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Sample records for inhibit lipid peroxidation

  1. Phytic Acid Inhibits Lipid Peroxidation In Vitro

    PubMed Central

    Węglarz, Ludmiła; Dzierżewicz, Zofia

    2013-01-01

    Phytic acid (PA) has been recognized as a potent antioxidant and inhibitor of iron-catalyzed hydroxyl radical formation under in vitro and in vivo conditions. Therefore, the aim of the present study was to investigate, with the use of HPLC/MS/MS, whether PA is capable of inhibiting linoleic acid autoxidation and Fe(II)/ascorbate-induced peroxidation, as well as Fe(II)/ascorbate-induced lipid peroxidation in human colonic epithelial cells. PA at 100 μM and 500 μM effectively inhibited the decay of linoleic acid, both in the absence and presence of Fe(II)/ascorbate. The observed inhibitory effect of PA on Fe(II)/ascorbate-induced lipid peroxidation was lower (10–20%) compared to that of autoxidation. PA did not change linoleic acid hydroperoxides concentration levels after 24 hours of Fe(II)/ascorbate-induced peroxidation. In the absence of Fe(II)/ascorbate, PA at 100 μM and 500 μM significantly suppressed decomposition of linoleic acid hydroperoxides. Moreover, PA at the tested nontoxic concentrations (100 μM and 500 μM) significantly decreased 4-hydroxyalkenal levels in Caco-2 cells which structurally and functionally resemble the small intestinal epithelium. It is concluded that PA inhibits linoleic acid oxidation and reduces the formation of 4-hydroxyalkenals. Acting as an antioxidant it may help to prevent intestinal diseases induced by oxygen radicals and lipid peroxidation products. PMID:24260736

  2. Triacontanol inhibits both enzymatic and nonenzymatic lipid peroxidation.

    PubMed

    Ramanarayan, K; Bhat, A; Shripathi, V; Swamy, G S; Rao, K S

    2000-09-01

    The effect of the plant growth regulator, triacontanol (TRIA) on lipid peroxidation was studied in three different systems: (i) isolated chloroplasts of spinach (Spinacea oleracea L.) leaves; (ii) egg lecithin liposomes; and (iii) soybean lipoxygenase (LOX) system. The nonenzymatic lipid peroxidation in isolated chloroplasts and egg lecithin liposomes was measured as the amount of thiobarbituric acid reactive substances (TBARS) formed. Inhibition of Fe2+ and/or light-induced lipid peroxidation by TRIA was observed in both isolated chloroplasts and egg lecithin liposomes. The kinetics of soybean lipoxygenase-1 (LOX-1) was studied using linoleic acid as the substrate. The enzyme was competitively inhibited by TRIA. The Ki for TRIA inhibition of the enzyme was estimated to be 3.2-5.0 microM according to different methods of estimation. TRIA has been known to exhibit anti-inflammatory action in animals and this anti-inflammatory effect of TRIA might be mediated through inhibition of lipid peroxidation. Since LOX inhibitors have been extensively used as therapeutic agents, TRIA, being a natural compound has been suggested to be an effective anti-inflammatory drug. PMID:11021645

  3. Synthesis of benzylideneacetophenones and their inhibition of lipid peroxidation.

    PubMed

    Arty, I S; Timmerman, H; Samhoedi, M; Sastrohamidjojo; Sugiyanto; van der Goot, H

    2000-04-01

    A series of benzylideneacetophenone derivatives have been synthesized and found to show potent inhibition of the lipid peroxidation (LPO) in rat liver microsomes. All 19 compounds prepared in this series are LPO inhibitors. The highest activity was found in para hydroxy derivatives with two meta tert-butyl substituents. PMID:10858605

  4. Inhibition of nonenzymic lipid peroxidation by benzylisoquinoline alkaloids.

    PubMed

    Martínez, L A; Ríos, J L; Payá, M; Alcaraz, M J

    1992-01-01

    A group of benzylisoquinoline alkaloids, including five simple benzylisoquinolines, three phtalideisoquinolines, six aporphines, three protoberberines, and two benzophenanthridines, have been studied as inhibitors of lipid peroxidation stimulated by Fe2+/cysteine in rat liver microsomal fractions. Protopapaverine, apomorphine, laudanosoline, tetrahydroberberine, isoboldine, bulbocapnine, boldine, anonaine, glaucine, and stepholidine showed antiperoxidative effects, and structure-activity relationships were established. In simple benzylisoquinolines, the presence of phenolic hydroxyls or similar reactive groups is necessary for inhibition of peroxidation, while in aporphines and protoberberines nonhydroxylated compounds can exert antiperoxidative effects. The phtalideisoquinolines and benzophenanthridines tested were inactive. PMID:1577331

  5. Lipid bilayer membrane affinity rationalizes inhibition of lipid peroxidation by a natural lignan antioxidant.

    PubMed

    Podloucká, Pavlína; Berka, Karel; Fabre, Gabin; Paloncýová, Markéta; Duroux, Jean-Luc; Otyepka, Michal; Trouillas, Patrick

    2013-05-01

    Lipid peroxidation is a degenerative oxidative process that modifies the structure of membranes, influencing their biological functions. Lignans, natural polyphenolic antioxidants widely distributed in plants, can prevent this membrane damage by free-radical scavenging. Here, we rationalize the difference in lipid peroxidation inhibition activity of argenteane, a natural dilignan isolated from wild nutmeg, and 3,3'-dimethoxy-1,1'-biphenyl-2,2'-diol, which represents the central part of argenteane responsible for its antioxidant activity. Although both compounds have the same capacity to scavenge free radicals, argenteane is a more active inhibitor of lipid peroxidation. We show that both compounds penetrate into DOPC and PLPC lipid bilayers and adopt similar positions and orientations, which therefore does not explain the difference in their lipid peroxidation inhibition activity. However, free energy profiles indicate that argenteane has a significantly higher affinity to the lipid bilayer, and thus a higher effective concentration to scavenge radicals formed during lipid peroxidation. This finding explains the higher activity of argenteane to inhibit lipid peroxidation. PMID:23560800

  6. Dihydrolipoic acid inhibits 15-lipoxygenase-dependent lipid peroxidation.

    PubMed

    Lapenna, Domenico; Ciofani, Giuliano; Pierdomenico, Sante Donato; Giamberardino, Maria Adele; Cuccurullo, Franco

    2003-11-15

    The potential antioxidant effects of the hydrophobic therapeutic agent lipoic acid (LA) and of its reduced form dihydrolipoic acid (DHLA) on the peroxidation of either linoleic acid or human non-HDL fraction catalyzed by soybean 15-lipoxygenase (SLO) and rabbit reticulocyte 15-lipoxygenase (RR15-LOX) were investigated. DHLA, but not LA, did inhibit SLO-dependent lipid peroxidation, showing an IC(50) of 15 microM with linoleic acid and 5 microM with the non-HDL fraction. In specific experiments performed with linoleic acid, inhibition of SLO activity by DHLA was irreversible and of a complete, noncompetitive type. In comparison with DHLA, the well-known lipoxygenase inhibitor nordihydroguaiaretic acid and the nonspecific iron reductant sodium dithionite inhibited SLO-dependent linoleic acid peroxidation with an IC(50) of 4 and 100 microM, respectively, while the hydrophilic thiol N-acetylcysteine, albeit possessing iron-reducing and radical-scavenging properties, was ineffective. Remarkably, DHLA, but not LA, was also able to inhibit the peroxidation of linoleic acid and of the non-HDL fraction catalyzed by RR15-LOX with an IC(50) of, respectively, 10 and 5 microM. Finally, DHLA, but once again not LA, could readily reduce simple ferric ions and scavenge efficiently the stable free radical 1,1-diphenyl-2-pycrylhydrazyl in ethanol; DHLA was considerably less effective against 2,2'-azobis(2-amidinopropane) dihydrochloride-mediated, peroxyl radical-induced non-HDL peroxidation, showing an IC(50) of 850 microM. Thus, DHLA, at therapeutically relevant concentrations, can counteract 15-lipoxygenase-dependent lipid peroxidation; this antioxidant effect may stem primarily from reduction of the active ferric 15-lipoxygenase form to the inactive ferrous state after DHLA-enzyme hydrophobic interaction and, possibly, from scavenging of fatty acid peroxyl radicals formed during lipoperoxidative processes. Inhibition of 15-lipoxygenase oxidative activity by DHLA could occur in

  7. Membrane lipid peroxidation: propagation and inhibition by antioxidants

    SciTech Connect

    Leung, H.W.

    1981-01-01

    Peroxidation studies in microsomes and liposomes were performed to evaluate the importance of the interaction between ascorbate and ..cap alpha..-tocopherol. The peroxidation of rat liver microsomes by FeSO/sub 4/ in the presence of ascorbate was delayed compared to when NADPH replaced ascorbate as the electron donor. To further investigate the cooperation between ascorbate and vitamin E, a liposomal system containing polyunsaturated phospholipids was used. Ascorbic acid alone (30 to 100 ..mu..M) delayed peroxidation by 20, and at higher concentrations, 60 minutes. Physiological levels of vitamin E decreased peroxidation at early times but was apparently consumed during incubation. Vitamin C and vitamin E together suppressed peroxidation at early times at approximately the sum of the individual inhibitions. At longer times, the mixture was more effective than the sum of both vitamins alone. The role of glutathione and the significance of its interaction with ascorbate were studied. Glutathione was able to reduce dehydroascorbic acid, but ascorbic acid was unable to reduce oxidized glutathione disulfide. Glutathione and ascorbic acid were oxidized by NO/sub 2/ in vitro. Pulmonary levels of glutathione and ascorbic acid in guinea pigs exposed to NO/sub 2/ were lowered. After the administration of diethyl maleate, the glutathione concentration was decreased, but the ascorbic acid concentration was unaffected. Simultaneous exposure further depressed glutathione concentration, but not the ascorbic acid concentration. (ERB)

  8. NADPH- and iron-dependent lipid peroxidation inhibit aromatase activity in human placental microsomes.

    PubMed

    Milczarek, Ryszard; Sokołowska, Ewa; Hallmann, Anna; Kaletha, Krystian; Klimek, Jerzy

    2008-06-01

    During pregnancy placenta is the most significant source of lipid hydroperoxides and other reactive oxygen species (ROS). The increased production of lipid peroxides and other ROS is often linked to pre-eclampsia. It is already proved that placental endoplasmic reticulum may be an important place of lipid peroxides and superoxide radical production. In the present study we revealed that NADPH- and iron-dependent lipid peroxidation in human placental microsomes (HPM) inhibit placental aromatase--a key enzyme of estrogen biosynthesis in human placenta. We showed that significant inhibition of this enzyme is caused by small lipid peroxidation (TBARS (thiobarbituric acid-reactive substances)<4nmol/mg microsomal protein (m.p.)). More intensive lipid peroxidation (TBARS>9nmol/mg microsomal protein) diminishes aromatase activity to value being less than 5% of initial value. NADPH- and iron-dependent lipid peroxidation also causes disappearance of cytochrome P450 parallel to observed aromatase activity inhibition. EDTA, alpha-tocopherol, MgCl(2) and superoxide dismutase (SOD) prevent aromatase activity inhibition and cytochrome P450(AROM) degradation. Mannitol and catalase have not effect on TBARS synthesis, aromatase activity and cytochrome P450 degradation. In view of the above we postulate that the inhibition of aromatase activity observed is mainly a consequence of cytochrome P450(AROM) degradation induced by lipid radicals. The role of hydroxyl radical in cytochrome P450 degradation is negligible in our experimental conditions. The results presented here also suggest that the inhibition of aromatase activity can also take place in placenta at in vivo conditions. PMID:18499441

  9. Inhibition of xanthine oxidase-xanthine-iron mediated lipid peroxidation by eugenol in liposomes.

    PubMed

    Nagababu, E; Lakshmaiah, N

    1997-01-01

    The effect of eugenol on xanthine oxidase (XO) xanthine(X)-Fe+3-ADP mediated lipid peroxidation was studied in liver microsomal lipid liposomes. Eugenol inhibited the lipid peroxidation in a dose dependent manner as assessed by formation of thiobarbituric acid reactive substances. When tested for its effect on XO activity per se, (by measuring uric acid formation) eugenol inhibited the enzyme to an extent of 85% at 10 microm concentration and hence formation of O2.- also. However, the concentration of eugenol required for XO inhibition was more in presence of metal chelators such as EDTA, EGTA and DETAPAC, but not in presence of deferoxamine, ADP and citrate. The antiperoxidative effect of eugenol was about 35 times more and inhibition of XO was about 5 times higher as compared to the effect of allopurinol. Eugenol did not scavenge O2.- generated by phenazine methosulfate and NAD but inhibited propagation of peroxidation catalyzed by Fe2+ EDTA and lipid hydroperoxide containing liposomes. Eugenol inhibits XO-X-Fe+3 ADP mediated peroxidation by inhibiting the XO activity per se in addition to quenching various radical species. PMID:9046022

  10. Inhibition of lipid peroxidation by ternatin, a tetramethoxyflavone from Egletes viscosa L.

    PubMed

    Souza, M F; Rao, V S; Silveira, E R

    1997-03-01

    Ternatin, the 4',5-dihydroxy-3,3',7,8-tetramethoxyflavone from Egletes viscosa L. (Asteraceae) was evaluated for its antiperoxidative effect against lipid peroxidation using CCl(4)-induced hepatotoxicity and adriamycin-induced hind-paw edema in mice as test models. An increase of melondialdehyde (MDA), a product of lipid peroxidation in liver homogenates and marked elevations of serum ALT, AST and HDL were detected 1 day after carbon tetrachloride (CCl(4)) administration. These increases were significantly inhibited in ternatin (25 and 50mg/kg i. p.) pretreated mice in a dose dependent way. Also, ternatin at a dose of 50 mg/kg but not at 25 mg/kg caused a significant inhibition of hind-paw edema induced by adriamycin, in a manner similar to vitamin E (300 mg/kg, p. o.), a compound known to be highly effective in protecting against membrane lipid peroxidation. These observations provide in vivo evidence of an antiperoxidative property of ternatin and suggest that it may offer therapeutic potential for the control of lipid peroxided mediated pathologies. PMID:23195242

  11. Inhibition of protein carbonyl formation and lipid peroxidation by glutathione in rat liver microsomes.

    PubMed

    Palamanda, J R; Kehrer, J P

    1992-02-14

    The peroxidation of rat liver microsomal lipids is stimulated in the presence of iron by the addition of NADPH or ascorbate and is inhibited by the addition of glutathione (GSH). The fate of GSH and the oxidative modification of proteins under these conditions have not been well studied. Rat liver microsomes were incubated at 37 degrees C under 95% O2:5% CO2 in the presence of 10 microM ferric chloride, 400 microM ADP, and either 450 microM ascorbic acid or 400 microM NADPH. Lipid peroxidation was assessed in the presence 0, 0.2, 0.5, 1, or 5 mM GSH by measuring thiobarbituric acid reactive substance (TBARS) and oxidative modification of proteins by measuring protein thiol and carbonyl groups. GSH inhibited TBARS and protein carbonyl group formation in both ascorbate and NADPH systems in a dose-dependent manner. Heat denaturing of microsomes or treatment with trypsin resulted in the loss of this protection. The formation of protein carbonyl groups could be duplicated by incubating microsomes with 4-hydroxynonenal. Ascorbate-dependent peroxidation caused a loss of protein thiol groups which was diminished by GSH only in fresh microsomes. Both boiling and trypsin treatment significantly decreased the basal protein thiol content of microsomes and enhanced ascorbate-stimulated lipid peroxidation. Protection against protein carbonyl group formation by GSH correlated with the inhibition of lipid peroxidation and appeared not to be due to the formation of the GSH conjugate of 4-hydroxynonenal as only trace amounts of this conjugate were detected. Ninety percent of the GSH lost after 60 min of peroxidation was recoverable as borohydride reducible material in the supernatant fraction. The remaining 10% could be accounted for as GSH-bound protein mixed disulfides. However, only 75% of the GSH lost during peroxidation appeared as glutathione disulfide, suggesting that some was converted to other soluble borohydride reducible forms. These data support a role for protein thiol

  12. Acetaminophen inhibits hemoprotein-catalyzed lipid peroxidation and attenuates rhabdomyolysis-induced renal failure

    PubMed Central

    Boutaud, Olivier; Moore, Kevin P.; Reeder, Brandon J.; Harry, David; Howie, Alexander J.; Wang, Shuhe; Carney, Clare K.; Masterson, Tina S.; Amin, Taneem; Wright, David W.; Wilson, Michael T.; Oates, John A.; Roberts, L. Jackson

    2010-01-01

    Hemoproteins, hemoglobin and myoglobin, once released from cells can cause severe oxidative damage as a consequence of heme redox cycling between ferric and ferryl states that generates radical species that induce lipid peroxidation. We demonstrate in vitro that acetaminophen inhibits hemoprotein-induced lipid peroxidation by reducing ferryl heme to its ferric state and quenching globin radicals. Severe muscle injury (rhabdomyolysis) is accompanied by the release of myoglobin that becomes deposited in the kidney, causing renal injury. We previously showed in a rat model of rhabdomyolysis that redox cycling between ferric and ferryl myoglobin yields radical species that cause severe oxidative damage to the kidney. In this model, acetaminophen at therapeutic plasma concentrations significantly decreased oxidant injury in the kidney, improved renal function, and reduced renal damage. These findings also provide a hypothesis for potential therapeutic applications for acetaminophen in diseases involving hemoprotein-mediated oxidative injury. PMID:20133658

  13. Inhibition of lipid peroxidation by extracts/subfractions of Chickrassy ( Chukrasia tabularis A. Juss.)

    NASA Astrophysics Data System (ADS)

    Kaur, Rajbir; Thind, Tarunpreet Singh; Singh, Bikram; Arora, Saroj

    2009-01-01

    Polyphenols and polyphenol-rich fractions of plants have been reported to have protective effects against lipid peroxidation, most probably by serving as scavengers of free radicals and/or by chelating metal ions. In the present study, the effect of different extracts/subfractions of Chickrassy ( Chukrasia tabularis) on peroxyl radical mediated damage to the polyunsaturated fatty acids was investigated. Liver homogenate was used as experimental material. The production of malondialdehyde served as a marker of lipid peroxidation and oxidative stress. It was observed that polyphenol-rich fractions, particularly the ethyl acetate fractions of bark and leaves, showed the highest protective activity of 83.02% and 88.62% inhibition, respectively. This study will help in knowing the scientific validation of this plant, for its use in ayurvedic formulations.

  14. Inhibition by the bioflavonoid ternatin of aflatoxin B1-induced lipid peroxidation in rat liver.

    PubMed

    Souza, M F; Tomé, A R; Rao, V S

    1999-02-01

    Aflatoxin B1, a metabolite of Aspergillus flavus is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damage are the principal manifestations of aflatoxin B1-induced toxicity which could be mitigated by antioxidants. Many plant constituents, e.g. flavonoids, lignans and spice principles (capsaicin, curcumin, eugenol, etc.) have been reported to prevent liver damage associated with lipid peroxidation. In this study we investigated ternatin, a tetramethoxyflavone isolated from Egletes viscosa, for possible protection against liver injury induced by aflatoxin B1 in rats. Seventy two hours after a single intraperitoneal dose of aflatoxin B1 (1 mg kg(-1)), the concentration of malondialdehyde, the product of lipid peroxidation in liver homogenates, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly elevated (P<0.001). Subcutaneous ternatin (25 mg kg(-1)) pretreatment greatly reduced aflatoxin B1-induced increases in the levels of serum enzymes (ALT from 5071+/-763 to 293+/-66 international units L(-1) and AST from 4241+/-471 to 449+/-108 international units L(-1)) and elevated malondialdehyde levels (from 11.37+/-1.27 to 0.79+/-0.22 nmol (mg wet tissue)(-1)) in a manner similar to oral vitamin E (300 mg kg(-1)), a standard antioxidant. Further, histological changes induced by aflatoxin B1 such as hepatocellular necrosis and bile-duct proliferation were markedly inhibited in animals pretreated with ternatin or vitamin E. These data provide evidence that ternatin inhibits lipid peroxidation and affords protection against liver damage induced by aflatoxin B1. Ternatin might, therefore, be a suitable candidate for the chemoprevention of aflatoxicosis associated liver cancer. PMID:10217309

  15. Vitamin E reduces glucocorticoid-induced growth inhibition and lipid peroxidation in rats.

    PubMed

    Ohtsuka, A; Ohtani, T; Horiguchi, H; Kojima, H; Hayashi, K

    1998-04-01

    This experiment was conducted to study the effects of vitamin E on growth inhibition and lipid peroxidation in rats treated with different levels of corticosterone (CTC). Rats (Sprague-Dawley strain, 5 weeks of age) were divided into two groups: control group receiving a basal diet containing 60 mg DL-alpha-tocopheryl acetate/kg diet, and vitamin E group receiving the same diet supplemented with 5,000 mg tocopherol. After 6 days, rats of both diet groups were further divided into three groups by dose levels of CTC treatment (0, 25, and 100 mg CTC/kg body weight/d). CTC was administered to the rats by subcutaneous injection for 4 d. Growth was dose-dependently inhibited by the CTC treatment. Feeding the vitamin E diet significantly (p < 0.05) improved growth retardation. Feed efficiency was lowered by CTC treatment, while this was significantly (p < 0.05) minimized by feeding the vitamin E diet. Lipid peroxidation (TBARS) in the liver was elevated by the CTC treatment (p < 0.001) when the rats were fed the basal diet. The increment in TBARS was significantly (p < 0.001) reduced by vitamin E. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly reduced by the CTC treatment in a dose-dependent manner in both dietary groups. Feeding vitamin E significantly (p < 0.001) improved the reduction in GST activity. The SOD activity showed some tendency. The present results demonstrate the effectiveness of vitamin E in improving growth retardation in glucocorticoid-treated rats and suggest that reductions in increased lipid peroxidation due to CTC may be an important factor of the action of vitamin E. PMID:9675704

  16. Antioxidant activity of tetrandrine and its inhibition of quartz-induced lipid peroxidation.

    PubMed

    Shi, X; Mao, Y; Saffiotti, U; Wang, L; Rojanasakul, Y; Leonard, S S; Vallyathan, V

    1995-10-01

    Tetrandrine is a benzylisoquinoline alkaloid that has been used in China as an antifibrotic drug to treat the lesions of silicosis. Its mechanism in the treatment of silicosis is unclear. Electron spin resonance (ESR) spin trapping was employed to investigate the antioxidant properties of tetrandrine. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide (DMPO). Tetrandine efficiently reacted with hydroxyl (.OH) radicals with a reaction rate of approximately 1.4 x 10(10) M-1 s-1. The .OH radicals were generated by the Fenton reaction [Fe(II) + H2O2) as well as by reaction of chromium(V) with H2O2. Similar results were obtained using .OH radicals generated by reaction of freshly fractured quartz particles with aqueous medium. Tetrandrine also scavenged superoxide (O2-) radicals produced from xanthine/xanthine oxidase. The effect of tetrandrine on lipid peroxidation induced by freshly fractured quartz particles was evaluated using linoleic acid as a model lipid. The results showed that tetrandrine caused a significant inhibition on freshly fractured quartz-induced lipid peroxidation. PMID:7563220

  17. Inhibition of iron-induced lipid peroxidation by newly identified bacterial carotenoids in model gastric conditions: comparison with common carotenoids.

    PubMed

    Sy, Charlotte; Caris-Veyrat, Catherine; Dufour, Claire; Boutaleb, Malika; Borel, Patrick; Dangles, Olivier

    2013-04-30

    Newly identified spore-forming pigmented marine bacteria, Bacillus indicus HU36 and Bacillus firmus GB1, are sources of carotenoids (mainly 15 yellow and orange pigments and 13 pink pigments, respectively) with original structures. These bacterial carotenoids were evaluated for their ability to inhibit the iron-induced peroxidation of linoleic acid micelles, or sunflower oil-in-water emulsions, in comparison with β-carotene, lycopene and astaxanthin. Lipid peroxidation was carried out in acidic conditions and initiated by dietary heme or non-heme iron (metmyoglobin or Fe(II), respectively) so as to simply simulate the postprandial gastric medium, a possible site for dietary oxidative stress. Lipid hydroperoxide formation and carotenoid consumption were followed by UV-vis spectroscopy and appropriate indicators of the antioxidant activity were estimated in each model. The bacterial carotenoids were found to be better inhibitors of heme-induced lipid peroxidation than the reference carotenoids as a likely consequence of their location closer to the interface in micelles and lipid droplets. However, this trend was not confirmed in lipid peroxidation induced by non-heme iron, possibly because of the redox recycling of Fe(II) by carotenoids. The quantitative kinetic analysis of the peroxidation curves suggests that the carotenoids mainly inhibit the propagation phase of lipid peroxidation by direct scavenging of the lipid peroxyl radicals, in agreement with independent experiments showing that carotenoids are unable to reduce the one-electron oxidized form of metmyoglobin (ferrylmyoglobin), a model of initiating species in heme-induced lipid peroxidation. Overall, carotenoids from Bacillus indicus HU36 and Bacillus firmus GB1 were found to be interesting antioxidants to fight postprandial oxidative stress in the stomach. PMID:23411789

  18. Lipid peroxidation and coupled vitamin oxidation in simulated and human gastric fluid inhibited by dietary polyphenols: health implications.

    PubMed

    Gorelik, Shlomit; Lapidot, Tair; Shaham, Inbal; Granit, Rina; Ligumsky, Moshe; Kohen, Ron; Kanner, Joseph

    2005-05-01

    The Western diet contains large quantities of oxidized lipids, because a large proportion of the food in the diet is consumed in a fried, heated, processed, or stored form. We investigated the reaction that could occur in the acidic pH of the stomach and accelerate the generation of lipid hydroperoxides and cooxidation of dietary vitamins. To estimate the oxygen content in the stomach after food consumption, oxygen released from masticated bread (20 g) into deoxygenated water (100 mL) was measured. Under these conditions, the oxygen concentration rose by 250 microM and reached a full oxygen saturation. The present study demonstrated that heated red meat homogenized in human gastric fluid, at pH 3.0, generated hydroperoxides and malondialdehyde. The cross-reaction between free radicals produced during this reaction cooxidized vitamin E, beta-carotene, and vitamin C. Both lipid peroxidation and cooxidation of vitamin E and beta-carotene were inhibited at pH 3.0 by red wine polyphenols. Ascorbic acid (44 mg) at a concentration that represented the amount that could be ingested during a meal inhibited lipid peroxidation only slightly. Red wine polyphenols failed to prevent ascorbic acid oxidation significantly but, in conjunction with ascorbic acid, did inhibit lipid peroxidation. In the presence of catechin, a well-known polyphenol found in red wine, ascorbic acid at pH 3.0 works in a synergistic manner preventing lipid peroxidation and beta-carotene cooxidation. The present data may explain the major benefits to our health and the crucial role of consuming food products rich in dietary antioxidants such as fruits, vegetables, red wines, or green tea during the meal. PMID:15853378

  19. 4-hydroxynonenal, a lipid peroxidation product, rapidly accumulates following traumatic spinal cord injury and inhibits glutamate uptake.

    PubMed

    Springer, J E; Azbill, R D; Mark, R J; Begley, J G; Waeg, G; Mattson, M P

    1997-06-01

    Traumatic injury to the spinal cord initiates a host of pathophysiological events that are secondary to the initial insult. One such event is the accumulation of free radicals that damage lipids, proteins, and nucleic acids. A major reactive product formed following lipid peroxidation is the aldehyde, 4-hydroxynonenal (HNE), which cross-links to side chain amino acids and inhibits the function of several key metabolic enzymes. In the present study, we used immunocytochemical and immunoblotting techniques to examine the accumulation of protein-bound HNE, and synaptosomal preparations to study the effects of spinal cord injury and HNE formation on glutamate uptake. Protein-bound HNE increased in content in the damaged spinal cord at early times following injury (1-24 h) and was found to accumulate in myelinated fibers distant to the site of injury. Immunoblots revealed that protein-bound HNE levels increased dramatically over the same postinjury interval. Glutamate uptake in synaptosomal preparations from injured spinal cords was decreased by 65% at 24 h following injury. Treatment of control spinal cord synaptosomes with HNE was found to decrease significantly, in a dose-dependent fashion, glutamate uptake, an effect that was mimicked by inducers of lipid peroxidation. Taken together, these findings demonstrate that the lipid peroxidation product HNE rapidly accumulates in the spinal cord following injury and that a major consequence of HNE accumulation is a decrease in glutamate uptake, which may potentiate neuronal cell dysfunction and death through excitotoxic mechanisms. PMID:9166741

  20. Lipid peroxide formation in microsomes. Relationship of hydroxylation to lipid peroxide formation

    PubMed Central

    Wills, E. D.

    1969-01-01

    1. Aminopyrine strongly inhibits NADPH-induced lipid peroxide formation in rat liver microsomes, but ascorbate-induced peroxidation is inhibited to a smaller extent. 2. Aminopyrine oxidation is stimulated by Mg2+ but inhibited by Ca2+. Concentrated solutions (10mm) of iron-chelating agents inhibit aminopyrine oxidation, but the more dilute solutions (0·5mm) of chelators that block lipid peroxide formation do not inhibit aminopyrine oxidation. Microsomes prepared from sucrose–EDTA homogenates rapidly oxidize aminopyrine, but do not form lipid peroxide when incubated with ascorbate or NADPH. 3. Aminopyrine oxidation is strongly inhibited by p-chloromercuribenzoate, less by iodoacetamide and weakly by N-ethylmaleimide. The site of action of these compounds is considered to be a ferredoxin-type protein. GSH and cysteine also inhibit. 4. Other drugs oxidized by microsomes such as caffeine, phenobarbitone and hexobarbitone had either no or little effect on lipid peroxide formation, but codeine inhibited. 5. Most aliphatic hydrocarbons, alcohols, ketones and aldehydes did not affect lipid peroxide formation, but chloroform and carbon tetrachloride inhibited. 6. Many aromatic compounds inhibited lipid peroxide formation. Only aromatic acids were without any effect and phenols and amines were very strong inhibitors. 7. Induction of lipid peroxide formation in microsomes by incubation with ascorbate or NADPH or by treatment with ionizing radiation leads to a sharp decline in the ability of microsomes to oxidize aminopyrine or hydroxylate aniline. 8. It is considered that the two processes of hydroxylation and lipid peroxide formation are closely linked in microsomes. They probably depend on the same electron-transport chain, and peroxide formation, which involves membrane disintegration, may be part of the normal membrane remodelling process. PMID:4390103

  1. Essential oil from lemon peels inhibit key enzymes linked to neurodegenerative conditions and pro-oxidant induced lipid peroxidation.

    PubMed

    Oboh, Ganiyu; Olasehinde, Tosin A; Ademosun, Ayokunle O

    2014-01-01

    This study sought to investigate the effects of essential oil from lemon (Citrus limoni) peels on acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities in vitro. The essential oil was extracted by hydrodistillation, dried with anhydrous Na2SO4 and characterized using gas chromatography. Antioxidant properties of the oil and inhibition of pro-oxidant-induced lipid peroxidation in rats brain homogenate were also assessed. The essential oil inhibited AChE and BChE activities in a concentration-dependent manner. GC analysis revealed the presence of sabinene, limonene, α-pinene, β-pinene, neral, geranial, 1,8-cineole, linalool, borneol, α-terpineol, terpinen-4-ol, linalyl acetate and β-caryophyllene. Furthermore, the essential oil exhibited antioxidant activities as typified by ferric reducing property, Fe(2+)-chelation and radicals [DPPH, ABTS, OH, NO] scavenging abilities. The inhibition of AChE and BChE activities, inhibition of pro-oxidant induced lipid peroxidation and antioxidant activities could be possible mechanisms for the use of the essential oil in the management and prevention of oxidative stress-induced neurodegeneration. PMID:24599102

  2. Lipid peroxidation and tissue damage.

    PubMed

    Mylonas, C; Kouretas, D

    1999-01-01

    In recent years it has become apparent that the oxidation of lipids, or lipid peroxidation, is a crucial step in the pathogenesis of several disease states in adult and infant patients. Lipid peroxidation is a process generated naturally in small amounts in the body, mainly by the effect of several reactive oxygen species (hydroxyl radical, hydrogen peroxide etc.). It can also be generated by the action of several phagocytes. These reactive oxygen species readily attack the polyunsaturated fatty acids of the fatty acid membrane, initiating a self-propagating chain reaction. The destruction of membrane lipids and the end-products of such lipid peroxidation reactions are especially dangerous for the viability of cells, even tissues. Enzymatic (catalase, superoxide dismutasse) and nonenzymatic (vitamins A and E) natural antioxidant defence mechanisms exist; however, these mechanisms may be overcome, causing lipid peroxidation to take place. Since lipid peroxidation is a self-propagating chain-reaction, the initial oxidation of only a few lipid molecules can result in significant tissue damage. Despite extensive research in the field of lipid peroxidation it has not yet been precisely determined if it is the cause or an effect of several pathological conditions. Lipid peroxidation has been implicated in disease states such as atherosclerosis, IBD, ROP, BPD, asthma, Parkinson's disease, kidney damage, preeclampsia and others. PMID:10459507

  3. Inhibition of oxidative stress and lipid peroxidation by anthocyanins from defatted Canarium odontophyllum pericarp and peel using in vitro bioassays.

    PubMed

    Khoo, Hock Eng; Azlan, Azrina; Ismail, Amin; Abas, Faridah; Hamid, Muhajir

    2014-01-01

    Canarium odontophyllum, also known as CO, is a highly nutritious fruit. Defatted parts of CO fruit are potent sources of nutraceutical. This study aimed to determine oxidative stress and lipid peroxidation effects of defatted CO pericarp and peel extracts using in vitro bioassays. Cell cytotoxic effect of the CO pericarp and peel extracts were also evaluated using HUVEC and Chang liver cell lines. The crude extracts of defatted CO peel and pericarp showed cytoprotective effects in t-BHP and 40% methanol-induced cell death. The crude extracts also showed no toxic effect to Chang liver cell line. Using CD36 ELISA, NAD(+) and LDL inhibition assays, inhibition of oxidative stress were found higher in the crude extract of defatted CO peel compared to the pericarp extract. Hemoglobin and LDL oxidation assays revealed both crude extracts had significantly reduced lipid peroxidation as compared to control. TBARS values among defatted CO pericarp, peel, and cyanidin-3-glucoside showed no significant differences for hemoglobin and LDL oxidation assays. The protective effects of defatted CO parts, especially its peel is related to the presence of high anthocyanin that potentially offers as a pharmaceutical ingredient for cardioprotection. PMID:24416130

  4. Curcumin Blocks Naproxen-Induced Gastric Antral Ulcerations through Inhibition of Lipid Peroxidation and Activation of Enzymatic Scavengers in Rats.

    PubMed

    Kim, Jeong-Hwan; Jin, Soojung; Kwon, Hyun Ju; Kim, Byung Woo

    2016-08-28

    Curcumin is a polyphenol derived from the plant Curcuma longa, which is used for the treatment of diseases associated with oxidative stress and inflammation. The present study was undertaken to determine the protective effect of curcumin against naproxen-induced gastric antral ulcerations in rats. Different doses (10, 50, and 100 mg/kg) of curcumin or vehicle (curcumin, 0 mg/kg) were pretreated for 3 days by oral gavage, and then gastric mucosal lesions were caused by 80 mg/kg naproxen applied for 3 days. Curcumin significantly inhibited the naproxen-induced gastric antral ulcer area and lipid peroxidation in a dose-dependent manner. In addition, curcumin markedly increased activities of radical scavenging enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase in a dose-dependent manner. Specifically, 100 mg/kg curcumin completely protected the gastric mucosa against the loss in the enzyme, resulting in a drastic increase of activities of radical scavenging enzymes up to more than the level of untreated normal rats. Histological examination obviously showed that curcumin prevents naproxen-induced gastric antral ulceration as a result of direct protection of the gastric mucosa. These results suggest that curcumin blocks naproxen-induced gastric antral ulcerations through prevention of lipid peroxidation and activation of radical scavenging enzymes, and it may offer a potential remedy of gastric antral ulcerations. PMID:27197667

  5. PHARMACOLOGICAL INHIBITION OF LIPID PEROXIDATION ATTENUATES CALPAIN-MEDIATED CYTOSKELETAL DEGRADATION AFTER TRAUMATIC BRAIN INJURY

    PubMed Central

    Mustafa, Ayman G.; Wang, Juan A.; Carrico, Kimberly M.; Hall, Edward D.

    2011-01-01

    Free radical-induced lipid peroxidation (LP) is critical in the evolution of secondary injury following traumatic brain injury (TBI). Previous studies in our laboratory demonstrated that U-83836E, a potent LP inhibitor, can reduce post-TBI LP along with an improved maintenance of mouse cortical mitochondrial bioenergetics and calcium (Ca++) buffering following severe (1.0 mm; 3.5 m/sec) controlled cortical impact TBI (CCI-TBI). Based upon this preservation of a major Ca++ homeostatic mechanism, we have now performed dose-response and therapeutic window analyses of the ability of U-83836e to reduce posttraumatic calpain-mediated cytoskeletal (α-spectrin) proteolysis in ipsilateral cortical homogenates at its 24 h post-TBI peak. In the dose-response analysis, mice were treated with a single i.v. dose of vehicle or U-83836e (0.1, 0.3, 1.3, 3.0, 10.0 or 30.0 mg/kg) at 15 min. after injury. U-83836e produced a dose-related attenuation of α-spectrin degradation with the maximal decrease being achieved at 3.0 mg/kg. Next, the therapeutic window was tested by delaying the single 3 mg/kg i.v. dose from 15 min. post-injury out to 1, 3, 6 or 12 h. No reduction in α-spectrin degradation was observed when the treatment delay was 1 h or longer. However, in a third experiment, we re-examined the window with repeated U-83836e dosing (3.0 mg/kg i.v. followed by 10 mg/kg i.p. maintenance doses at 1 and 3 h after the initial i.v. dose) which significantly reduced 24 h α-α-spectrin degradation even when treatment initiation was withheld until 12 h post-TBI. These results demonstrate the relationship between post-TBI LP, disruptions in neuronal Ca++ homeostasis and calpain-mediated cytoskeletal damage. PMID:21361959

  6. Crocidolite-induced lipid peroxidation. II. Role of antioxidants

    SciTech Connect

    Gulumian, M.; Kilroe-Smith, T.A.

    1987-12-01

    Asbestos fibers in vitro produce lipid peroxidation in rat lung microsomes. Butylated hydroxytoluene prevented this peroxidation. Ascorbate in low concentrations enhanced peroxidation of lipids but inhibited it at concentrations above 4 mmole/liter so that it partially protected membrane lipids from peroxidation produced by asbestos fibers. Reduced glutathione added to microsomes gave increased peroxidation at increased concentrations up to 20 mmol/liter. At 40 mmol/liter peroxidation was prevented. Glutathione had no obvious effect on the level of peroxidation produced by asbestos fibers. The 105,000g supernatant cell fraction added either with or without glutathione gave a decrease in the amount of lipid peroxidation produced by asbestos fibers. The protective action of these reducing agents suggests a possible use as prophylactic agents against the harmful effects of inhaled asbestos.

  7. Topical alpha-tocotrienol supplementation inhibits lipid peroxidation but fails to mitigate increased transepidermal water loss after benzoyl peroxide treatment of human skin.

    PubMed

    Weber, Stefan U; Thiele, Jens J; Han, Nancy; Luu, Chate; Valacchi, Giuseppe; Weber, Stefanie; Packer, Lester

    2003-01-15

    Benzoyl peroxide (BPO) is a commonly used drug in the treatment of acne vulgaris, but it induces unwanted side effects related to stratum corneum (SC) function. Since it has been recently shown to oxidize SC antioxidants, it was hypothesized that antioxidant supplementation may mitigate the BPO-induced SC changes. To test this, 11 subjects were selected to be topically supplemented with alpha-tocotrienol (5% w/vol) for 7 d on defined regions of the upper back, while the contralateral region was used for vehicle-only controls. Starting on day 8, all test sites were also treated with BPO (10%) for 7 d; the alpha-tocotrienol supplementation was continued throughout the study. A single dose of BPO depleted 93.2% of the total vitamin E. While continuing the BPO exposure for 7 d further depleted vitamin E in both vehicle-only and alpha-tocotrienol-treated sites, significantly more vitamin E remained in the alpha-tocotrienol-treated areas. Seven BPO applications increased lipid peroxidation. Alpha-tocotrienol supplementation significantly mitigated the BPO-induced lipid peroxidation. The transepidermal water loss was increased 1.9-fold by seven BPO applications, while there was no difference between alpha-tocotrienol treatment and controls. The data suggest that alpha-tocotrienol supplementation counteracts the lipid peroxidation but not the barrier perturbation in the SC induced by 10% BPO. PMID:12521598

  8. Antioxidant effect of bisphosphonates and simvastatin on chondrocyte lipid peroxidation

    SciTech Connect

    Dombrecht, E.J.; De Tollenaere, C.B.; Aerts, K.; Cos, P.; Schuerwegh, A.J.; Bridts, C.H.; Van Offel, J.F.; Ebo, D.G.; Stevens, W.J. . E-mail: immuno@ua.ac.be; De Clerck, L.S.

    2006-09-22

    The objective of this study was to evaluate the effect of bisphosphonates (BPs) and simvastatin on chondrocyte lipid peroxidation. For this purpose, a flow cytometrical method using C11-BODIPY{sup 581/591} was developed to detect hydroperoxide-induced lipid peroxidation in chondrocytes. Tertiary butylhydroperoxide (t-BHP) induced a time and concentration dependent increase in chondrocyte lipid peroxidation. Addition of a Fe{sup 2+}/EDTA complex to t-BHP or hydrogen peroxide (H{sub 2}O{sub 2}) clearly enhanced lipid peroxidation. The lipophilic simvastatin demonstrated a small inhibition in the chondrocyte lipid peroxidation. None of three tested BPs (clodronate, pamidronate, and risedronate) had an effect on chondrocyte lipid peroxidation induced by t-BHP. However, when Fe{sup 2+}/EDTA complex was added to t-BHP or H{sub 2}O{sub 2}, BPs inhibited the lipid peroxidation process varying from 25% to 58%. This study demonstrates that BPs have antioxidant properties as iron chelators, thereby inhibiting the chondrocyte lipid peroxidation. These findings add evidence to the therapeutic potential of bisphosphonates and statins in rheumatoid arthritis.

  9. Inhibiting LDL glycation ameliorates increased cholesteryl ester synthesis in macrophages and hypercholesterolemia and aortic lipid peroxidation in streptozotocin diabetic rats

    PubMed Central

    Cohen, Margo P.; Shea, Elizabeth A.; Wu, Van-Yu

    2009-01-01

    Increased nonenzymatic glycation of apoB-containing lipoproteins impairs uptake and metabolism by the high affinity low density lipoprotein (LDL) receptor, and is one of the post-secretory modifications contributory to accelerated atherosclerosis in diabetes. The present study evaluated in vitro and in vivo effects of 2,2-chlorophenylaminophenylacetate (CAP22) to probe the influence of glycated lipoprotein on cholesterol homeostasis. This compound prevented the increased formation of glycated products in LDL incubated with 200 mM glucose and the increased cholesteryl ester synthesis in THP-1 macrophages induced by apoB-containing lipoproteins preincubated with high glucose concentration. The elevated circulating concentrations of glycated lipoprotein and cholesterol and higher vascular levels of lipid peroxidation products observed in streptozotocin diabetic rats compared to nondiabetic controls were significantly reduced in diabetic animals treated for six months with test compound. These results are the first to demonstrate that inhibiting nonenzymatic glycation of apoB-containing lipoproteins ameliorates abnormalities contributory to hypercholesterolemia and atherogenic risk in diabetes. PMID:19922964

  10. Paraquat and NADPH-dependent lipid peroxidation in lung microsomes

    SciTech Connect

    Misra, H.P.; Gorsky, L.D.

    1981-10-10

    Since there exists some controversy in the literature as to whether paraquat augments microsomal lipid peroxidation via superoxide anion (O/sub 2//sup -/), the role of paraquat and active oxygen species in NADPH-dependent lung microsomal lipid peroxidation was investigated. Incubation of buffered aerobic mixture of bovine lung microsome and NADPH, in the presence or absence of exogenously added iron, resulted in a progressive formation of lipid peroxides whose accumulation could be followed at 535 nm as malondialdehyde. Paraquat strongly inhibited this lipid peroxidation, Thus, malondialydehyde formation was 50% inhibited by 4 X 10/sup -5/ M paraquat in the reaction mixture. The malondialdehyde color development by lipid peroxides was not affected by this concentration of paraquat. Lipid peroxidation was also strongly inhibited by singlet oxygen scavengers, e.g. dimethylfuran and diphenylfuran, and by catalase. Hydroxyl radical scavengers, e.g. mannitol, benzoate, and ethanol, had little effect in malondialydehyde production. Superoxide dismutase, which removes O/sub 2//sup -/ efficiently, did not inhibit malondialdehyde production by lung microsomes and rather enhanced its formation. A scheme in which paraquat and active O/sub 2/ species may be involved with microsomal lipid peroxidation is presented.

  11. Mechanism of inhibition of lipid peroxidation by gamma-terpinene, an unusual and potentially useful hydrocarbon antioxidant.

    PubMed

    Foti, Mario C; Ingold, K U

    2003-04-23

    gamma-Terpinene (TH), a monoterpene hydrocarbon present in essential oils, retards the peroxidation of linoleic acid (LH). The peroxidation of TH has been shown to yield p-cymene as the only organic product in a chain reaction in which the chain carrier is the hydroperoxyl radical, HOO(.). The peroxidation of LH is well-known to be a chain reaction in which the chains are carried by linoleylperoxyl radicals, LOO., and the products are linoleyl hydroperoxides. The retardation of LH peroxidation by TH has been found to be due to rapid chain termination via a very fast cross-reaction between HOO. and LOO. radicals. This antioxidant mechanism is completely different from the mechanism of antioxidant action of vitamin E. Since vitamin E becomes a prooxidant at high concentrations, the addition of essential oils containing TH to edible lipids may provide an alternative or supplementary strategy for obtaining large increases in their oxidative stability and shelf life, something that cannot be achieved by simply adding more and more vitamin E. PMID:12696969

  12. Lipocarbazole, an efficient lipid peroxidation inhibitor anchored in the membrane.

    PubMed

    Fabre, Gabin; Hänchen, Anne; Calliste, Claude-Alain; Berka, Karel; Banala, Srinivas; Otyepka, Michal; Süssmuth, Roderich D; Trouillas, Patrick

    2015-08-01

    Lipid peroxidation is a major deleterious effect caused by oxidative stress. It is involved in various diseases such as atherosclerosis, rheumatoid arthritis and neurodegenerative diseases. In order to inhibit lipid peroxidation, antioxidants must efficiently scavenge free radicals and penetrate inside biological membranes. Lipocarbazole has recently been shown to be a powerful antioxidant in solution. Here, we show its powerful capacity as lipid peroxidation inhibitor. Its mechanism of action is rationalized based on molecular dynamics simulations on a biomembrane model, quantum calculations and experimental evaluation. The role of the lipocarbazole side chain is particularly highlighted as a critical chemical feature responsible for its antioxidant activity. PMID:26068016

  13. Lipid Peroxidation in Higher Plants 1

    PubMed Central

    Schmidt, Arno; Kunert, Karl Josef

    1986-01-01

    To study the role of glutathione reductase in lipid peroxidation, bean leaves (Phaseolus vulgaris) cv Fori were treated with the herbicide acifluorfen-sodium (sodium 5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoic acid). Acifluorfen is a potent inducer of lipid peroxidation. In beans, decrease of acid-soluble SH-compounds and lipid peroxidation, measured as ethane evolution, were the toxic events after treatment of leaves with acifluorfen. As a primary response to peroxidation, increased production of antioxidants, such as vitamin C and glutathione, was found. This was followed by elevation of glutathione reductase activity. Enhanced activity of the enzyme prevented both further decline of acid-soluble SH-compounds and lipid peroxidation. Increased production of antioxidants and elevated activity of antioxidative enzymes, like glutathione reductase, seem to be a general strategy to limit toxic peroxidation in plants. PMID:16665095

  14. Water Extractable Phytochemicals from Peppers (Capsicum spp.) Inhibit Acetylcholinesterase and Butyrylcholinesterase Activities and Prooxidants Induced Lipid Peroxidation in Rat Brain In Vitro

    PubMed Central

    Ogunruku, Omodesola O.; Ademosun, Ayokunle O.

    2014-01-01

    Background. This study sought to investigate antioxidant capacity of aqueous extracts of two pepper varieties (Capsicum annuum var. accuminatum (SM) and Capsicum chinense (RO)) and their inhibitory effect on acetylcholinesterase and butyrylcholinesterase activities. Methods. The antioxidant capacity of the peppers was evaluated by the 2,2′-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS) radical scavenging ability and ferric reducing antioxidant property. The inhibition of prooxidant induced lipid peroxidation and cholinesterase activities in rat brain homogenates was also evaluated. Results. There was no significant difference (P > 0.05) in the total phenol contents of the unripe and ripe Capsicum spp. extracts. Ripe and unripe SM samples had significantly higher (P < 0.05) ABTS* scavenging ability than RO samples, while the ripe fruits had significantly higher (P < 0.05) ferric reducing properties in the varieties. Furthermore, the extracts inhibited Fe2+ and quinolinic acid induced lipid peroxidation in rats brain homogenates in a dose-dependent manner. Ripe and unripe samples from SM had significantly higher AChE inhibitory abilities than RO samples, while there was no significant difference in the BuChE inhibitory abilities of the pepper samples. Conclusion. The antioxidant and anticholinesterase properties of Capsicum spp. may be a possible dietary means by which oxidative stress and symptomatic cognitive decline associated with neurodegenerative conditions could be alleviated. PMID:26904640

  15. Water Extractable Phytochemicals from Peppers (Capsicum spp.) Inhibit Acetylcholinesterase and Butyrylcholinesterase Activities and Prooxidants Induced Lipid Peroxidation in Rat Brain In Vitro.

    PubMed

    Ogunruku, Omodesola O; Oboh, Ganiyu; Ademosun, Ayokunle O

    2014-01-01

    Background. This study sought to investigate antioxidant capacity of aqueous extracts of two pepper varieties (Capsicum annuum var. accuminatum (SM) and Capsicum chinense (RO)) and their inhibitory effect on acetylcholinesterase and butyrylcholinesterase activities. Methods. The antioxidant capacity of the peppers was evaluated by the 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid) (ABTS) radical scavenging ability and ferric reducing antioxidant property. The inhibition of prooxidant induced lipid peroxidation and cholinesterase activities in rat brain homogenates was also evaluated. Results. There was no significant difference (P > 0.05) in the total phenol contents of the unripe and ripe Capsicum spp. extracts. Ripe and unripe SM samples had significantly higher (P < 0.05) ABTS(*) scavenging ability than RO samples, while the ripe fruits had significantly higher (P < 0.05) ferric reducing properties in the varieties. Furthermore, the extracts inhibited Fe(2+) and quinolinic acid induced lipid peroxidation in rats brain homogenates in a dose-dependent manner. Ripe and unripe samples from SM had significantly higher AChE inhibitory abilities than RO samples, while there was no significant difference in the BuChE inhibitory abilities of the pepper samples. Conclusion. The antioxidant and anticholinesterase properties of Capsicum spp. may be a possible dietary means by which oxidative stress and symptomatic cognitive decline associated with neurodegenerative conditions could be alleviated. PMID:26904640

  16. Lipid Peroxidation Inhibition Blunts Nuclear Factor-κB Activation, Reduces Skeletal Muscle Degeneration, and Enhances Muscle Function in mdx Mice

    PubMed Central

    Messina, Sonia; Altavilla, Domenica; Aguennouz, M’hammed; Seminara, Paolo; Minutoli, Letteria; Monici, Maria C.; Bitto, Alessandra; Mazzeo, Anna; Marini, Herbert; Squadrito, Francesco; Vita, Giuseppe

    2006-01-01

    Duchenne muscular dystrophy (DMD) is a progressive muscle-wasting disease resulting from lack of the sarcolemmal protein dystrophin. However, the mechanism leading to the final disease status is not fully understood. Several lines of evidence suggest a role for nuclear factor (NF)-κB in muscle degeneration as well as regeneration in DMD patients and mdx mice. We investigated the effects of blocking NF-κB by inhibition of oxidative stress/lipid peroxidation on the dystrophic process in mdx mice. Five-week-old mdx mice received three times a week for 5 weeks either IRFI-042 (20 mg/kg), a strong antioxidant and lipid peroxidation inhibitor, or its vehicle. IRFI-042 treatment increased forelimb strength (+22%, P < 0.05) and strength normalized to weight (+23%, P < 0.05) and decreased fatigue (−45%, P < 0.05). It also reduced serum creatine kinase levels (P < 0.01) and reduced muscle-conjugated diene content and augmented muscle-reduced glutathione (P < 0.01). IRFI-042 blunted NF-κB DNA-binding activity and tumor necrosis factor-α expression in the dystrophic muscles (P < 0.01), reducing muscle necrosis (P < 0.01) and enhancing regeneration (P < 0.05). Our data suggest that oxidative stress/lipid peroxidation represents one of the mechanisms activating NF-κB and the consequent pathogenetic cascade in mdx muscles. Most importantly, these new findings may have clinical implications for the pharmacological treatment of patients with DMD. PMID:16507907

  17. Inhibition of key enzymes linked to type 2 diabetes and sodium nitroprusside induced lipid peroxidation in rats' pancreas by phenolic extracts of avocado pear leaves and fruit.

    PubMed

    Oboh, Ganiyu; Isaac, Adelusi Temitope; Akinyemi, Ayodele Jacobson; Ajani, Richard Akinlolu

    2014-09-01

    Persea americana fruit and leaves had been known in folk medicine for their anti-diabetic prowess. Therefore, this study sought to investigate the inhibitory effect of phenolic extract from avocado pear (Persea americana) leaves and fruits on some key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase); and sodium nitroprusside (SNP) induced lipid peroxidation in rats' pancreas in vitro. The phenolic extracts of Persea americana fruit and leaves were extracted using methanol and 1M HCl (1:1 v/v). Thereafter, their inhibitory effects on sodium nitroprusside induced lipid peroxidation and key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase) were determined in vitro. The result revealed that the leaves had fruit of avocado pear inhibit both α-amylase and α-glucosidase activities in a dose dependent manner. However, the Peel had the highest α-amylase inhibitory activity while the leaf had the highest α-glucosidase inhibitory activity as revealed by their IC50 value. Furthermore, incubation of the rat pancreas in the presence of 5 mM SNP caused an increase in the malondialdehyde (MDA) content in the tissue, however, introduction of the phenolic extracts inhibited MDA produced in a dose dependent manner. The additive and/or synergistic action of major phenolic compounds such as syringic acid, eugenol, vnillic acid, isoeugenol, guaiacol, kaemferol, catechin, ρ-hydroxybenzoic acid, ferulic acid, apigenin, naringenin, epigallocatechin, epicatechin, lupeol and epigallocatechin-3-O-gallate in avocado pear using gas chromatography (GC) could have contributed to the observed medicinal properties of the plant. Therefore, inhibition of some key enzymes linked to type 2 diabetes and prevention of oxidative stress in the pancreas could be some of the possible mechanism by which they exert their anti-diabetic properties. PMID:25324703

  18. Inhibition of Key Enzymes Linked to Type 2 Diabetes and Sodium Nitroprusside Induced Lipid Peroxidation in Rats’ Pancreas by Phenolic Extracts of Avocado Pear Leaves and Fruit

    PubMed Central

    Oboh, Ganiyu; Isaac, Adelusi Temitope; Akinyemi, Ayodele Jacobson; Ajani, Richard Akinlolu

    2014-01-01

    Persea americana fruit and leaves had been known in folk medicine for their anti-diabetic prowess. Therefore, this study sought to investigate the inhibitory effect of phenolic extract from avocado pear (Persea americana) leaves and fruits on some key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase); and sodium nitroprusside (SNP) induced lipid peroxidation in rats’ pancreas in vitro. The phenolic extracts of Persea americana fruit and leaves were extracted using methanol and 1M HCl (1:1 v/v). Thereafter, their inhibitory effects on sodium nitroprusside induced lipid peroxidation and key enzymes linked to type 2 diabetes (α-amylase and α-glucosidase) were determined in vitro. The result revealed that the leaves had fruit of avocado pear inhibit both α-amylase and α-glucosidase activities in a dose dependent manner. However, the Peel had the highest α-amylase inhibitory activity while the leaf had the highest α-glucosidase inhibitory activity as revealed by their IC50 value. Furthermore, incubation of the rat pancreas in the presence of 5 mM SNP caused an increase in the malondialdehyde (MDA) content in the tissue, however, introduction of the phenolic extracts inhibited MDA produced in a dose dependent manner. The additive and/or synergistic action of major phenolic compounds such as syringic acid, eugenol, vnillic acid, isoeugenol, guaiacol, kaemferol, catechin, ρ-hydroxybenzoic acid, ferulic acid, apigenin, naringenin, epigallocatechin, epicatechin, lupeol and epigallocatechin-3-O-gallate in avocado pear using gas chromatography (GC) could have contributed to the observed medicinal properties of the plant. Therefore, inhibition of some key enzymes linked to type 2 diabetes and prevention of oxidative stress in the pancreas could be some of the possible mechanism by which they exert their anti-diabetic properties PMID:25324703

  19. Acetaminophen Attenuates Lipid Peroxidation in Children Undergoing Cardiopulmonary Bypass

    PubMed Central

    Simpson, Scott A.; Zaccagni, Hayden; Bichell, David P.; Christian, Karla G.; Mettler, Bret A.; Donahue, Brian S.; Roberts, L. Jackson; Pretorius, Mias

    2014-01-01

    Objective Hemolysis, occurring during cardiopulmonary bypass (CPB), is associated with lipid peroxidation and postoperative acute kidney injury (AKI). Acetaminophen (ApAP) inhibits lipid peroxidation catalyzed by hemeproteins and in an animal model attenuated rhabdomyolysis-induced AKI. This pilot study tests the hypothesis that ApAP attenuates lipid peroxidation in children undergoing CPB. Design Single center prospective randomized double blinded study. Setting University-affiliated pediatric hospital. Patients Thirty children undergoing elective surgical correction of a congenital heart defect. Interventions Patients were randomized to ApAP (OFIRMEV® (acetaminophen) injection, Cadence Pharmaceuticals, San Diego, CA) or placebo every 6 hours for 4 doses starting before the onset of CPB. Measurement and Main Results Markers of hemolysis, lipid peroxidation (isofurans and F2-isoprostanes) and AKI were measured throughout the perioperative period. CPB was associated with a significant increase in free hemoglobin (from a pre-bypass level of 9.8±6.2 mg/dl to a peak of 201.5±42.6 mg/dl post-bypass). Plasma and urine isofuran and F2-isoprostane concentrations increased significantly during surgery. The magnitude of increase in plasma isofurans was greater than the magnitude in increase in plasma F2-isoprostanes. ApAP attenuated the increase in plasma isofurans compared to placebo (P=0.02 for effect of study drug). There was no significant effect of ApAP on plasma F2-isoprostanes or urinary makers of lipid peroxidation. ApAP did not affect postoperative creatinine, urinary neutrophil gelatinase-associated lipocalin or prevalence of AKI. Conclusion CPB in children is associated with hemolysis and lipid peroxidation. ApAP attenuated the increase in plasma isofuran concentrations. Future studies are needed to establish whether other therapies that attenuate or prevent the effects of free hemoglobin result in more effective inhibition of lipid peroxidation in patients

  20. A Trypsin Inhibitor from Tecoma stans Leaves Inhibits Growth and Promotes ATP Depletion and Lipid Peroxidation in Candida albicans and Candida krusei.

    PubMed

    Patriota, Leydianne L S; Procópio, Thamara F; de Souza, Maria F D; de Oliveira, Ana Patrícia S; Carvalho, Lidiane V N; Pitta, Maira G R; Rego, Moacyr J B M; Paiva, Patrícia M G; Pontual, Emmanuel V; Napoleão, Thiago H

    2016-01-01

    Tecoma stans (yellow elder) has shown medicinal properties and antimicrobial activity. Previous reports on antifungal activity of T. stans preparations and presence of trypsin inhibitor activity from T. stans leaves stimulated the investigation reported here. In this work, we proceeded to the purification and characterization of a trypsin inhibitor (TesTI), which was investigated for anti-Candida activity. Finally, in order to determine the potential of TesTI as a new natural chemotherapeutic product, its cytotoxicity to human peripheral blood mononuclear cells (PBMCs) was evaluated. TesTI was isolated from saline extract by ammonium sulfate fractionation followed by ion exchange and gel filtration chromatographies. Antifungal activity was evaluated by determining the minimal inhibitory (MIC) and fungicide (MFC) concentrations using fungal cultures containing only yeast form or both yeast and hyphal forms. Candida cells treated with TesTI were evaluated for intracellular ATP levels and lipid peroxidation. Cytotoxicity of TesTI to PBMCs was evaluated by MTT assay. TesTI (39.8 kDa, pI 3.41, K i 43 nM) inhibited similarly the growth of both C. albicans and C. krusei culture types at MIC of 100 μg/mL. The MFCs were 200 μg/mL for C. albicans and C. krusei. Time-response curves revealed that TesTI (at MIC) was more effective at inhibiting the replication of C. albicans cells. At MIC, TesTI promoted reduction of ATP levels and lipid peroxidation in the Candida cells, being not cytotoxic to PBMCs. In conclusion, TesTI is an antifungal agent against C. albicans and C. krusei, without toxicity to human cells. PMID:27199940

  1. A Trypsin Inhibitor from Tecoma stans Leaves Inhibits Growth and Promotes ATP Depletion and Lipid Peroxidation in Candida albicans and Candida krusei

    PubMed Central

    Patriota, Leydianne L. S.; Procópio, Thamara F.; de Souza, Maria F. D.; de Oliveira, Ana Patrícia S.; Carvalho, Lidiane V. N.; Pitta, Maira G. R.; Rego, Moacyr J. B. M.; Paiva, Patrícia M. G.; Pontual, Emmanuel V.; Napoleão, Thiago H.

    2016-01-01

    Tecoma stans (yellow elder) has shown medicinal properties and antimicrobial activity. Previous reports on antifungal activity of T. stans preparations and presence of trypsin inhibitor activity from T. stans leaves stimulated the investigation reported here. In this work, we proceeded to the purification and characterization of a trypsin inhibitor (TesTI), which was investigated for anti-Candida activity. Finally, in order to determine the potential of TesTI as a new natural chemotherapeutic product, its cytotoxicity to human peripheral blood mononuclear cells (PBMCs) was evaluated. TesTI was isolated from saline extract by ammonium sulfate fractionation followed by ion exchange and gel filtration chromatographies. Antifungal activity was evaluated by determining the minimal inhibitory (MIC) and fungicide (MFC) concentrations using fungal cultures containing only yeast form or both yeast and hyphal forms. Candida cells treated with TesTI were evaluated for intracellular ATP levels and lipid peroxidation. Cytotoxicity of TesTI to PBMCs was evaluated by MTT assay. TesTI (39.8 kDa, pI 3.41, Ki 43 nM) inhibited similarly the growth of both C. albicans and C. krusei culture types at MIC of 100 μg/mL. The MFCs were 200 μg/mL for C. albicans and C. krusei. Time-response curves revealed that TesTI (at MIC) was more effective at inhibiting the replication of C. albicans cells. At MIC, TesTI promoted reduction of ATP levels and lipid peroxidation in the Candida cells, being not cytotoxic to PBMCs. In conclusion, TesTI is an antifungal agent against C. albicans and C. krusei, without toxicity to human cells. PMID:27199940

  2. Lipid Peroxidation by Human Blood Phagocytes

    PubMed Central

    Stossel, Thomas P.; Mason, Robert J.; Smith, Arnold L.

    1974-01-01

    Cell suspensions enriched in human blood monocytes, obtained from normal peripheral blood by sedimentation on sodium diatrizoate-Ficoll gradients or from the blood of patients with neutropenia and monocytosis, accumulated malonyldialdehyde, a labile catabolite of lipid peroxidation, during incubations with polystyrene beads or heat-killed Staphylococcus epidermidis. Mixed blood leukocytes principally composed of granulocytes or granulocytes purified by density gradient sedimentation did not accumulate malonyldialdehyde during incubations with these particles, but did when ingesting particles containing linolenate. The phospholipid fatty acid composition of monocyte-enriched and purified granulocyte preparations from the same donors were compared. The molar fraction of arachidonate (20:4) in phospholipids from monocyte-rich preparations was 62% greater than that of purified granulocytes. The findings indicate that human monocytes, possibly because of a greater content of polyunsaturated fatty acids in their membranes, peroxidize a greater quantity of endogenous lipids than granulocytes during endocytosis. Normal human granulocytes have the capacity to peroxidize ingested lipids. However, mixed leukocytes from two patients with chronic granulomatous disease produced little malonyldialdehyde when engulfing linolenate-containing particles. Therefore the capacity to peroxidize lipid is related to cellular oxygen metabolism, a function in which chronic granulomatous disease granulocytes are dificient. Malonyldialdehyde chemically prepared by hydrolysis of tetramethoxypropane, by extraction from peroxidized linolenic acid, or purified from extracts of phagocytizing rabbit alveolar macrophages had bactericidal activity against Escherichia coli and S. epidermidis. Therefore, toxic catabolites of lipid hydroperoxides may potentiate the bactericidal activity of hydrogen peroxide in mononuclear phagocytes. PMID:4853010

  3. Hepatic drug metabolism and lipid peroxidation in thiamine deficient rats.

    PubMed

    Galdhar, N R; Pawar, S S

    1976-01-01

    In vitro metabolism of aminopyrene, ethylmorphine (Type I substrates), N-methylaniline and acetanilide (Type II substrates) in liver microsomal fraction from thiamine deficient male and female rats was studied. No significant change in microsomal protein content was noticed during the period of thiamine deficiency. However, a significant increase in the in vitro oxidation of aminopyrene, ethylmorphine, N-methylaniline and hydroxylation of acetanilide was observed. The NADPH linked and ascorbate induced lipid peroxidation was also increased during thiamine deficiency. The levels of NADPH cytochrome c-reductase, cytochrome b5 and heme were noticeably increased in thiamine deficient animals as compared to normal rats. Phenobarbital treatment induced the activities of all drug enzymes and inhibited the lipid peroxidation in either sex during the period of thiamine deficiency. It appears that thiamine intake is an important determination in drug metabolism and lipid peroxidation. PMID:816749

  4. [Effect of alkylresorcin on biological membranes during activation of lipid peroxidation].

    PubMed

    Erin, A N; Davitashvili, N G; Prilipko, L L; Boldyrev, A A; Lushchak, V I

    1987-07-01

    The effect of alkyl resorcin isolated from the cells of Azotobacter chroococcum and of its structural analog devoid of the alkyl chain (resorcin) on liver microsomes and brain synaptosomes of the rat as well as on rabbit skeletal muscle sarcoplasmic reticulum fragments during activation of lipid peroxidation was studied. Alkyl resorcin was shown to produce a much more potent antioxidant effect as compared with resorcin, since it inhibited lipid peroxidation in all the three types of membranes under study at much lower concentrations. Both alkyl resorcin and resorcin which inhibit lipid peroxidation prevented lipid peroxidation-induced structural-functional damages of synaptosomal and sarcoplasmic reticulum fragment membranes. Unlike resorcin, alkyl resorcin exerted an additional effect on brain synaptosomal membranes which consisted in the stabilization of barrier functions of membranes during incomplete inhibition of lipid peroxidation. The cumulative data suggest that stabilization necessitates the presence of both resorcin radical and alkyl chain in the alkyl resorcin molecule. PMID:3663757

  5. Hepatic drug hydroxylation and lipid peroxidation in riboflavin-deficient rats*

    PubMed Central

    Patel, J. M.; Galdhar, N. R.; Pawar, S. S.

    1974-01-01

    The effect of riboflavin deficiency and phenobarbital pretreatment on drug hydroxylation and lipid peroxidation was investigated. A significant decrease in aniline and acetanilide hydroxylation as well as NADPH-linked and ascorbate-induced lipid peroxidation was observed during 4- and 7-week riboflavin deficiency in both adult male and adult female rats. The drug-hydroxylation and lipid-peroxidation activities were further lowered with the increase in riboflavin deficiency. The phenobarbital pretreatment induced aniline and acetanilide hydroxylase activity even in riboflavin-deficient animals. Drug hydroxylation inhibits lipid peroxidation in both deficient and normal rats. The administration of riboflavin was followed by a significant increase in drug hydroxylation and lipid peroxidation. PMID:4374935

  6. Hepatic drug hydroxylation and lipid peroxidation in riboflavin-deficient rats.

    PubMed

    Patel, J M; Galdhar, N R; Pawar, S S

    1974-06-01

    The effect of riboflavin deficiency and phenobarbital pretreatment on drug hydroxylation and lipid peroxidation was investigated. A significant decrease in aniline and acetanilide hydroxylation as well as NADPH-linked and ascorbate-induced lipid peroxidation was observed during 4- and 7-week riboflavin deficiency in both adult male and adult female rats. The drug-hydroxylation and lipid-peroxidation activities were further lowered with the increase in riboflavin deficiency. The phenobarbital pretreatment induced aniline and acetanilide hydroxylase activity even in riboflavin-deficient animals. Drug hydroxylation inhibits lipid peroxidation in both deficient and normal rats. The administration of riboflavin was followed by a significant increase in drug hydroxylation and lipid peroxidation. PMID:4374935

  7. Lipid peroxidation, calcium, iron, and TCDD toxicity in rats

    SciTech Connect

    Al-Bayati, Z.A.F.

    1986-01-01

    2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been studied as a prototype of halogenated aromatic hydrocarbons. Previous studies have shown that TCDD enhances hepatic lipid peroxidation. This study on TCDD administration to rats was conducted to: measure induction of lipid peroxidation in hepatic and extrahepatic tissues; compare lipid peroxidation between sexes; determine the contributions of H/sub 2/O/sub 2/ and other reactive oxygen species and associated enzymes on hepatic lipid peroxidation: determine the role of iron in TCDD-induced lipid peroxidation; and investigate the relationship between TCDD-induced alterations in lipid peroxidation, calcium homeostasis, reduced glutathione content (GSH) and selenium-dependent glutathione peroxidase activity (GSH-Px). The results demonstrated that TCDD induces changes in microsomal lipid peroxidation in hepatic and extrahepatic tissues. The rates of microsomal lipid peroxidation in male rats were less than in microsomes from female rats. TCDD treatment produced a significant increase in lipid peroxidation which preceded an increase in whole homogenate and mitochondrial calcium content, but paralleled an increase in microsomal calcium content. TCDD treatment produced dose and time dependent decreases in hepatic GSH content and GSH-Px activity in female rats. H/sub 2/O/sub 2/ and possibly hydroxyl radical and singlet oxygen are involved in TCDD-induced hepatic microsomal lipid peroxidation. The results support the hypothesis that the toxicity of TCDD and its lack of tissue selectivity in male and female rats may be due in part to lipid peroxidation. Lipid peroxidation may alter membrane permeability to calcium and lead to sequestration of calcium.

  8. Protective effects of a 21-aminosteroid against copper-induced erythrocyte and plasma lipid peroxidation.

    PubMed

    Fernandes, A C; Filipe, P M; Manso, C F

    1992-09-22

    The 21-aminosteroids, or lazaroids, are a novel class of antioxidant drugs designed to inhibit iron-dependent lipid peroxidation in biological lipid environments. They have been shown to be of therapeutic value in several animal models of traumatic, ischemic and hemorrhagic injury of the central nervous system. Our purpose was to evaluate the ability of 21-aminosteroids to protect human erythrocytes and plasma against oxidative damage in vitro. We found that the 21-aminosteroid U74500A inhibited erythrocyte and plasma lipid peroxidation. U74500A at 1 microM significantly reduced copper-induced and hydrogen peroxide-induced erythrocyte lipid peroxidation by 76.5 and 27.6%, respectively. The inhibition of erythrocyte lipid peroxidation was accompanied by an inhibition of hemolysis. Copper-induced plasma lipid peroxidation was also significantly reduced by as little as 1 microM U74500A. These results suggest that 21-aminosteroids may prove useful in preventive or therapeutic interventions in situations where erythrocyte or plasma components are subjected to oxidative stress and in situations related to copper-induced oxidative damage. PMID:1425992

  9. The NADPH- and iron-dependent lipid peroxidation in human placental microsomes.

    PubMed

    Milczarek, Ryszard; Sokolowska, Ewa; Hallmann, Anna; Klimek, Jerzy

    2007-01-01

    In pregnant females, placenta is the most important source of lipid hydroperoxides and other reactive oxygen species (ROS). The increased production of lipid peroxides is often linked to preeclampsia. In our study, we revealed that NADPH- and iron-dependent lipid peroxidation in human placental microsomes (HPM) occurred. In the presence of Fe2+ ion, HPM produced small amounts of thiobarbituric acid-reactive substances (TBARS) - a final product of lipid peroxidation. NADPH caused a strong increase of iron stimulated TBARS formation. TBARS formation was inhibited by superoxide dismutase, butylated hydroxytoluene and alpha-tocopherol but not by mannitol or catalase. TBARS and superoxide radical production was inhibited in similar manner by cytochrome P450 inhibitors. The results obtained led us to the following conclusions: (1) microsomal lipid peroxidation next to mitochondrial lipid peroxidation may by an important source of lipid hydroperoxides in blood during pregnancy and (2) superoxide radical released by microsomal cytochrome P450 is an important factor in NADPH- and iron-dependent lipid peroxidation in HPM. PMID:16896536

  10. Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

    PubMed Central

    Muñoz, Mario F.; Argüelles, Sandro

    2014-01-01

    Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown. PMID:24999379

  11. Lipid peroxidation in ethanol poisoning: a critical reconsideration.

    PubMed

    Dianzani, M U

    1985-01-01

    Evidence for the existence of increased lipid peroxidation in the liver after ethanol administration to rats is discussed. A criticism of the methods used to measure lipid peroxidation is also given. Most authors who are in favour of the presence of lipid peroxidation after ethanol have used the detection of thiobarbituric acid (TBA)-reacting substances as a measure of lipid peroxidation. This test is not entirely satisfactory, because: (1) it is not specific; (2) it mostly measures malonaldehyde, a substance of low toxicity, following a 1-2 hr incubation time; (3) several aldehydes produced during lipid peroxidation do not react with TBA. However, it is now clear that the aldehydes produced during lipid peroxidation are actively metabolized by homogenates, so differences in catabolism may influence the result of a TBA test. Measurement of the diene conjugation band, the other test usually used to detect lipid peroxidation, produces information only on the presence of dienes at a given moment, but does not give any information on the production or decomposition rates of such dienes. Thus differences in production or decomposition kinetics may mask the results. Notwithstanding these criticisms, most of the evidence at present is in favour of some involvement of lipid peroxidation in ethanol intoxication. One hypothesis is that of the direct impact of ethanol-derived free radicals. Another is that ethanol provokes the formation of oxygen free radical species, which can start lipid peroxidation either directly, or by exhausting anti-oxidant substances in the cell so as to change the balance in favour of increased peroxidation. Finally, a third hypothesis is that acetaldehyde, the main product of ethanol oxidation, is able to stimulate lipid peroxidation, possibly through the formation of free radicals, or depletion of levels of antioxidant substances. Experiments consisting of measuring total glutathione (GSH and GSSG) during lipid peroxidation stimulated by ethanol

  12. In vitro inhibition activity of polyphenol-rich extracts from Syzygium aromaticum (L.) Merr. & Perry (Clove) buds against carbohydrate hydrolyzing enzymes linked to type 2 diabetes and Fe2+-induced lipid peroxidation in rat pancreas

    PubMed Central

    Adefegha, Stephen Adeniyi; Oboh, Ganiyu

    2012-01-01

    Objective To investigate and compare the inhibitory properties of free and bound phenolic extracts of clove bud against carbohydrate hydrolyzing enzymes (alpha-amylase & alpha-glucosidase) and Fe2+-induced lipid peroxidation in rat pancreas in vitro. Methods The free phenolics were extracted with 80% (v/v) acetone, while bound phenolics were extracted from the alkaline and acid hydrolyzed residue with ethyl acetate. Then, the interaction of the extracts with alpha-amylase and alpha-glucosidase was subsequently assessed. Thereafter, the total phenolic contents and antioxidant activities of the extracts were determined. Results The result revealed that both extracts inhibited alpha-amylase and alpha-glucosidase in a dose-dependent manner. However, the alpha-glucosidase inhibitory activity of the extracts were significantly (P<0.05) higher than their alpha-amylase inhibitory activity. The free phenolics (31.67 mg/g) and flavonoid (17.28 mg/g) contents were significantly (P<0.05) higher than bound phenolic (23.52 mg/g) and flavonoid (13.70 mg/g) contents. Both extracts also exhibited high antioxidant activities as typified by their high reducing power, 1,1 diphenyl-2- picrylhydrazyl (DPPH) and 2, 2-azinobis-3-ethylbenzo-thiazoline-6-sulfonate (ABTS) radical scavenging abilities, as well as inhibition of Fe2+-induced lipid peroxidation in rat pancreas in vitro. Conclusions This study provides a biochemical rationale by which clove elicits therapeutic effect on type 2 diabetes. PMID:23569846

  13. Lipid peroxidation induced by maternal cadmium exposure in mouse pups

    SciTech Connect

    Baohui Xu |; Yapin Jin; Zhaoliang Feng; Zhaofa Xu; Matsushita, Toshio

    1993-11-01

    Cadmium as an environmental pollutant has received considerable attention and its toxic effects have been studied extensively in human and adult animals. Moreover, an International Task Group on Metal Accumulation (1973) has established that although it is in a limited quantity cadmium can be transported across placenta and excreted through milk in animals. Likewise, it can pass through placenta in humans. Furthermore, the fact is that women in the cadmium-polluted areas are continuously exposed to cadmium during gestation and lactation. Even if they are removed from the exposure, the body burden of cadmium probably remains high because of the very long biological half-time of cadmium which is estimated to be between 17.6 and 33 years. Thus, it is possible that fetuses and pups may be exposed to cadmium during maternal gestation and lactation. Although placenta affords some protection from cadmium exposure, cadmium exposure prior to day 10-11 when placenta forms may be deleterious. Cadmium exposure during pregnancy and its effects on offsprings, which were mainly focused on litter size, pup survival, pup growth and cadmium contents in pups following maternal cadmium exposure have been reported. Lipid peroxide has been considered as a sensitive toxicological index for environmental pollutants. The inhibited antioxidant enzymes and enhanced lipid peroxidation due to cadmium exposure have been demonstrated both in humans and animals. Therefore, the present study was designed to evaluate the toxic effects of maternal cadmium exposure on mouse pups using both the indices used in the previous studies and determinations of lipid peroxide concentrations in various pup organs. In conclusion, data from the present study indicate that the detection of LPO concentration in selected pup tissues is a sensitive index for evaluating the effects of maternal cadmium exposure on mouse pups. 16 refs., 4 tabs.

  14. Interaction of aldehydes derived from lipid peroxidation and membrane proteins

    PubMed Central

    Pizzimenti, Stefania; Ciamporcero, Eric; Daga, Martina; Pettazzoni, Piergiorgio; Arcaro, Alessia; Cetrangolo, Gianpaolo; Minelli, Rosalba; Dianzani, Chiara; Lepore, Alessio; Gentile, Fabrizio; Barrera, Giuseppina

    2013-01-01

    A great variety of compounds are formed during lipid peroxidation of polyunsaturated fatty acids of membrane phospholipids. Among them, bioactive aldehydes, such as 4-hydroxyalkenals, malondialdehyde (MDA) and acrolein, have received particular attention since they have been considered as toxic messengers that can propagate and amplify oxidative injury. In the 4-hydroxyalkenal class, 4-hydroxy-2-nonenal (HNE) is the most intensively studied aldehyde, in relation not only to its toxic function, but also to its physiological role. Indeed, HNE can be found at low concentrations in human tissues and plasma and participates in the control of biological processes, such as signal transduction, cell proliferation, and differentiation. Moreover, at low doses, HNE exerts an anti-cancer effect, by inhibiting cell proliferation, angiogenesis, cell adhesion and by inducing differentiation and/or apoptosis in various tumor cell lines. It is very likely that a substantial fraction of the effects observed in cellular responses, induced by HNE and related aldehydes, be mediated by their interaction with proteins, resulting in the formation of covalent adducts or in the modulation of their expression and/or activity. In this review we focus on membrane proteins affected by lipid peroxidation-derived aldehydes, under physiological and pathological conditions. PMID:24027536

  15. Therapies targeting lipid peroxidation in traumatic brain injury.

    PubMed

    Anthonymuthu, Tamil Selvan; Kenny, Elizabeth Megan; Bayır, Hülya

    2016-06-01

    Lipid peroxidation can be broadly defined as the process of inserting a hydroperoxy group into a lipid. Polyunsaturated fatty acids present in the phospholipids are often the targets for peroxidation. Phospholipids are indispensable for normal structure of membranes. The other important function of phospholipids stems from their role as a source of lipid mediators - oxygenated free fatty acids that are derived from lipid peroxidation. In the CNS, excessive accumulation of either oxidized phospholipids or oxygenated free fatty acids may be associated with damage occurring during acute brain injury and subsequent inflammatory responses. There is a growing body of evidence that lipid peroxidation occurs after severe traumatic brain injury in humans and correlates with the injury severity and mortality. Identification of the products and sources of lipid peroxidation and its enzymatic or non-enzymatic nature is essential for the design of mechanism-based therapies. Recent progress in mass spectrometry-based lipidomics/oxidative lipidomics offers remarkable opportunities for quantitative characterization of lipid peroxidation products, providing guidance for targeted development of specific therapeutic modalities. In this review, we critically evaluate previous attempts to use non-specific antioxidants as neuroprotectors and emphasize new approaches based on recent breakthroughs in understanding of enzymatic mechanisms of lipid peroxidation associated with specific death pathways, particularly apoptosis. We also emphasize the role of different phospholipases (calcium-dependent and -independent) in hydrolysis of peroxidized phospholipids and generation of pro- and anti-inflammatory lipid mediators. This article is part of a Special Issue entitled SI:Brain injury and recovery. PMID:26872597

  16. Induction of lipid peroxidation by hexachlorocyclohexane, dieldrin, TCDD, carbon tetrachloride, and hexachlorobenzene in rats

    SciTech Connect

    Goel, M.R.; Shara, M.A.; Stohs, S.J.

    1988-02-01

    Hexachlorobenzene (HCB), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), hexachlorocyclohexane (HCCH) and dieldrin are all halogenated lipophilic environmental contaminants. A common biologic property of these compounds is their ability to induce hepatic microsomal drug metabolizing enzymes. Furthermore, exposure of laboratory animals to these xenobiotics elicits a number of similar effects including porphyria, hypothyroidism, a wasting syndrome and lethality. Perturbation of membrane lipids and lipid peroxidation may be responsible for at least part of the toxic effects of HCCH. TCDD has been shown to induce lipid peroxidation in hepatic and extrahepatic tissues. Based on the similar toxic manifestations of HCB, HCCH, TCDD and dieldrin, the authors have examined the effects of these xenobiotics on hepatic lipid peroxidation following an acutely toxic dose. Lipid peroxidation was assessed by determining the content of thiobarbituric acid reactive substance (TBARS) in the liver, employing malondialdehyde as the standard. Animals were also treated with carbon tetrachloride, a well know inducer of lipid peroxidation, as a positive control. Furthermore, the ability of these xenobiotics to inhibit selenium dependent glutathione peroxidase (GSHPX) activity was determined.

  17. The oxidation of benzo[a]pyrene mediated by lipid peroxidation in irradiated synthetic diets.

    PubMed

    Gower, J D; Wills, E D

    1986-03-01

    The effect of gamma-irradiation (1000-4000 Gy) on the formation of lipid peroxides and on the oxidation of the environmental carcinogen benzo[a]pyrene (BP) has been studied in mixtures of starch/fat and BP which were used as models for natural foods. When mixtures containing polyunsaturated fats (mackerel oil and cod-liver oil which contain relatively large proportions of C20:5 and C22:6) were exposed to gamma-irradiation, large concentrations of lipid peroxide were formed and a concomitant oxidation of BP to mutagenic and toxic BP quinones took place. The rate of BP oxidation was closely related to the extent of peroxidation of the lipids in the starch mixtures and was dependent on the dose of gamma-irradiation and the presence of air. Mackerel oil also underwent peroxidation during the storage of both irradiated and unirradiated starch/mackerel oil/BP mixtures and this resulted in a significant oxidation of the BP present in these samples. Antioxidants such as vitamin E and BHA inhibited both lipid peroxidation and BP oxidation resulting from gamma-irradiation. These results demonstrate that the species generated during the peroxidation of unsaturated fats in foodstuffs can react with polycyclic aromatic hydrocarbons such as BP and convert them into active mutagenic and toxic products. This has important toxicological implications, particularly as the consumption of polyunsaturated fat in the Western world is increasing and gamma-irradiation may soon be widely used for food sterilization. PMID:3485594

  18. Resistance to lipid peroxidation by cultured neoplastic cells

    SciTech Connect

    Arneson, R.M.; Wander, J.D.; Cabot, M.C.; Tan, E.L.; Schenley, R.L.; Hsie, A.W.

    1982-01-01

    The membranes of murine neuroblastoma cells (C1300) and human leukemia cells (HL-60) exhibit markedly increased resistance to peroxidation and undifferentiated Friend erythroleukemia cells were highly resistant to peroxidation. These findings suggest that high resistance to peroxidation and changes in the level of resistance occur commonly in cultured cells. Both cytosolic and membrane-associated factors that can prevent the onset of lipid peroxidation are present in differentiating neuroblastoma cells. A highly sensitive, single-phase assay for antioxidant activity failed to detect the presence of an antioxidant that could be associated with increased resistance to peroxidation in neuroblastoma cells. Likewise, lipid analyses of neuroblastoma cells revealed no parameter that could be related to this increase; however, this resistance phenomenon is abolished by adding arachidonic acid to the culture medium at levels that do not affect cell growth or viability. Protective factors exist in the cytosolic fraction of rat liver homogenate, which are able to neutralize the toxic products of lipid peroxidation rather than prevent the initiation of peroxidation. These protective factors were detected, and could possibly be isolated, by a cytotoxicity assay employing Chinese hamster ovary cells. In the course of this work, we discovered an antioxidant artifact that is widely distributed in commercial tissue culture media. A simple procedure has been developed to detect this antioxidant in lots of culture media.

  19. Essential Oil from Clove Bud (Eugenia aromatica Kuntze) Inhibit Key Enzymes Relevant to the Management of Type-2 Diabetes and Some Pro-oxidant Induced Lipid Peroxidation in Rats Pancreas in vitro.

    PubMed

    Oboh, Ganiyu; Akinbola, Ifeoluwa A; Ademosun, Ayokunle O; Sanni, David M; Odubanjo, Oluwatoyin V; Olasehinde, Tosin A; Oyeleye, Sunday I

    2015-01-01

    The inhibition of enzymes involved in the breakdown of carbohydrates is considered a therapeutic approach to the management of type-2 diabetes. This study sought to investigate the effects of essential oil from clove bud on α-amylase and α-glucosidase activities. Essential oil from clove bud was extracted by hydrodistillation, dried with anhydrous Na2SO4 and characterized using gas chromatography-mass spectrometry (GC-MS). The effects of the essential oil on α-amylase and α-glucosidase activities were investigated. The antioxidant properties of the oil and the inhibition of Fe(2+) and sodium nitroprusside-induced malondialdehyde (MDA) production in rats pancreas homogenate were also carried out. The essential oil inhibited α-amylase (EC50=88.9 μl/L) and α-glucosidase (EC50=71.94 μl/L) activities in a dose-dependent manner. Furthermore, the essential oil inhibited Fe(2+) and SNP-induced MDA production and exhibited antioxidant activities through their NO*, OH*, scavenging and Fe(2+)- chelating abilities. The total phenolic and flavonoid contents of the essential oil were 12.95 mg/g and 6.62 mg/g respectively. GC-MS analysis revealed the presence of α-pinene, β-pinene, neral, geranial, gamma terpinene, cis-ocimene, allo ocimene, 1,8-cineole, linalool, borneol, myrcene and pinene-2-ol in significant amounts. Furthermore, the essential oils exhibited antioxidant activities as typified by hydroxyl (OH) and nitric oxide (NO)] radicals scavenging and Fe(2+)-chelating abilities. The inhibition of α-amylase and α-glucosidase activities, inhibition of pro-oxidant induced lipid peroxidation in rat pancreas and antioxidant activities could be possible mechanisms for the use of the essential oil in the management and prevention of oxidative stress induced type-2 diabetes. PMID:25994557

  20. Stimulation of lipid peroxidation by methyl mercury in rats

    SciTech Connect

    Yonaha, M.; Saito, M.; Sagai, M.

    1983-03-28

    As an index of lipid peroxidation, thiobarbituric acid (TBA)-reactive substances in the liver, kidney, and serum, and hydrocarbons (ethane and pentane) in the exhalation of rats injected subcutaneously with 10 mg/kg/day of methylmercuric chloride (MMC) were determined. Formation of TBA-reactive substances in the liver and kidney of rats was significantly increased 4 and 2 days after initial injection of MMC, respectively. The result for serum was similar to that for the kidney. The maximum ethane production in the exhaled gases was observed 4 days after initial injection of MMC, and thereafter decreased slowly. Pentane production was significantly increased 5 days after initial injection of MMC, and thereafter continued to increase. Glutathione peroxidase activity and amount of vitamin C in the liver were depleted 4 days after initial injection of MMC; vitamin E was not depleted. In the kidney, significant decreases of glutathione peroxidase activity and vitamin C content were also seen 4 days after initial injection of MMC, but vitamin E content was unaltered. Thus, a clear increase of lipid peroxidation as determined by measurement of TBA-reactive substances in tissues and of hydrocarbons in the exhaled gases of rats after MMC treatment was demonstrated, though there was a lag phase of several days before the increase of lipid peroxidation. It is suggested that the significant increase of lipid peroxide formation may be a result of depletion of defending factors against lipid peroxidation.

  1. Effects of lipid peroxidation on membrane-bound enzymes of the endoplasmic reticulum

    PubMed Central

    Wills, E. D.

    1971-01-01

    1. Induction of the formation of lipid peroxide in suspensions of liver microsomal preparations by incubation with ascorbate or NADPH, or by treatment with ionizing radiation, leads to a marked decrease of the activity of glucose 6-phosphatase. 2. The effect of peroxidation can be imitated by treating microsomal suspensions with detergents such as deoxycholate or with phospholipases. 3. The substrate, glucose 6-phosphate, protects the glucose 6-phosphatase activity of microsomal preparations against peroxidation or detergents. 4. The loss of glucose 6-phosphatase activity is not due to the formation of hydroperoxide or formation of malonaldehyde or other breakdown products of peroxidation, all of which are not toxic to the enzyme. 5. All experiments lead to the conclusion that the loss of activity of glucose 6-phosphatase resulting from peroxidation is a consequence of loss of membrane structure essential for the activity of the enzyme. 6. In addition to glucose 6-phosphatase, oxidative demethylation of aminopyrine or p-chloro-N-methylaniline, hydroxylation of aniline, NADPH oxidation and menadione-dependent NADPH oxidation are also strongly inhibited by peroxidation. However, another group of enzymes separated with the microsomal fraction, including NAD+/NADP+ glycohydrolase, adenosine triphosphatase, esterase and NADH–cytochrome c reductase are not inactivated by peroxidation. This group is not readily inactivated by treatment with detergents. 7. Lipid peroxidation, by controlling membrane integrity, may exert a regulating effect on the oxidative metabolism and carbohydrate metabolism of the endoplasmic reticulum in vivo. PMID:4399403

  2. Turmeric and black pepper spices decrease lipid peroxidation in meat patties during cooking

    PubMed Central

    Zhang, Yanjun; Henning, Susanne M.; Lee, Ru-Po; Huang, Jianjun; Zerlin, Alona; Li, Zhaoping; Heber, David

    2015-01-01

    Abstract Spices are rich in natural antioxidants and have been shown to be potent inhibitors of lipid peroxidation during cooking of meat. Turmeric contains unique conjugated curcuminoids with strong antioxidant activity. Piperine, one of the main constituents of black pepper, is known to increase the bioavailability of curcuminoids in mouse and human studies when consumed with turmeric. We investigated whether adding black pepper to turmeric powder may further inhibit lipid peroxidation when added to meat patties prior to cooking. The addition of black pepper to turmeric significantly decreased the lipid peroxidation in hamburger meat. When investigating the antioxidant activity of the main chemical markers, we determined that piperine did not exhibit any antioxidant activity. Therefore, we conclude that other black pepper ingredients are responsible for the increased antioxidant activity of combining black pepper with turmeric powder. PMID:25582173

  3. Turmeric and black pepper spices decrease lipid peroxidation in meat patties during cooking.

    PubMed

    Zhang, Yanjun; Henning, Susanne M; Lee, Ru-Po; Huang, Jianjun; Zerlin, Alona; Li, Zhaoping; Heber, David

    2015-05-01

    Spices are rich in natural antioxidants and have been shown to be potent inhibitors of lipid peroxidation during cooking of meat. Turmeric contains unique conjugated curcuminoids with strong antioxidant activity. Piperine, one of the main constituents of black pepper, is known to increase the bioavailability of curcuminoids in mouse and human studies when consumed with turmeric. We investigated whether adding black pepper to turmeric powder may further inhibit lipid peroxidation when added to meat patties prior to cooking. The addition of black pepper to turmeric significantly decreased the lipid peroxidation in hamburger meat. When investigating the antioxidant activity of the main chemical markers, we determined that piperine did not exhibit any antioxidant activity. Therefore, we conclude that other black pepper ingredients are responsible for the increased antioxidant activity of combining black pepper with turmeric powder. PMID:25582173

  4. Lipid peroxidation and cytotoxicity induced by respirable volcanic ash.

    PubMed

    Cervini-Silva, Javiera; Antonio-Nieto-Camacho; Gomez-Vidales, Virginia; Ramirez-Apan, María Teresa; Palacios, Eduardo; Montoya, Ascención; Kaufhold, Stephan; Abidin, Zeanal; Theng, Benny K G

    2014-06-15

    This paper reports that the main component of respirable volcanic ash, allophane, induces lipid peroxidation (LP), the oxidative degradation of lipids in cell membranes, and cytotoxicity in murin monocyle/macrophage cells. Naturally-occurring allophane collected from New Zealand, Japan, and Ecuador was studied. The quantification of LP was conducted using the Thiobarbituric Acid Reactive Substances (TBARS) assay. The cytotoxic effect was determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide colorimetric assay. Electron-Paramagnetic Resonance (EPR) determinations of naturally-occurring allophane confirmed the incorporation in the structure and clustering of structural Fe(3+), and nucleation and growth of small-sized Fe (oxyhydr)oxide or gibbsite. LP induced by allophane varied with time, and solid concentration and composition, reaching 6.7 ± 0.2 nmol TBARS mg prot(-1). LP was surface controlled but not restricted by structural or surface-bound Fe(3+), because redox processes induced by soluble components other than perferryl iron. The reactivity of Fe(3+) soluble species stemming from surface-bound Fe(3+) or small-sized Fe(3+) refractory minerals in allophane surpassed that of structural Fe(3+) located in tetrahedral or octahedral sites of phyllosilicates or bulk iron oxides. Desferrioxamine B mesylate salt (DFOB) or ethylenediaminetetraacetic acid (EDTA) inhibited LP. EDTA acted as a more effective inhibitor, explained by multiple electron transfer pathways. Registered cell-viability values were as low as 68.5 ± 6.7%. PMID:24793297

  5. Lipid peroxidation causes endosomal antigen release for cross-presentation.

    PubMed

    Dingjan, Ilse; Verboogen, Daniëlle Rj; Paardekooper, Laurent M; Revelo, Natalia H; Sittig, Simone P; Visser, Linda J; Mollard, Gabriele Fischer von; Henriet, Stefanie Sv; Figdor, Carl G; Ter Beest, Martin; van den Bogaart, Geert

    2016-01-01

    Dendritic cells (DCs) present foreign antigen in major histocompatibility complex (MHC) class I molecules to cytotoxic T cells in a process called cross-presentation. An important step in this process is the release of antigen from the lumen of endosomes into the cytosol, but the mechanism of this step is still unclear. In this study, we show that reactive oxygen species (ROS) produced by the NADPH-oxidase complex NOX2 cause lipid peroxidation, a membrane disrupting chain-reaction, which in turn results in antigen leakage from endosomes. Antigen leakage and cross-presentation were inhibited by blocking ROS production or scavenging radicals and induced when using a ROS-generating photosensitizer. Endosomal antigen release was impaired in DCs from chronic granulomatous disease (CGD) patients with dysfunctional NOX2. Thus, NOX2 induces antigen release from endosomes for cross-presentation by direct oxidation of endosomal lipids. This constitutes a new cellular function for ROS in regulating immune responses against pathogens and cancer. PMID:26907999

  6. Lipid peroxidation causes endosomal antigen release for cross-presentation

    PubMed Central

    Dingjan, Ilse; Verboogen, Daniëlle RJ; Paardekooper, Laurent M; Revelo, Natalia H; Sittig, Simone P; Visser, Linda J; Mollard, Gabriele Fischer von; Henriet, Stefanie SV; Figdor, Carl G; ter Beest, Martin; van den Bogaart, Geert

    2016-01-01

    Dendritic cells (DCs) present foreign antigen in major histocompatibility complex (MHC) class I molecules to cytotoxic T cells in a process called cross-presentation. An important step in this process is the release of antigen from the lumen of endosomes into the cytosol, but the mechanism of this step is still unclear. In this study, we show that reactive oxygen species (ROS) produced by the NADPH-oxidase complex NOX2 cause lipid peroxidation, a membrane disrupting chain-reaction, which in turn results in antigen leakage from endosomes. Antigen leakage and cross-presentation were inhibited by blocking ROS production or scavenging radicals and induced when using a ROS-generating photosensitizer. Endosomal antigen release was impaired in DCs from chronic granulomatous disease (CGD) patients with dysfunctional NOX2. Thus, NOX2 induces antigen release from endosomes for cross-presentation by direct oxidation of endosomal lipids. This constitutes a new cellular function for ROS in regulating immune responses against pathogens and cancer. PMID:26907999

  7. Inhibitory Response of Raphanus sativus on Lipid Peroxidation in Albino Rats.

    PubMed

    Chaturvedi, P

    2008-03-01

    In the present study, inhibitory effect of the methanol extract of Raphanus sativus root on lipid peroxidation has been carried out in normal rats. Graded doses of methanol extract of root of the plant (40, 80 and 120 mg kg(-1) body weight) were administered orally for 15 days to experimental treated rats. Distilled water was administered to experimental control rats. At the end of experiment, rats were killed by decapitation after ether anesthesia. Blood and liver were collected to measure thiobarbituric acid reactive substance, reduced glutathione and activity of catalase. Results indicated that the extract of R. sativus root reduced the levels of thiobarbituric acid reactive substance significantly in all experimental treated groups (P < 0.05) as compared to the experimental control group. It also increased the levels of reduced glutathione and increased the activity of catalase. In vitro experiments with the liver of experimental control and experimental treated rats were also carried out against cumene hydroperoxide induced lipid peroxidation. The extract inhibited in vitro cumene hydroperoxide induced lipid peroxidation. R. sativus inhibits lipid peroxidation in vivo and in vitro. It provides protection by strengthening the antioxidants like glutathione and catalase. Inclusion of this plant in every day diet would be beneficial. PMID:18317549

  8. Fluoresceinated phosphoethanolamine for flow-cytometric measurement of lipid peroxidation.

    PubMed

    Maulik, G; Kassis, A I; Savvides, P; Makrigiorgos, G M

    1998-10-01

    A new lipophilic fluorescein probe (fluor-DHPE) has been identified that can assay lipid peroxidation in mammalian cells on a cell-by-cell or selected-cell-subpopulation basis by flow cytometry. Application of this approach requires that the fluorescent probe be nonexchangeable among cells. Fluorescein is an appropriate fluorophore, since its fluorescence matches the specifications of common flow cytometers and the compound loses its fluorescence upon reaction with peroxyl radicals. Upon examination of four lipophilic derivatives of fluorescein, fluor-DHPE was found to be the only probe that was nonexchangeable among labeled and unlabeled rat RBC for at least 24 h. The exposure of fluor-DHPE-labeled RBC to benzoyl peroxide followed by mixing the sample with RBC unexposed to peroxide led to a decrease in fluorescence. Furthermore, the flow cytometer could clearly select the subpopulation of cells undergoing lipid peroxidation from those cells that were not. Fluor-DHPE-labeled-RBC obtained from rats and exposed to cumene hydroperoxide also displayed a gradual decrease in fluorescence. This decrease was preventable by either regulation of the vitamin E content in the animal diet or in vitro supplementation of cells with vitamin E. We conclude that fluor-DHPE is a stable and nonexchangeable probe for monitoring lipid peroxidation in cell subpopulations by flow cytometry. PMID:9801063

  9. [Fatty acid and lipid peroxidation in human atherosclerosis].

    PubMed

    Loeper, J; Goy, J; Emerit, J; Rozensztajn, L; Jeny, C; Bedu, O

    1983-06-01

    Plasma fatty acids and lipid peroxidation were studied in human atherosclerosis. Analysis of fatty acids in 16 controls and 32 hyperlipidemic patients showed, in the latter, a decrease in saturated fatty acids, especially palmitic and stearic acids, and an increase in unsaturated fatty acids, especially arachidonic acid. Compared to hyperlipidemic patients without arterial injury, patients with arterial injury exhibit a significant increase in malonaldehyde (MDA). In the former, MDA concentrations are significantly increased compared to controls. Therefore, peroxidation of unsaturated fatty acids may have a deleterious effect on arteries in atheroma, through the release of toxic endoperoxydes and the metabolization of arachidonic acid into thromboxane, which is a platelet aggregator. Lipid peroxidation can also be demonstrated in other diseases: we found very high MDA concentration in 11 alcoholic patients (alcoholic hepatitis, cirrhosis) and 6 patients with inflammatory conditions such as Crohn disease. PMID:6308785

  10. The role of lipid peroxidation in neurological disorders

    PubMed Central

    Shichiri, Mototada

    2014-01-01

    There has been much evidence demonstrating the involvement of oxidative stress in the pathology of neurological disorders. Moreover, the vulnerability of the central nervous system to reactive oxygen species mediated injury is well established since neurons consume large amounts of oxygen, the brain has many areas containing high iron content, and neuronal mitochondria generate large amounts of hydrogen peroxide. Furthermore, neuronal membranes are rich in polyunsaturated fatty acids, which are particularly susceptible to oxidative stress. Recently, the biological roles of products produced by lipid peroxidation have received much attention, not only for their pathological mechanisms associated with neurological disorders, but also for their practical clinical applications as biomarkers. Here, we discuss the production mechanisms of reactive oxygen species in some neurological disorders, including Alzheimer’s disease, Down syndrome, Parkinson’s disease, and stroke. We also describe lipid peroxidation biomarkers for evaluating oxidative stress. PMID:24895477

  11. Biomarkers of lipid peroxidation related to hypertension in aging.

    PubMed

    Yavuzer, Hakan; Yavuzer, Serap; Cengiz, Mahir; Erman, Hayriye; Doventas, Alper; Balci, Huriye; Erdincler, Deniz Suna; Uzun, Hafize

    2016-05-01

    The aim of this clinical study was to evaluate the influence of aging on the levels of lipid peroxidation (quantified as thiobarbituric acid-reactive substances (TBARS) content), lipid hydroperoxide (LOOH), hexanoyl lysine (HEL), 8-iso-prostaglandin F2α (8-iso-PGF2α) and total antioxidant capacity (TAC), and determine their relationships to the demographic and cardiovascular risk factors in elderly hypertensive (HT) patients. This study consisted of four groups: two elderly groups with 30 HT patients (11 males, 19 females) and 30 normotensive healthy volunteers (15 males, 15 females), and two young groups with 30 HT patients (13 males, 17 females) and 30 normotensive healthy volunteers (12 males, 18 females). In the elderly control group, the TBARS, LOOH, HEL and 8-iso-PGF2α levels, and the carotid intima media thickness (CIMT) were significantly higher than in the young control group. The TBARS, LOOH, HEL and 8-iso-PGF2α levels and the CIMT measurements were significantly higher in the elderly HT group than in the young HT group. In addition, the TAC levels were significantly lower in the elderly and young HT groups than in the elderly and young control groups. The CIMT was significantly positively correlated with TBARS (r=0.40, P<0.001), HEL (r= 0.30, P=0.001), LOOH (r= 0.44, P<0.001) and 8-iso-PGF2α (r= 0.32, P<0.001) in all of the HT groups. It seems that in elderly patients, the LOOH and TBARS are better biomarkers of lipid peroxidation in hypertension in terms of sensitivity. In all of the HT groups, 8-iso-PGF2α had the highest sensitivity. Hypertension is associated with lipid peroxidation due to an impaired oxidant/antioxidant status. Increased lipid peroxidation and decreased antioxidants with aging indicate that peroxidative damage further increases with higher blood pressure and the aging process. PMID:26763852

  12. Measurement of doxorubicin-induced lipid peroxidation under the conditions that determine cytotoxicity in cultured tumor cells.

    PubMed

    Benchekroun, M N; Robert, J

    1992-03-01

    We have investigated doxorubicin-induced lipid peroxidation by the measure of malondialdehyde (MDA) formation in rat glioblastoma cells and human breast carcinoma cells in culture. There was a significant production of MDA when the cells were incubated with pharmacologically relevant doxorubicin concentrations, i.e., concentrations that produce a significant cytotoxicity (0.1 micrograms/ml). At equitoxic doses, vincristine provided no lipid peroxidation, indicating that MDA formation is not a consequence of cell death. Doxorubicin-induced lipid peroxidation was maximal 24 h after incubation of the cells with doxorubicin, indicating that a delay was necessary for the free radical-mediated membrane damage induced by doxorubicin. In the presence of alpha-tocopherol in the culture medium, the doxorubicin-induced MDA formation was inhibited. The development of this method will help in defining the role of free radicals and lipid peroxidation in the cytotoxicity of doxorubicin. PMID:1632521

  13. Lipid peroxidation products and antioxidants in human disease.

    PubMed Central

    Romero, F J; Bosch-Morell, F; Romero, M J; Jareño, E J; Romero, B; Marín, N; Romá, J

    1998-01-01

    Lipid peroxidation (LPO) is a free radical-related process that in biologic systems may occur under enzymatic control, e.g., for the generation of lipid-derived inflammatory mediators, or nonenzymatically. This latter form is associated mostly with cellular damage as a result of oxidative stress, which also involves cellular antioxidants in this process. This article focuses on the relevance of two LPO products, malondialdehyde (MDA) and 4-hydroxynonenal (HNE), to the pathophysiology of human disease. The former has been studied in human serum samples of hepatitis C virus-infected adults and human immunodeficiency virus-infected children. In these two cases it is shown that the specific assay of serum MDA is useful for the clinical management of these patients. The presence of MDA in subretinal fluid of patients with retinal detachment suggests the involvement of oxidative stress in this process. Moreover, we were able to report the dependence of this involvement on the degree of myopia in these patients. The assay of MDA contents in the peripheral nerves of rats fed a chronic alcohol-containing diet or diabetic mice also confirms the pathophysiologic role of oxidative stress in these experimental models. In these two cases, associated with an increase in tissue LPO products content, we detected a decrease of glutathione peroxidase (GSHPx) activity in peripheral nerve, among other modifications. We have demonstrated that in vitro HNE is able to inhibit GSHPx activity in an apparent competitive manner, and that glutathione may partially protect and/or prevent this inactivation. The accumulation of LPO products in the brain of patients with Alzheimer's disease has also been described, and it is on the basis of this observation that we have tried to elucidate the role of oxidative stress and cellular antioxidants in beta-amyloid-induced apoptotic cell death of rat embryo neurons. Finally, we discuss the possible role of the observed vascular effects of HNE on human

  14. Enhancement of lipid peroxidation and its amelioration by vitamin E in a subject with mutations in the SBP2 gene.

    PubMed

    Saito, Yoshiro; Shichiri, Mototada; Hamajima, Takashi; Ishida, Noriko; Mita, Yuichiro; Nakao, Shohei; Hagihara, Yoshihisa; Yoshida, Yasukazu; Takahashi, Kazuhiko; Niki, Etsuo; Noguchi, Noriko

    2015-11-01

    Selenocysteine (Sec) insertion sequence-binding protein 2 (SBP2) is essential for the biosynthesis of Sec-containing proteins, termed selenoproteins. Subjects with mutations in the SBP2 gene have decreased levels of several selenoproteins, resulting in a complex phenotype. Selenoproteins play a significant role in antioxidative defense, and deficiencies in these proteins can lead to increased oxidative stress. However, lipid peroxidation and the effects of antioxidants in subjects with SBP2 gene mutations have not been studied. In the present study, we evaluated the lipid peroxidation products in the blood of a subject (the proband) with mutations in the SBP2 gene. We found that the proband had higher levels of free radical-mediated lipid peroxidation products, such as 7β-hydroxycholesterol, than the control subjects. Treatment of the proband with vitamin E (α-tocopherol acetate, 100 mg/day), a lipid-soluble antioxidant, for 2 years reduced lipid peroxidation product levels to those of control subjects. Withdrawal of vitamin E treatment for 7 months resulted in an increase in lipid peroxidation products. Collectively, these results clearly indicate that free radical-mediated oxidative stress is increased in the subject with SBP2 gene mutations and that vitamin E treatment effectively inhibits the generation of lipid peroxidation products. PMID:26411970

  15. Effects of zinc on copper-induced and spontaneous lipid peroxidation.

    PubMed

    Filipe, P M; Fernandes, A C; Manso, C F

    1995-01-01

    Zinc (Zn) is an essential nonredox metal that has been regarded as having antioxidant properties. Some epidemiological indications and therapeutic results point to a role of Zn in restricting the development and the progression of some diseases. Redox-active metals like iron and copper are involved in oxidative injury mechanisms, and a decrease in the Zn:Cu ratio may be associated with certain pathologies. We studied the effect of Zn on the copper-induced lipid peroxidation in diluted human plasma. Lipid peroxidation was evaluated by measuring the formation of conjugated dienes and of thiobarbituric acid reactive products. We found that 20 microM Zn reduced the 125-microM copper-dependent formation of conjugated dienes by 27% and of thiobarbituric acid reactive products by 49%, during a 3-h incubation period. The inhibition of lipid peroxidation by 125 microM Zn is almost total in the same conditions. The time-course study of the inhibitory effect of 125 microM Zn showed that it lasted for 7 h, which was the maximum incubation period tested. We also found that Zn had an inhibitory effect on the spontaneous lipid peroxidation in rat brain whole homogenates. Our results support the antioxidant properties of Zn, which may be potentially relevant to the protection of human plasma constituents, competing with the transition metals for redox reactions. PMID:7779575

  16. Regulation of collagen synthesis in human dermal fibroblasts by ascorbic-induced lipid peroxidation

    SciTech Connect

    Geesin, J.C. Johnson and Johnson Consumer Products, Inc., Skillman, NJ ); Gordon, J.S. ); Gordon, J.S. ); Berg, R.A. )

    1991-03-11

    Ascorbic acid has been shown to stimulate collagen synthesis through the induction of lipid peroxidation which leads to increased transcription of the collagen genes. To test the ability of aldehyde products of lipid peroxidation to mediate this effect, the authors treated cultured fibroblasts with 1-200{mu}M of malondialdehyde, acetaldehyde, glyoxal or hexenal in the presence of lipid peroxidation inducing or noninducing concentrations of ascorbic acid. The treatment process involved either pretreatment of cells for 66hrs with either concentration of ascorbate before a 6hr treatment in the presence of ascorbate and the aldehydes, or 6 or 72hr treatment of the cells in the presence of either concentration of ascorbate plus the aldehydes. No effect of any of these aldehydes was seen on ascorbate-stimulated collagen synthesis. Also, pretreatment of fibroblasts for 24hrs with 100nM phorbol myristate acetate (PMA), which produces down regulation of protein kinase C(PKC), failed to alter the ascorbate-stimulation of collagen synthesis. Additionally, the authors tested the ability of benzamide, a poly ACP ribosylation inhibitor, to inhibit the ascorbate response with no specific effect noted. These results do not support the proposed roles for aldehydes, PKC, or poly ADP ribosylation in the mediation of the lipid peroxidation induced stimulation of collagen synthesis.

  17. Fish oil changes the lifespan of Caenorhabditis elegans via lipid peroxidation

    PubMed Central

    Sugawara, Soko; Honma, Taro; Ito, Junya; Kijima, Ryo; Tsuduki, Tsuyoshi

    2013-01-01

    Recently, we administered fish oil containing eicosapentaenoic acid and docosahexaenoic acid (DHA) to senescence-accelerated mice P8 (SAMP8), in order to investigate the effects on lifespan. Surprisingly, the lifespan of SAMP8 that were fed fish oil was shortened significantly, through a mechanism that likely involved lipid peroxidation. In this study, we investigated this phenomenon in further detail. To examine whether this phenomenon occurs only in SAMP8, we investigated the effect of fish oil on the lifespan of another organism species, Caenorhabditis elegans (C. elegans). C. elegans fed fish oil were cultured and the lifespan monitored. As a consequence of the provision of large amounts of fish oil the lifespan of C. elegans was shortened significantly, whereas an appropriate amount of fish oil extended their lifespan significantly. Lipid peroxide levels in C. elegans that were fed fish oil increased significantly in a dose-dependent manner. However, lipid peroxide levels in C. elegans were inhibited by the addition of fish oil and an antioxidant, α-tocopherol, and completely abrogated the changes in the lifespan. To further confirm whether the oxidation of n-3 polyunsaturated fatty acid in fish oil would change the lifespan of C. elegans, the effect of oxidized DHA was examined. Large amounts of oxidized DHA were found to shorten their lifespan significantly. Thus, fish oil changes the lifespan of C. elegans through lipid peroxidation. PMID:23526170

  18. Lipid peroxidation and antioxidants as biomarkers of tissue damage.

    PubMed

    Gutteridge, J M

    1995-12-01

    Disturbance of the balance between the production of reactive oxygen species such as superoxide; hydrogen peroxide; hypochlorous acid; hydroxyl, alkoxyl, and peroxyl radicals; and antioxidant defenses against them produces oxidative stress, which amplifies tissue damage by releasing prooxidative forms of reactive iron that are able to drive Fenton chemistry and lipid peroxidation and by eroding away protective sacrificial antioxidants. The body has a hierarchy of defense strategies to deal with oxidative stress within different cellular compartments, and superimposed on these are gene-regulated defenses involving the heat-shock and oxidant stress proteins. PMID:7497639

  19. Role of lipid composition and lipid peroxidation in the sensitivity of fungal plant pathogens to aluminum chloride and sodium metabisulfite.

    PubMed

    Avis, Tyler J; Michaud, Mélanie; Tweddell, Russell J

    2007-05-01

    Aluminum chloride and sodium metabisulfite have shown high efficacy at low doses in controlling postharvest pathogens on potato tubers. Direct effects of these two salts included the loss of cell membrane integrity in exposed pathogens. In this work, four fungal potato pathogens were studied in order to elucidate the role of membrane lipids and lipid peroxidation in the relative sensitivity of microorganisms exposed to these salts. Inhibition of mycelial growth in these fungi varied considerably and revealed sensitivity groups within the tested fungi. Analysis of fatty acids in these fungi demonstrated that sensitivity was related to high intrinsic fatty acid unsaturation. When exposed to the antifungal salts, sensitive fungi demonstrated a loss of fatty acid unsaturation, which was accompanied by an elevation in malondialdehyde content (a biochemical marker of lipid peroxidation). Our data suggest that aluminum chloride and sodium metabisulfite could induce lipid peroxidation in sensitive fungi, which may promote the ensuing loss of integrity in the plasma membrane. This direct effect on fungal membranes may contribute, at least in part, to the observed antimicrobial effects of these two salts. PMID:17337539

  20. [Effects of essential oil on lipid peroxidation and lipid metabolism in patients with chronic bronchitis].

    PubMed

    Siurin, S A

    1997-01-01

    Natural concentrations of some essential oils were examined for effects on the system lipid peroxidation-antioxidant defense and lipid metabolism in 150 patients with chronic bronchitis. Lowering of plasm levels of dienic conjugates and ketons, activation of catalase in red cells characteristic of antioxidant effect were observed in exposure to essential oils of rosemary, basil, fir, eucalyptus. Lavender essential oil promotes normalization of the level of total lipids, ratio of total cholesterol to its alpha-fraction. PMID:9490339

  1. Lipid peroxidation: pathophysiological and pharmacological implications in the eye.

    PubMed

    Njie-Mbye, Ya Fatou; Kulkarni-Chitnis, Madhura; Opere, Catherine A; Barrett, Aaron; Ohia, Sunny E

    2013-01-01

    Oxygen-derived free radicals such as hydroxyl and hydroperoxyl species have been shown to oxidize phospholipids and other membrane lipid components leading to lipid peroxidation. In the eye, lipid peroxidation has been reported to play an important role in degenerative ocular diseases (age-related macular degeneration, cataract, glaucoma, diabetic retinopathy). Indeed, ocular tissues are prone to damage from reactive oxygen species due to stress from constant exposure of the eye to sunlight, atmospheric oxygen and environmental chemicals. Furthermore, free radical catalyzed peroxidation of long chain polyunsaturated acids (LCPUFAs) such as arachidonic acid and docosahexaenoic acid leads to generation of LCPUFA metabolites including isoprostanes and neuroprostanes that may further exert pharmacological/toxicological actions in ocular tissues. Evidence from literature supports the presence of endogenous defense mechanisms against reactive oxygen species in the eye, thereby presenting new avenues for the prevention and treatment of ocular degeneration. Hydrogen peroxide (H2O2) and synthetic peroxides can exert pharmacological and toxicological effects on tissues of the anterior uvea of several mammalian species. There is evidence suggesting that the retina, especially retinal ganglion cells can exhibit unique characteristics of antioxidant defense mechanisms. In the posterior segment of the eye, H2O2 and synthetic peroxides produce an inhibitory action on glutamate release (using [(3)H]-D-aspartate as a marker), in vitro and on the endogenous glutamate and glycine concentrations in vivo. In addition to peroxides, isoprostanes can elicit both excitatory and inhibitory effects on norepinephrine (NE) release from sympathetic nerves in isolated mammalian iris ciliary bodies. Whereas isoprostanes attenuate dopamine release from mammalian neural retina, in vitro, these novel arachidonic acid metabolites exhibit a biphasic regulatory effect on glutamate release from retina

  2. Lipid peroxidation: pathophysiological and pharmacological implications in the eye

    PubMed Central

    Njie-Mbye, Ya Fatou; Kulkarni-Chitnis, Madhura; Opere, Catherine A.; Barrett, Aaron; Ohia, Sunny E.

    2013-01-01

    Oxygen-derived free radicals such as hydroxyl and hydroperoxyl species have been shown to oxidize phospholipids and other membrane lipid components leading to lipid peroxidation. In the eye, lipid peroxidation has been reported to play an important role in degenerative ocular diseases (age-related macular degeneration, cataract, glaucoma, diabetic retinopathy). Indeed, ocular tissues are prone to damage from reactive oxygen species due to stress from constant exposure of the eye to sunlight, atmospheric oxygen and environmental chemicals. Furthermore, free radical catalyzed peroxidation of long chain polyunsaturated acids (LCPUFAs) such as arachidonic acid and docosahexaenoic acid leads to generation of LCPUFA metabolites including isoprostanes and neuroprostanes that may further exert pharmacological/toxicological actions in ocular tissues. Evidence from literature supports the presence of endogenous defense mechanisms against reactive oxygen species in the eye, thereby presenting new avenues for the prevention and treatment of ocular degeneration. Hydrogen peroxide (H2O2) and synthetic peroxides can exert pharmacological and toxicological effects on tissues of the anterior uvea of several mammalian species. There is evidence suggesting that the retina, especially retinal ganglion cells can exhibit unique characteristics of antioxidant defense mechanisms. In the posterior segment of the eye, H2O2 and synthetic peroxides produce an inhibitory action on glutamate release (using [3H]-D-aspartate as a marker), in vitro and on the endogenous glutamate and glycine concentrations in vivo. In addition to peroxides, isoprostanes can elicit both excitatory and inhibitory effects on norepinephrine (NE) release from sympathetic nerves in isolated mammalian iris ciliary bodies. Whereas isoprostanes attenuate dopamine release from mammalian neural retina, in vitro, these novel arachidonic acid metabolites exhibit a biphasic regulatory effect on glutamate release from retina and

  3. Laser-based assessment of lipid peroxidation in humans

    NASA Astrophysics Data System (ADS)

    Giubileo, Gianfranco

    1998-07-01

    Infrared absorption spectroscopy can be performed at very high resolution by tunable diode laser (TDL) based optical systems for any gas with well resolved absorption spectra. In a double beam setup atmospheric trace gas concentration can be measured down to ppb levels. The analysis of trace gases may have useful applications in detecting chemicals in the human breath for non invasive medical diagnostic. The capability of TDL based breath analysis was well demonstrated by monitoring ammonia and methane. In the human body the formation of free radicals does induce oxidative degradation of polyunsaturated fatty acids (lipid peroxidation) which is a damage for cells and organs in the organism. Specific volatile hydrocarbons generated as end product by lipid peroxidation (LP) can be found inside circulating blood and expired breath. TDL based analysis of those specific hydrocarbons (ethane and pentane) in the expired breath can allow a non invasive assessment of the LP extent.

  4. Lipid Peroxidation Is a Consequence of Elicitor Activity 1

    PubMed Central

    Rogers, Kim R.; Albert, Fred; Anderson, Anne J.

    1988-01-01

    Elicitor-active preparations from the fungal pathogen of bean Colletotrichum lindemuthianum stimulated the accumulation of products characteristic of lipid peroxidation in treated bean tissues. Bean suspension cells treated with crude and purified elicitors accumulated `lipofuscin-like pigment' (LEP) and malondialdehyde. The accumulation of LFP after about 6 h of treatment coincided with the onset of visible browning and production of the bean phytoalexins kievitone, phaseollin, and phaseollinisoflavan. The induction of phytoalexins and accumulation of LFP were also triggered by treatments with generators of activated oxygen species, xanthine:xanthine oxidase and Fe:ethylenediaminedi-o-hydroxyphenylacetic acid. These data suggest that generation of active oxygen species may be involved in lipid peroxidation triggered by elicitors. PMID:16665944

  5. Prevention of lipid peroxidation induced by ochratoxin A in Vero cells in culture by several agents.

    PubMed

    Baudrimont, I; Ahouandjivo, R; Creppy, E E

    1997-04-18

    Ochratoxin A (OTA) is a mycotoxin produced by Aspergillus ochraceus as well as other moulds. This mycotoxin contaminates animal feed and food and is nephrotoxic for all animal species studied so far. OTA is immunosuppressive, genotoxic, teratogenic and carcinogenic. It is a structural analogue of phenylalanine and contains a chlorinated dihydroisocoumarinic moiety. Ochratoxin A inhibits protein synthesis by competition with phenylalanine in the phenylalanine-tRNA aminoacylation reaction. Recently lipid peroxidation induced by OTA has been reported, indicating that the lesions induced by this toxin could also be related to oxidative damage. An attempt to prevent its toxic effect, mainly the lipid peroxidation, has been made using aspartame (L-aspartyl-L-phenylalanine methyl ester) a structural analogue of both OTA and phenylalanine, piroxicam, a non steroidal anti-inflammatory drug and superoxide dismutase+catalase (endogenous oxygen radical scavengers). Lipid peroxidation was assayed in monkey kidney cells (Vero cells) treated by increasing concentrations of OTA (5-50 microM). After 24 h incubation OTA induced lipid peroxidation in Vero cells in a concentration dependent manner, as measured by malonaldehyde (MDA) production. The MDA production, in Vero cells, was significantly increased by 50.5% from 694.1 +/- 21.0 to 1041.5 +/- 23.5 pmol/mg of protein. In the presence of superoxide dismutase (SOD)+catalase (25 micrograms/ml each) the MDA production induced by OTA was significantly decreased. At 50 microM of OTA concentration (optimal production of MDA) the MDA production decreased from 1041.5 +/- 23.5 to 827.5 +/- 21.3 pmol/mg of protein. SOD and catalase, when applied prior to the toxin, seemed to prevent lipid peroxidation more efficiently than piroxicam (at a ten-fold higher concentration than OTA) and aspartame (at equimolar concentration). These molecules also partially prevented the OTA-induced leakage of MDA in the culture medium. PMID:9158693

  6. Lipid peroxidation in Rheumatoid arthritis; consequences and monitoring.

    PubMed

    Luczaj, Wojciech; Jarocka-Karpinska, Iwona; Sierakowski, Stanislaw; Andrisic, Luka; Zarkovic, Neven; Skrzydlewska, Elzbieta

    2014-10-01

    The epidemiological studies have shown that rheumatoid arthritis (RA) leads to oxidative stress formation. Therefore the aim of this study has been to estimate the lipid peroxidation in RA patients. Moreover the reasons and consequences of changes in lipid peroxidation were estimated. 73 patients with RA and 62 healthy subjects were included into the study. Lipid peroxidation was estimated by the measurement of phospholipid arachidonic acid (AA) and linoleic acid (LA) as well as aldehydes: 4-hydroxynonenal (4-HNE), 4-hydroxyhexenal (4-HHE), malondialdehyde (MDA), acrolein, crotonaldehyde, and 4-oxononenal (4-ONE) that were determined by GC and GCMS, while 8-isoprostanes (8-isoPGF2a) - was determined by LCMS. Phospholipase A2 (PLA2), platelet-activating factor acetylhydrolase (PAF-AH) and glutathione peroxidase (GSH-Px) activity were determined spectrophotometrically, while vitamin E was determined by HPLC. Plasma of RA patients was characterized by higher vitamin E level and decreased GSH-Px activity as well as the level of phospholipid AA and LA compared to healthy subjects. The level of all examined aldehydes was significantly increased in plasma patients but higher increase was observed in urine of RA patients in comparison with control group. The 8-isoprostanes level was approximately 9-fold higher in the plasma and 3-fold higher in the urine of RA patients compared to healthy subjects, but in the urine the changes in 8-isoprostanes level was correlated with RA progression. A significant increase in 4-HNE-modified protein adducts level as well as a decrease in the activity of PAF-AH and PLA2 were observed in the plasma of RA patients. The level of lipid peroxidation products in the plasma and the urine may be the indicator of RA, but additionally urine 8-isoprostanes may be the useful and reliable biomarker of RA progression. PMID:26461394

  7. Effect of Semecarpus anacardium nuts on lipid peroxidation.

    PubMed

    Tripathi, Y B; Singh, A V

    2001-08-01

    Alcoholic extract of pericarp showed significant protection against FeSO4 induced lipid peroxidation, as compared with whole native nut and seeds. Mechanism of action may be through metal chelation or activation of endogenous antioxidant enzymes, because the extract did not show hydroxyl and super oxide anion scavenging property. Further in vitro experiments against FeSO4, it did not maintain the level of reduced glutathione. PMID:12018583

  8. The effect of ghee (clarified butter) on serum lipid levels and microsomal lipid peroxidation.

    PubMed

    Sharma, Hari; Zhang, Xiaoying; Dwivedi, Chandradhar

    2010-04-01

    Ghee, also known as clarified butter, has been utilized for thousands of years in Ayurveda as a therapeutic agent. In ancient India, ghee was the preferred cooking oil. In the last several decades, ghee has been implicated in the increased prevalence of coronary artery disease (CAD) in Asian Indians due to its content of saturated fatty acids and cholesterol and, in heated ghee, cholesterol oxidation products. Our previous research on Sprague-Dawley outbred rats, which serve as a model for the general population, showed no effect of 5 and 10% ghee-supplemented diets on serum cholesterol and triglycerides. However, in Fischer inbred rats, which serve as a model for genetic predisposition to diseases, results of our previous research showed an increase in serum total cholesterol and triglyceride levels when fed a 10% ghee-supplemented diet. In the present study, we investigated the effect of 10% dietary ghee on microsomal lipid peroxidation, as well as serum lipid levels in Fischer inbred rats to assess the effect of ghee on free radical mediated processes that are implicated in many chronic diseases including cardiovascular disease. Results showed that 10% dietary ghee fed for 4 weeks did not have any significant effect on levels of serum total cholesterol, but did increase triglyceride levels in Fischer inbred rats. Ghee at a level of 10% in the diet did not increase liver microsomal lipid peroxidation or liver microsomal lipid peroxide levels. Animal studies have demonstrated many beneficial effects of ghee, including dose-dependent decreases in serum total cholesterol, low density lipoprotein (LDL), very low density lipoprotein (VLDL), and triglycerides; decreased liver total cholesterol, triglycerides, and cholesterol esters; and a lower level of nonenzymatic-induced lipid peroxidation in liver homogenate. Similar results were seen with heated (oxidized) ghee which contains cholesterol oxidation products. A preliminary clinical study showed that high doses of

  9. The mechanism of the hypochlorite-induced lipid peroxidation.

    PubMed

    Panasenko, O M

    1997-01-01

    The article reviews data related to the role of exogenic hypochlorite (HOCl/OCl-) and hypochlorite produced by myeloperoxidase catalysis in initiation of lipid peroxidation (LPO) in phospholipid membranes and human blood lipoproteins (LP). It has been shown that HOCl/OCl- promotes free radical lipid oxidation in liposomes and LP that is followed by the formation of LPO products; hydroperoxides, conjugated dienes, TBARS, and fluorescent products. Water soluble reactive substances (.O2-, H2O2, Fe2+) which can be present in the reaction mixture as a dopant are not the source of free radicals and do not participate in HOCl/OCl(-)-induced LPO at the initiation step. The main reaction of HOCl/OCl- with unsaturated lipid is probably the generation of chlorohydrins. However, this reaction is not accompanied by generation of free radicals and LPO. HOCl/OCl- reacts efficiently with TBARS of aldehydic nature. It is likely that the reaction proceeds without the participation of free radicals. Among the compounds of a peroxide nature (hydro-, dialkyl-, diacyl-, alkyl-acyl-peroxide groups and epoxides) only hydroperoxides react with HOCl/OCl-. This reaction is accompanied by the production of free radicals (but not singlet oxygen), probably alkoxyl radicals, which may play a role in the initiation of HOCl/OCl(-)-induced LPO. PMID:9260000

  10. [The effect of cadmium chloride and hydrogen peroxide on the lipid peroxidation and fractional composition of lipids in hepatocytes of rats].

    PubMed

    Borikov, O Iu; Kaliman, P A

    2004-01-01

    The isolated hepatocytes were incubated in the medium, containing cadmium chloride or hydrogen peroxide. Influence of the latter on the intensity of lipid peroxidation and contents of some lipids fractions, as well as viability of hepatocytes in these conditions has been studied. It is shown that under such cultivation conditions the activation of lipid peroxidation in the hepatocytes takes place. Its activation in presence of cadmium chloride was one of the factors of the membranes damage. The changes in the content of some fractions of lipids were similar both under the incubations of the cells with cadmium chloride and hydrogen peroxide. This allows one to suppose that cadmium chloride causes changes in the lipid composition of membranes as a result of intensification of lipid peroxidation. PMID:15915720

  11. Analysis of the kinetics of lipid peroxidation in terms of characteristic time-points.

    PubMed

    Pinchuk, Ilya; Lichtenberg, Dov

    2014-02-01

    Measuring peroxidation of aggregated lipids in model systems (liposomes, micelles, emulsions or microemulsions) as well as in samples of biological origin ex vivo (isolated lipoproteins, blood sera or plasma) is widely used in medical and biological investigations, to evaluate the oxidative stress, antioxidants' efficiency and lipid oxidizability in different pathophysiological states. To avoid possible artifacts, such investigations must be based on the time course of peroxidation (i.e. on kinetic studies). To be able to compare complex kinetic profiles, it is important to characterize them in terms of mechanistically meaningful and experimentally unequivocal parameters. In this review, we characterize the typically observed continuous kinetic profiles in terms of a limited number of characteristic time-points (both commonly used and additional time-points and their combinations) that can be derived from experimental time-dependencies. The meaning of each of the experimentally observed characteristic parameters is presented in terms of rate constants and concentrations, derived on the basis of mechanistic considerations. Theoretical expressions for these characteristic parameters are based on a model that includes both the inhibited peroxidation and the uninhibited peroxidation occurring after consumption of the antioxidant(s). Comparison between theoretically predicted dependencies and experimental data support our treatment considered with special emphasis on transition metals-induced peroxidation of lipoproteins. PMID:24333462

  12. Effects of various compounds on lipid peroxidation mediated by detergent-solubilized rat liver NADPH-cytochrome C reductase.

    PubMed

    Kamataki, T; Sugita, O; Naminohira, S; Kitagawa, H

    1978-12-01

    A reconstituted lipid peroxidation system containing NADPH-cytochrome c reductase isolated from detergent-solubilized rat liver microsomes was used to determine the effects of several compounds, including drugs, on the lipid peroxidation activity. EDTA and ferrous ion were essential requirements for reconstitution of the activity. The addition of 1,10-phenanthroline to the system containing both EDTA and ferrous ion further enhanced the activity. Pyrocatecol, thymol, p-aminophenol, imipramine, p-chloromercuribenzoate (PCMB) and alpha-tocopherol exhibited strong inhibition, aniline, N-monomethylaniline, aminopyrine, benzphetamine, SKF 525-A and NADP exhibited moderate inhibition, and phenol, benzoic acid, acetanilide and nicotinamide exhibited less or no inhibition at the concentrations lower than 1000 micron M. Metal ions such as Hg+, Hg2+, Co2+, Cu2+, Mn2+ and U6+ inhibited lipid peroxidation strongly. In addition, Cd2+, St2+ and Ca2+ exhibited less potent to moderate inhibition, and Ba2+ and Mg2+ were without effects on the activity. Among sulfhydryl compounds tested, dithiothreitol inhibited lipid peroxidation to a greater extent than did the other three compounds, glutathione, cysteine and mercaptoethanol. PMID:106178

  13. Pantothenic acid and its derivatives protect Ehrlich ascites tumor cells against lipid peroxidation.

    PubMed

    Slyshenkov, V S; Rakowska, M; Moiseenok, A G; Wojtczak, L

    1995-12-01

    Preincubation of Ehrlich ascites tumor cells at 22 or 32 degrees C, but not at 0 degree C, with pantothenic acid, 4'-phosphopantothenic acid, pantothenol, or pantethine reduced lipid peroxidation (measured by production of thiobarbituric acid-reactive compounds) induced by the Fenton reaction (Fe2+ + H2O2) and partly protected the plasma membrane against the leakiness to cytoplasmic proteins produced by the same reagent. Pantothenic acid and its derivatives did not inhibit (Fe2+ + H2O2)-induced peroxidation of phospholipid multilamellar vesicles, thus indicating that their effect on the cells was not due to the scavenging mechanism. Homopantothenic acid and its 4'-phosphate ester (which are not precursors of CoA) neither protected Ehrlich ascites tumor cells against lipid peroxidation nor prevented plasma membrane leakiness under the same conditions. Incubation of the cells with pantothenic acid, 4'-phosphopantothenic acid, pantothenol, or pantethine significantly increased the amount of cellular CoA and potentiated incorporation of added palmitate into phospholipids and cholesterol esters. It is concluded that pantothenic acid and its related compounds protect the plasma membrane of Ehrlich ascites tumor cells against the damage by oxygen free radicals due to increasing cellular level of CoA. The latter compound may act by diminishing propagation of lipid peroxidation and promoting repair mechanisms, mainly the synthesis of phospholipids. PMID:8582649

  14. Measuring oxidative stress: the confounding effect of lipid concentration in measures of lipid peroxidation.

    PubMed

    Pérez-Rodríguez, Lorenzo; Romero-Haro, Ana A; Sternalski, Audrey; Muriel, Jaime; Mougeot, Francois; Gil, Diego; Alonso-Alvarez, Carlos

    2015-01-01

    Lipid peroxidation products are widely used as markers of oxidative damage in the organism. To properly interpret the information provided by these markers, it is necessary to know potential sources of bias and control confounding factors. Here, we investigated the relationship between two indicators of lipid mobilization (circulating levels of triglycerides and cholesterol) and two common markers of oxidative damage (plasma levels of malondialdehyde and hydroperoxides; the latter estimated from the d-ROMs assay kit). The following five avian species were studied: red-legged partridge (Alectoris rufa), zebra finch (Taeniopygia guttata), spotless starling (Sturnus unicolor), marsh harrier (Circus aeroginosus), and Montagu's harrier (Circus pygargus). In all cases, plasma triglyceride levels positively and significantly correlated with lipid peroxidation markers, explaining between 8% and 34% of their variability. Plasma cholesterol, in contrast, showed a significant positive relationship only among spotless starling nestlings and a marginally significant association in zebra finches. These results indicate that lipid peroxidation marker levels covary with circulating lipid levels. We discuss the potential causes and implications of this covariation and recommend that future studies that measure oxidative damage using lipid peroxidation markers report both raw and relative levels (i.e., corrected for circulating triglycerides). Whether the observed pattern also holds for other tissues and in other taxa would deserve further research. PMID:25860832

  15. An in vitro model to test relative antioxidant potential: Ultraviolet-induced lipid peroxidation in liposomes

    SciTech Connect

    Pelle, E.; Maes, D.; Padulo, G.A.; Kim, E.K.; Smith, W.P. )

    1990-12-01

    Since antioxidants have been shown to play a major role in preventing some of the effects of aging and photoaging in skin, it is important to study this phenomenon in a controlled manner. This was accomplished by developing a simple and reliable in vitro technique to assay antioxidant efficacy. Inhibition of peroxidation by antioxidants was used as a measure of relative antioxidant potential. Liposomes, high in polyunsaturated fatty acids (PUFA), were dispersed in buffer and irradiated with ultraviolet (UV) light. Irradiated liposomes exhibited a significantly higher amount of hydroperoxides than liposomes containing antioxidants in a dose- and concentration-dependent manner. Lipid peroxidation was determined spectrophotometrically by an increase in thiobarbituric acid reacting substances. To further substantiate the production of lipid peroxides, gas chromatography was used to measure a decrease in PUFA substrate. In order of decreasing antioxidant effectiveness, the following results were found among lipophilic antioxidants: BHA greater than catechin greater than BHT greater than alpha-tocopherol greater than chlorogenic acid. Among hydrophilic antioxidants, ascorbic acid and dithiothreitol were effective while glutathione was ineffective. In addition, ascorbic acid was observed to act synergistically with alpha-tocopherol, which is in agreement with other published reports on the interaction of these two antioxidants. Although peroxyl radical scavengers seem to be at a selective advantage in this liposomal/UV system, these results demonstrate the validity of this technique as an assay for measuring an antioxidant's potential to inhibit UV-induced peroxidation.

  16. Lipid peroxides as endogenous oxidants forming 8-oxo-guanosine and lipid-soluble antioxidants as suppressing agents

    PubMed Central

    Kanazawa, Kazuki; Sakamoto, Miku; Kanazawa, Ko; Ishigaki, Yoriko; Aihara, Yoshiko; Hashimoto, Takashi; Mizuno, Masashi

    2016-01-01

    The oxidation of guanosine to 8-oxo-2'-deoxyguanosine (8-oxo-dG) in DNA is closely associated with induction of various diseases, but the endogenous oxidant species involved remains unclear. Hydrogen peroxides (H2O2) have been considered to be the oxidant, while lipid peroxides are another possible oxidant because generated easily in bio-membranes surrounding DNA. The oxidant potency was compared between lipid peroxides and H2O2. Linoleic acid hydroperoxides (LOOH) formed 8-oxo-dG at a higher level than H2O2 in guanosine or double-stranded DNA. In the presence of a physiological concentration of Fe2+ to produce hydroxyl radicals, LOOH was also a stronger oxidant. In a lipid micelle, LOOH markedly produced 8-oxo-dG at a concentration one-tenth of that of H2O2. Upon adding to rat hepatic mitochondria, phosphatidylcholine hydroperoxides produced 8-oxo-dG abundantly. Employing HepG2 cells after pretreated with glutathione peroxidase inhibitor, LOOH formed 8-oxo-dG more abundantly than H2O2. Then, antioxidants to suppress the 8-oxo-dG formation were examined, when the nuclei of pre-incubated HepG2 with antioxidants were exposed to LOOH. Water-soluble ascorbic acid, trolox, and N-acetyl cysteine showed no or weak antioxidant potency, while lipid-soluble 2,6-dipalmitoyl ascorbic acid, α-tocopherol, and lipid-soluble phytochemicals exhibited stronger potency. The present study shows preferential formation of 8-oxo-dG upon LOOH and the inhibition by lipid-soluble antioxidants. PMID:27499574

  17. Lipid peroxides as endogenous oxidants forming 8-oxo-guanosine and lipid-soluble antioxidants as suppressing agents.

    PubMed

    Kanazawa, Kazuki; Sakamoto, Miku; Kanazawa, Ko; Ishigaki, Yoriko; Aihara, Yoshiko; Hashimoto, Takashi; Mizuno, Masashi

    2016-07-01

    The oxidation of guanosine to 8-oxo-2'-deoxyguanosine (8-oxo-dG) in DNA is closely associated with induction of various diseases, but the endogenous oxidant species involved remains unclear. Hydrogen peroxides (H2O2) have been considered to be the oxidant, while lipid peroxides are another possible oxidant because generated easily in bio-membranes surrounding DNA. The oxidant potency was compared between lipid peroxides and H2O2. Linoleic acid hydroperoxides (LOOH) formed 8-oxo-dG at a higher level than H2O2 in guanosine or double-stranded DNA. In the presence of a physiological concentration of Fe(2+) to produce hydroxyl radicals, LOOH was also a stronger oxidant. In a lipid micelle, LOOH markedly produced 8-oxo-dG at a concentration one-tenth of that of H2O2. Upon adding to rat hepatic mitochondria, phosphatidylcholine hydroperoxides produced 8-oxo-dG abundantly. Employing HepG2 cells after pretreated with glutathione peroxidase inhibitor, LOOH formed 8-oxo-dG more abundantly than H2O2. Then, antioxidants to suppress the 8-oxo-dG formation were examined, when the nuclei of pre-incubated HepG2 with antioxidants were exposed to LOOH. Water-soluble ascorbic acid, trolox, and N-acetyl cysteine showed no or weak antioxidant potency, while lipid-soluble 2,6-dipalmitoyl ascorbic acid, α-tocopherol, and lipid-soluble phytochemicals exhibited stronger potency. The present study shows preferential formation of 8-oxo-dG upon LOOH and the inhibition by lipid-soluble antioxidants. PMID:27499574

  18. Oxidative Stress and Lipid Peroxidation Products in Cancer Progression and Therapy

    PubMed Central

    Barrera, Giuseppina

    2012-01-01

    The generation of reactive oxygen species (ROS) and an altered redox status are common biochemical aspects in cancer cells. ROS can react with the polyunsaturated fatty acids of lipid membranes and induce lipid peroxidation. The end products of lipid peroxidation, 4-hydroxynonenal (HNE), have been considered to be a second messenger of oxidative stress. Beyond ROS involvement in carcinogenesis, increased ROS level can inhibit tumor cell growth. Indeed, in tumors in advanced stages, a further increase of oxidative stress, such as that occurs when using several anticancer drugs and radiation therapy, can overcome the antioxidant defenses of cancer cells and drive them to apoptosis. High concentrations of HNE can also induce apoptosis in cancer cells. However, some cells escape the apoptosis induced by chemical or radiation therapy through the adaptation to intrinsic oxidative stress which confers drug resistance. This paper is focused on recent advances in the studies of the relation between oxidative stress, lipid peroxidation products, and cancer progression with particular attention to the pro-oxidant anticancer agents and the drug-resistant mechanisms, which could be modulated to obtain a better response to cancer therapy. PMID:23119185

  19. CALCIUM-INDUCED LIPID PEROXIDATION IS MEDIATED BY RHODNIUS HEME-BINDING PROTEIN (RHBP) AND PREVENTED BY VITELLIN.

    PubMed

    Paes, Marcia C; Silveira, Alan B; Ventura-Martins, Guilherme; Luciano, Monalisa; Coelho, Marsen G P; Todeschini, Adriane R; Bianconi, M Lucia; Atella, Georgia C; Silva-Neto, Mário A C

    2015-10-01

    Lipid peroxidation is promoted by the quasi-lipoxygenase (QL) activity of heme proteins and enhanced by the presence of free calcium. Unlike mammalian plasma, the hemolymph of Rhodnius prolixus, a vector of Chagas disease, contains both a free heme-binding protein (RHBP) and circulating lipoproteins. RHBP binds and prevents the heme groups of the proteins from participating in lipid peroxidation reactions. Herein, we show that despite being bound to RHBP, heme groups promote lipid peroxidation through a calcium-dependent QL reaction. This reaction is readily inhibited by the presence of ethylene glycol tetraacetic acid (EGTA), the antioxidant butylated hydroxytoluene or micromolar levels of the main yolk phosphoprotein vitellin (Vt). The inhibition of lipid peroxidation is eliminated by the in vitro dephosphorylation of Vt, indicating that this reaction depends on the interaction of free calcium ions with negatively charged phosphoamino acids. Our results demonstrate that calcium chelation mediated by phosphoproteins occurs via an antioxidant mechanism that protects living organisms from lipid peroxidation. PMID:26111116

  20. Lipid peroxidation and cyclooxygenase enzyme inhibitory activities of acidic aqueous extracts of some dietary supplements.

    PubMed

    Raman, Priyadarshini; Dewitt, David L; Nair, Muraleedharan G

    2008-02-01

    The botanical supplement market is growing at a fast pace with more and more people resorting to them for maintaining good health. Echinacea, garlic, ginkgo, ginseng, Siberian ginseng, grape seed extract, kava kava, saw palmetto and St John's wort are some of the popular supplements used for a variety of health benefits. These supplements are associated with various product claims, which suggest that they possess cyclooxygenase (COX) enzyme and lipid s inhibitory activities. COX enzymes are found to be at elevated levels in inflamed and cancerous cells. To test some of the product claims, selected supplements were analysed for their ability to inhibit COX-1 and -2 enzymes and lipid peroxidation in vitro. The supplements were extracted with acidified water (pH 2) at 37 degrees C to simulate the gastric environment. The supplements tested demonstrated varying degrees of COX enzyme inhibition (5-85% for COX-1 and 13-28% for COX-2). Interestingly, extracts of garlic (Meijer), ginkgo (Solaray), ginseng (Nature's Way), Siberian ginseng (GNC, Nutrilite, Solaray, Natrol), kava kava (GNC, Sundown, Solaray) and St John's wort (Nutrilite) selectively inhibited COX-2 enzyme. These supplements also inhibited lipid peroxidation in vitro (5-99%). The results indicated that the consumption of these botanical supplements studied possess health benefits. PMID:17726737

  1. Lycopene control of benzophenone-sensitized lipid peroxidation

    NASA Astrophysics Data System (ADS)

    Cvetković, Dragan; Marković, Dejan

    2012-05-01

    Lycopene antioxidant activity in the presence of two different mixtures of phospholipids in hexane solution, under continuous regime of UV-irradiation from three different ranges (UV-A, UV-B, and UV-C) has been evaluated in this work. Lycopene expected role was to control lipid peroxidation, by scavenging free radicals generated by UV-irradiation, in the presence and in the absence of selected photosensitizer, benzophenone. This work shows that lycopene undergoes to UV-induced destruction (bleaching), highly dependent on the incident photons energy input, more expressed in the presence than in the absence of benzophenone. The further increase ("excess") of its bleaching is undoubtedly related to the further increase of its antioxidant activity in the presence of benzophenone, having the same cause: increase of (phospholipids peroxidation) chain-breaking activities.

  2. [Age-related Peculiarities of Succinate Effect on Induced Lipid Peroxidation in Rat Liver Mitochondria].

    PubMed

    Grishina, E V; Khaustova, Ya V; Vasilieva, A A; Mayevsky, E I

    2015-01-01

    The antioxidant effect of succinate and 3-hydroxybutyrate oxidation on the kinetics of lipid peroxidation induced by ATP-Fe2+ complex in isolated rat liver mitochondria of old (1.0-1.5 years) and young (3 months) male rats was investigated. The rate of induced lipid peroxidation V(LPO) in rat liver mitochondria and the half-time of oxygen consumption Δt50, which included the lag period and the initiation. phase, was recorded polarographically. Without exogenous oxidative-substrates V(LPO) was slightly higher in mitochondria of old animals, but the onset of lipid peroxidation cascade was significantly earlier than in young animals. Incubation of mitochondria with 5mM succinate for 1 min inhibited V(LPO) by 15% in young animals and by 35% in old animals. However, only in mitochondria of old animals Δt50 increased by 19% as compared to lipid peroxidation without substrates. V(LPO) in mitochondria of young animals did not significantly change during 3-hydroxybutyrate oxidation, while in mitochondria of old animals it was reduced by 19% with a slight increase in Δt50. To simulate age-dependent dysfunction we damaged isolated mitochondria by a series of freeze-thaw cycles, which caused a significant increase of V(LPO) of.both age groups. Succinate oxidation inhibited V(LPO) in damaged mitochondria in all cases by 56%, as compared to V(LPO) without oxidative substrates and extended At50 twofold in mitochondria of young animals. Oxidation of 3-hydroxybutyrate had no effect on V(LPO) in damaged mitochondria regardless of animal, age and extended Δt50 by 48% in mitochondria of young animals. Thus, the antioxidant effect of succinate oxidation can prevent lipid peroxidation damage and may exhibit geroprotective action at the level of aging mitochondria. Therefore, the antioxidant effect is due to the process of substrate oxidation in the respiratory chain but not because of an interaction of their structures with membrane lipids per se. PMID:26394470

  3. 4-Hydroxy-nonenal—A Bioactive Lipid Peroxidation Product †

    PubMed Central

    Schaur, Rudolf J.; Siems, Werner; Bresgen, Nikolaus; Eckl, Peter M.

    2015-01-01

    This review on recent research advances of the lipid peroxidation product 4-hydroxy-nonenal (HNE) has four major topics: I. the formation of HNE in various organs and tissues, II. the diverse biochemical reactions with Michael adduct formation as the most prominent one, III. the endogenous targets of HNE, primarily peptides and proteins (here the mechanisms of covalent adduct formation are described and the (patho-) physiological consequences discussed), and IV. the metabolism of HNE leading to a great number of degradation products, some of which are excreted in urine and may serve as non-invasive biomarkers of oxidative stress. PMID:26437435

  4. Lipid peroxidation of plants under microgravity and its simulation

    NASA Astrophysics Data System (ADS)

    Zhadko, S. I.; Polulyakh, Yu. A.; Vorobyeva, T. V.; Baraboy, V. A.

    1994-08-01

    In series of space experiments a board the biosatellites ``Cosmos 1887'', ``Bion 9'', the orbital stations ``Salut'', ``Mir'' and under clinostating, changes of lipid peroxidation (LPO) and antioxidation activity (AOA) of Chlorella, Haplopappus tissue culture, wheat and pea roots were determined. The changes had a complex fluctuation character three steps of response were established; LPO decreasing accompanied by AOA increase; stabilization LPO⇄AOA balance; secondary LPO activation. Most early and highly amplitude decreasing of LPO were fixed in mitochondria. The rate of response have been increased on multicellular level of plants organization.

  5. Lipid diffusion in sperm plasma membranes exposed to peroxidative injury from oxygen free radicals.

    PubMed

    Christova, Yonka; James, Peter S; Jones, Roy

    2004-07-01

    Unsaturated lipids in sperm plasma membranes are very susceptible to peroxidation when exposed to reactive oxygen species (ROS). In this investigation we have incubated ram spermatozoa in the presence of two ROS generating systems, ascorbate/FeSO4 and potassium peroxychromate (K3CrO8), and examined their effects on membrane fluidity by measuring fluorescence recovery after photobleaching (FRAP) of a lipid reporter probe 5-(N-octadecanoyl)-aminofluorescein (ODAF). Peroxidation was monitored by malonaldehyde formation and changes in fluorescence emission of 4,4-difluoro-5-(4-phenyl-1,3-butadienyl)-4-bora-3a,4a-diaza-s-indacene-3-undecanoic acid (C11-BODIPY(581/591)). Ascorbate/FeSO4-induced peroxidation was inhibited by Vitamin E, butylated hydroxyanisole (BHA), 1,4-diazobicyclo(2,2,2)octane (DABCO), and to a lesser extent by ethanol. Added superoxide dismutase (SOD), gluthathione peroxidase (GPX), and catalase were ineffective scavengers. K3CrO8 induced very rapid peroxidation that could be delayed, but not prevented, by Vitamin E, BHT, DABCO, ethanol, and mannitol; once again SOD, GPX, and catalase were ineffective scavengers. Neither peroxidation with ascorbate/FeSO4 nor K3CrO8, or added H2O2 or malonaldehyde perturbed ODAF diffusion in any region of the sperm plasma membrane. Vitamin E tended to enhance diffusion rates. Exogenous cumene hydroperoxide, however, reduced ODAF diffusion to low levels on the sperm head. These results suggest that the adverse effects of ROS on spermatozoa are more likely to be caused by direct oxidation of proteins and membrane permeabilisation than disturbance of lipid fluidity. PMID:15112331

  6. Effect of occupation on lipid peroxidation and antioxidants' status in masons.

    PubMed

    Mallika, R; Srinivasan, K N; Pugalendi, K V

    2000-01-01

    Effect of occupation on haematological factors, lipid peroxidation and antioxidants' status was studied in masons and compared with normal subjects. Red blood corpuscles (RBC), haemoglobin (Hb), Vitamin C, Vitamin E, beta-carotene levels and glutathione peroxidase (GSHPx), superoxide dismutase (SOD) and catalase (CAT) activities decreased. Thiobarbituric acid reacting substances (TBARS) level increased. Occupational exposure to cement increased lipid peroxidation but decreased antioxidants' levels in masons. Increased lipid peroxidation seems to be responsible for the reduction in RBC and Hb. PMID:10919101

  7. Novel approaches to identify protein adducts produced by lipid peroxidation.

    PubMed

    Codreanu, S G; Liebler, D C

    2015-01-01

    Lipid peroxidation is responsible for the generation of chemically reactive, diffusible lipid-derived electrophiles (LDEs) that covalently modify cellular protein targets. These protein modifications modulate protein activity and macromolecular interactions and induce adaptive and toxic cell signaling. Protein modifications induced by LDEs can be identified and quantified by affinity enrichment and liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based techniques. Tagged LDE analog probes with different electrophilic groups can be covalently captured by click chemistry for LC-MS/MS analyses, thereby enabling in-depth studies of proteome damage at the protein and peptide sequence levels. Conversely, click-reactive, thiol-directed probes can be used to evaluate thiol damage caused by LDE by difference. These analytical approaches permit systematic study of the dynamics of protein damage caused by LDE and mechanisms by which oxidative stress contribute to toxicity and diseases. PMID:25819163

  8. Systemic complement activation, lung injury, and products of lipid peroxidation.

    PubMed Central

    Ward, P A; Till, G O; Hatherill, J R; Annesley, T M; Kunkel, R G

    1985-01-01

    Previously we have demonstrated that systemic activation of the complement system after intravenous injection of cobra venom factor (CVF) results in acute lung injury as reflected by increases in the vascular permeability of the lung as well as by morphologic evidence of damage to lung vascular endothelial cells. In using the vascular permeability of the lung as the reference, the current studies show a quantitative correlation between lung injury and the appearance in plasma of lipid peroxidation products (conjugated dienes) as well as increased concentrations of lactic dehydrogenase (LDH) and one of its isoenzymes (LDH-4). After injection of CVF, extracts of lungs also showed elevated levels of conjugated dienes, whereas no elevations were found in extracts of liver, kidney, and spleen. There was no evidence in CVF-injected rats of renal or hepatic injury as reflected by the lack of development of proteinuria and the failure to detect increased serum levels of liver-related enzymes. Other peroxidation products identified in plasma of CVF-injected rats involved hydroperoxides and fluorescent compounds with features of Schiff bases. Not surprisingly, malondialdehyde was not found to be a reliable plasma indicator of lipid peroxidation associated with oxygen radical-mediated lung vascular injury. In using a model of oxygen radical-independent lung injury induced by oleic acid, although large amounts of LDH and LDH-4 were found in the plasma, no increases in plasma levels of conjugated dienes were detected. In CVF-injected animals treated with interventions protective against lung injury (neutrophil depletion, catalase, hydroxyl radical scavengers, or iron chelators), there were striking reductions in the plasma levels of conjugated dienes, hydroperoxides, and fluorochromic products. Morphometric analysis of lung sections revealed that the protective interventions did not interfere with the accumulation of neutrophils in lung interstitial capillaries after systemic

  9. Exploring the biology of lipid peroxidation-derived protein carbonylation.

    PubMed

    Fritz, Kristofer S; Petersen, Dennis R

    2011-09-19

    The sustained overproduction of reactive oxygen and nitrogen species results in an imbalance of cellular prooxidant-antioxidant systems and is implicated in numerous disease states, including alcoholic liver disease, cancer, neurological disorders, inflammation, and cardiovascular disease. The accumulation of reactive aldehydes resulting from sustained oxidative stress and lipid peroxidation is an underlying factor in the development of these pathologies. Determining the biochemical factors that elicit cellular responses resulting from protein carbonylation remains a key element to developing therapeutic approaches and ameliorating disease pathologies. This review details our current understanding of the generation of reactive aldehydes via lipid peroxidation resulting in protein carbonylation, focusing on pathophysiologic factors associated with 4-hydroxynonenal-protein modification. Additionally, an overview of in vitro and in vivo model systems used to study the physiologic impact of protein carbonylation is presented. Finally, an update of the methods commonly used in characterizing protein modification by reactive aldehydes provides an overview of isolation techniques, mass spectrometry, and computational biology. It is apparent that research in this area employing state-of-the-art proteomics, mass spectrometry, and computational biology is rapidly evolving, yielding foundational knowledge concerning the molecular mechanisms of protein carbonylation and its relation to a spectrum of diseases associated with oxidative stress. PMID:21812433

  10. High levels of lipid peroxidation in semen of diabetic patients.

    PubMed

    La Vignera, S; Condorelli, R A; Vicari, E; D'Agata, R; Salemi, M; Calogero, A E

    2012-05-01

    The aim of this study was to evaluate the level of malondialdehyde (MDA) (one of the final products of lipid peroxidation and well-known marker of oxidative stress) in semen of infertile men with type 2 diabetes and to investigate its relationship with their glycaemic control. Forty infertile men with type 2 diabetes were evaluated. The mean ages were 36.5 ± 8.0. Men with diabetes were divided into two groups. Group A (n = 20) with glycated haemoglobin >10% and group B (n = 20) with glycated haemoglobin <7%. A single sample was examined according to the criteria of the World Health Organization (WHO Laboratory Manual for the Examination of Human Semen and Sperm-Cervical Mucus Interaction, 1999, Cambridge University Press). MDA was assessed using the thiobarbituric acid method. MDA concentration in semen of group A patients (0.95 ± 0.35 nmol ml(-1)) was significantly higher than in group B patients (0.43 ± 0.13 nmol ml(-1)) (P value < 0.05) and had negative relationship with sperm density (r = -.717; P value < 0.05), total sperm count (r = -.625; P value < 0.05), progressive motility (r = -.489; P value < 0.05) and normal forms (r = -.545; P value < 0.05). Based on these results, it could be concluded that increase in lipid peroxidation in men with diabetes with poor metabolic control was associated with low sperm quality. PMID:21919944

  11. Effects of glycyl-histidyl-lysyl chelated Cu(II) on ferritin dependent lipid peroxidation.

    PubMed

    Miller, D M; DeSilva, D; Pickart, L; Aust, S D

    1990-01-01

    The copper binding tripeptide, glycyl-L-histidyl-L-lysine [GHK:Cu(II)] has a plethora of biological effects related to the wound healing process. The presence of iron complexes in damaged tissues is detrimental to wound healing, due to local inflammation, as well as microbial infection mediated by iron. To test if the wound healing properties of GHK:Cu(II) are due to an affect on iron metabolism, we examined the effects of GHK:Cu(II) on iron catalyzed lipid peroxidation. GHK:Cu(II) inhibited lipid peroxidation only if the iron source was ferritin. Whereas GHK:Cu(II) inhibited ferritin iron release it did not exhibit significant superoxide dismutase-like or ceruloplasmin-like activity. We propose that GHK:Cu(II) binds to the channels of ferritin involved in iron release and physically prevents the release of Fe(II). Thus, a biological effect of GHK:Cu(II), possibly related to wound healing, may be the inhibition of ferritin iron release in damaged tissues, preventing inflammation and microbial infections. PMID:2244543

  12. Lipid peroxidation by "free" iron ions and myoglobin as affected by dietary antioxidants in simulated gastric fluids.

    PubMed

    Lapidot, Tair; Granit, Rina; Kanner, Joseph

    2005-05-01

    Grilled red turkey muscle (Doner Kabab) is a real "fast food" containing approximately 200 microM hydroperoxides, homogenized in simulated gastric fluid and oxidized more rapidly at pH 3.0 than at pH 5.0, after 180 min, producing 1200 and 600 microM hydroperoxides, respectively. The effects of "free" iron ions and metmyoglobin, two potential catalyzers of lipid peroxidation in muscle foods, were evaluated for linoleic acid peroxidation at pH 3.0 of simulated gastric fluid. The prooxidant effects of free iron ions on linoleic acid peroxidation in simulated gastric fluid was evaluated in the presence of ascorbic acid. At low concentrations of ascorbic acid, the effects were prooxidative, which was reversed at high concentrations. In the presence of metmyoglobin, ascorbic acid with or without free iron enhanced the antioxidative effect. Lipid peroxidation by an iron-ascorbic acid system was inhibited totally by 250-500 microM catechin at pH 3.0. The catechin antioxidant effect was determined also in the iron-ascorbic acid system containing metmyoglobin. In this system, catechin totally inhibited lipid peroxidation at a concentration 20-fold lower than without metmyoglobin. The ability of catechin to inhibit lipid peroxidation was also determined at a low pH with beta-carotene as a sensitive target molecule for oxidation. The results show that a significant protection was achieved only with almost 100-fold higher antioxidant concentration. Polyphenols from different groups were determined for the antioxidant activity at pH 3.0. The results show a high antioxidant activity of polyphenols with orthodihydroxylated groups at the B ring, unsaturation, and the presence of a 4-oxo group in the heterocyclic ring, as demonstrated by quercetin. PMID:15853376

  13. A spectrophotometric assay for lipid peroxides in serum lipoproteins using a commercially available reagent.

    PubMed

    el-Saadani, M; Esterbauer, H; el-Sayed, M; Goher, M; Nassar, A Y; Jürgens, G

    1989-04-01

    A method is described for measuring lipid peroxides by means of the color reagent of a commercially available test kit for cholesterol estimation. In principle, this assay makes use of the oxidative capacity of lipid peroxides to convert iodide to iodine, which can be measured photometrically at 365 nm. Calibration curves were obtained using peroxides such as H2O2, t-butyl hydroperoxide, and cumene hydroperoxide. A stoichiometric relationship was observed between the amount of organic peroxides assayed and the concentration of iodine produced. Concentrations of lipid peroxides as small as 1 nmol/ml could be measured. The ability to estimate lipid peroxides of isolated low density lipoprotein was demonstrated. PMID:2754343

  14. Obesity Induces Tissue-Specific Changes in Lipid Peroxidation Defense Enzymes

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Lipid peroxidation is thought to be a component of obesity-induced pathology. However, the tissue-dependent changes in lipid peroxidation (LOOH) and LOOH defense mechanisms in response to obesity are unclear. In this work, we utilized 14-week old male, obese Zucker rats and their control, lean litte...

  15. Visible Light-Induced Lipid Peroxidation of Unsaturated Fatty Acids in the Retina and the Inhibitory Effects of Blueberry Polyphenols.

    PubMed

    Liu, Yixiang; Zhang, Di; Hu, Jimei; Liu, Guangming; Chen, Jun; Sun, Lechang; Jiang, Zedong; Zhang, Xichun; Chen, Qingchou; Ji, Baoping

    2015-10-28

    The lipid peroxidation of unsaturated fatty acids (UFAs) in the retina not only threatens visual cells but also affects the physiological health of the retina. In this work, the potential damages caused by daily visible light exposure on retinal UFAs were evaluated via a simulated in vitro model. At the same time, the benefits of dietary supplementation of blueberries to the eyes were also assessed. After prolonged light exposure, lipid peroxidation occurred for both docosahexaenoic and arachidonic acids (DHA and AA, respectively). The oxidized UFAs presented obvious cytotoxicity and significantly inhibited cell growth in retinal pigment epithelium cells. Among the different blueberry polyphenol fractions, the flavonoid-rich fraction, in which quercetin was discovered as the main component, was considerably better in preventing visible light-induced DHA lipid peroxidation than the anthocyanin- and phenolic acid-rich fractions. Then the retinal protective activity of blueberry polyphenols against light-induced retinal injury was confirmed in vivo. On the basis of the above results, inhibiting lipid peroxidation of UFAs in the retina is proposed to be another important function mechanism for antioxidants to nourish eyes. PMID:26456696

  16. Lipid peroxidation in brain or spinal cord mitochondria after injury.

    PubMed

    Hall, Edward D; Wang, Juan A; Bosken, Jeffrey M; Singh, Indrapal N

    2016-04-01

    Extensive evidence has demonstrated an important role of oxygen radical formation (i.e., oxidative stress) as a mediator of the secondary injury process that occurs following primary mechanical injury to the brain or spinal cord. The predominant form of oxygen radical-induced oxidative damage that occurs in injured nervous tissue is lipid peroxidation (LP). Much of the oxidative stress in injured nerve cells initially begins in mitochondria via the generation of the reactive nitrogen species peroxynitrite (PN) which then can generate multiple highly reactive free radicals including nitrogen dioxide (•NO2), hydroxyl radical (•OH) and carbonate radical (•CO3). Each can readily induce LP within the phospholipid membranes of the mitochondrion leading to respiratory dysfunction, calcium buffering impairment, mitochondrial permeability transition and cell death. Validation of the role of LP in central nervous system secondary injury has been provided by the mitochondrial and neuroprotective effects of multiple antioxidant agents which are briefly reviewed. PMID:25595872

  17. 'Mitochondrial energy imbalance and lipid peroxidation cause cell death in Friedreich's ataxia'.

    PubMed

    Abeti, R; Parkinson, M H; Hargreaves, I P; Angelova, P R; Sandi, C; Pook, M A; Giunti, P; Abramov, A Y

    2016-01-01

    Friedreich's ataxia (FRDA) is an inherited neurodegenerative disease. The mutation consists of a GAA repeat expansion within the FXN gene, which downregulates frataxin, leading to abnormal mitochondrial iron accumulation, which may in turn cause changes in mitochondrial function. Although, many studies of FRDA patients and mouse models have been conducted in the past two decades, the role of frataxin in mitochondrial pathophysiology remains elusive. Are the mitochondrial abnormalities only a side effect of the increased accumulation of reactive iron, generating oxidative stress? Or does the progressive lack of iron-sulphur clusters (ISCs), induced by reduced frataxin, cause an inhibition of the electron transport chain complexes (CI, II and III) leading to reactive oxygen species escaping from oxidative phosphorylation reactions? To answer these crucial questions, we have characterised the mitochondrial pathophysiology of a group of disease-relevant and readily accessible neurons, cerebellar granule cells, from a validated FRDA mouse model. By using live cell imaging and biochemical techniques we were able to demonstrate that mitochondria are deregulated in neurons from the YG8R FRDA mouse model, causing a decrease in mitochondrial membrane potential (▵Ψm) due to an inhibition of Complex I, which is partially compensated by an overactivation of Complex II. This complex activity imbalance leads to ROS generation in both mitochondrial matrix and cytosol, which results in glutathione depletion and increased lipid peroxidation. Preventing this increase in lipid peroxidation, in neurons, protects against in cell death. This work describes the pathophysiological properties of the mitochondria in neurons from a FRDA mouse model and shows that lipid peroxidation could be an important target for novel therapeutic strategies in FRDA, which still lacks a cure. PMID:27228352

  18. 'Mitochondrial energy imbalance and lipid peroxidation cause cell death in Friedreich's ataxia'

    PubMed Central

    Abeti, R; Parkinson, M H; Hargreaves, I P; Angelova, P R; Sandi, C; Pook, M A; Giunti, P; Abramov, A Y

    2016-01-01

    Friedreich's ataxia (FRDA) is an inherited neurodegenerative disease. The mutation consists of a GAA repeat expansion within the FXN gene, which downregulates frataxin, leading to abnormal mitochondrial iron accumulation, which may in turn cause changes in mitochondrial function. Although, many studies of FRDA patients and mouse models have been conducted in the past two decades, the role of frataxin in mitochondrial pathophysiology remains elusive. Are the mitochondrial abnormalities only a side effect of the increased accumulation of reactive iron, generating oxidative stress? Or does the progressive lack of iron-sulphur clusters (ISCs), induced by reduced frataxin, cause an inhibition of the electron transport chain complexes (CI, II and III) leading to reactive oxygen species escaping from oxidative phosphorylation reactions? To answer these crucial questions, we have characterised the mitochondrial pathophysiology of a group of disease-relevant and readily accessible neurons, cerebellar granule cells, from a validated FRDA mouse model. By using live cell imaging and biochemical techniques we were able to demonstrate that mitochondria are deregulated in neurons from the YG8R FRDA mouse model, causing a decrease in mitochondrial membrane potential (▵Ψm) due to an inhibition of Complex I, which is partially compensated by an overactivation of Complex II. This complex activity imbalance leads to ROS generation in both mitochondrial matrix and cytosol, which results in glutathione depletion and increased lipid peroxidation. Preventing this increase in lipid peroxidation, in neurons, protects against in cell death. This work describes the pathophysiological properties of the mitochondria in neurons from a FRDA mouse model and shows that lipid peroxidation could be an important target for novel therapeutic strategies in FRDA, which still lacks a cure. PMID:27228352

  19. Effect of Hypericum perforatum Aqueous Extracts on Serum Lipids, Aminotransferases, and Lipid Peroxidation in Hyperlipidemic Rats

    PubMed Central

    Ghosian Moghaddam, Mohammad Hassan; Roghani, Mehrdad; Maleki, Maryam

    2016-01-01

    Background: Patients with high levels of total cholesterol (TCH), low-density lipoprotein cholesterol (LDL-CH), and triglyceride (TG) are at increased risk of coronary heart disease. Studies have shown that flavonoids and antioxidant compounds have beneficial effects on hyperlipidemia. Objectives: The aim of the present study was to evaluate the effects of extract of Hypericum perforatum (EHP) on the serum lipid profile (TCH, TG, and LDL-CH), aminotransferase, alkaline phosphatase, and lipid peroxidation in hyperlipidemic rats. Materials and Methods: Thirty-two male rats weighting 200 ± 10 g were randomly divided into four experimental groups: 1) control, 2) control + EHP, 3) hyperlipidemia, and 4) hyperlipidemia + EHP. The rats in the hyperlipidemic groups were fed a high-fat diet for 60 days, and EHP (300 mg/kg) was injected intraperitoneally for 2 weeks in the rats in the second and fourth groups. At the end of the experimental period, blood samples from each group were analyzed. Results: There was a significant reduction in LDL-CH in the control + EHP group and the hyperlipidemia + EHP group (P < 0.05). TCH was significantly reduced in the control + EHP group (P < 0.05). There were no significant changes in the levels of TG and HDL-CH. Malondialdehyde, aspartate aminotransferase, and alanine aminotransferase were significantly reduced in the hyperlipidemia + EHP group (P < 0.05), with no significant change in alkaline phosphatase. Conclusions: EHP was able to both reduce LDL-CH and to significantly decrease markers of oxidative stress and lipid peroxidation induced by hyperlipidemia. Therefore, this herb, as a new pharmacological component, could be used to reduce certain blood lipids, lipid peroxidation, and aminotransferase markers. PMID:26949689

  20. The generation of oxidation products of benzo(a)pyrene by lipid peroxidation: a study using gamma-irradiation

    SciTech Connect

    Gower, J.D.; Wills, E.D.

    1984-09-01

    The role which active oxygen and radicals generated by the peroxidation of unsaturated fatty acids could play in the oxidation of benzo(a)pyrene has been studied using gamma-irradiation. Irradiation of benzo(a)pyrene resulted in the formation of benzo(a)pyrene 1,6-, 3,6- and 6,12-quinones and other more polar products which were analysed by h.p.l.c. OH. radicals are believed to be involved in this oxidation. The presence of polyunsaturated fatty acids and polyunsaturated lipids stimulated the formation of benzo(a)pyrene products following gamma-irradiation. Oxidation of benzo(a)pyrene also occurred over a period of days in the presence of autoxidising mackerel oil. The rate of benzo(a)pyrene oxidation was related to the extent of lipid peroxidation as determined by malonaldehyde formation. Malonaldehyde production as a result of peroxidising lipids was inhibited by benzo(a)pyrene which suggested that benzo(a)pyrene reacted directly with lipid peroxy radicals or hydroperoxides generated in the process of lipid peroxidation. These results demonstrate that oxidation products of the peroxidation of lipids and fatty acids are able to react directly with benzo(a)pyrene to form products including benzo(a)pyrene quinones without the presence of enzymes such as the cytochrome P-450 mixed function oxidase system and prostaglandin synthetase. It is possible that benzo(a)pyrene may be activated by these types of reactions in vivo or in vitro when benzo(a)pyrene is in contact with polyunsaturated lipids in foodstuffs or the intestinal lumen and peroxidation of unsaturated fats may play an important role in human carcinogenesis.

  1. Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models

    PubMed Central

    2015-01-01

    Ferrostatin-1 (Fer-1) inhibits ferroptosis, a form of regulated, oxidative, nonapoptotic cell death. We found that Fer-1 inhibited cell death in cellular models of Huntington’s disease (HD), periventricular leukomalacia (PVL), and kidney dysfunction; Fer-1 inhibited lipid peroxidation, but not mitochondrial reactive oxygen species formation or lysosomal membrane permeability. We developed a mechanistic model to explain the activity of Fer-1, which guided the development of ferrostatins with improved properties. These studies suggest numerous therapeutic uses for ferrostatins, and that lipid peroxidation mediates diverse disease phenotypes. PMID:24592866

  2. Investigation of the effect of chamazulene on lipid peroxidation and free radical processes.

    PubMed

    Rekka, E A; Kourounakis, A P; Kourounakis, P N

    1996-06-01

    Oxygen toxicity and related free radical reactions are implicated in numerous pathophysiological conditions, like atherosclerosis, inflammation, gastric ulceration, neuronal degeneration, tumour promotion. The flowers of Matricaria chamomilla, Asteraceae, have been used therapeutically for conditions in which oxidative stress is supposed to be implicated. We considered interesting to investigate the effect of Chamazulene, the active substance of chamomile, on free radical processes. Membrane lipid peroxidation was induced by Fe2+/ascorbate and assessed as the 2-thiobarbituric acid reactive material. The hydroxyl radical scavenging activity was studied as the competition of Chamazulene with DMSO for HO. generated by Fe3+/ascorbate. Finally, the interaction of Chamazulene with the N-centered stable free radical DPPH was estimated photometrically (517 nm). It was found that Chamazulene inhibited lipid peroxidation in a concentration and time dependent manner presenting an IC50 of 18 microM after 45 min incubation. It could also inhibit the autoxidation of DMSO (33 mM) by 76% at 25 mM, and had a weak capacity to interact with DPPH. In conclusion, Chamazulene presents interesting properties concerning radical processes. PMID:8827832

  3. A meta-analysis of lipid peroxidation markers in major depression

    PubMed Central

    Mazereeuw, Graham; Herrmann, Nathan; Andreazza, Ana C; Khan, Maisha M; Lanctôt, Krista L

    2015-01-01

    Background Major depressive disorder (MDD) may be associated with oxidative damage to lipids, which can potentially affect mood-regulating pathways. This meta-analysis summarizes current knowledge regarding lipid peroxidation markers in clinical samples of MDD and the effects of antidepressant pharmacotherapy on those markers. Methods MEDLINE, EMBASE, CINAHL, PsycINFO, and Cochrane Collaboration were searched for original, peer-reviewed articles measuring markers of lipid peroxidation in patients with MDD and nondepressed healthy controls up to April 2015. Standardized mean differences (SMDs) were generated from random effects models summarizing mean (± standard deviations) concentrations of selected markers. Results Lipid peroxidation was greater in MDD than in controls (studies =17, N=857 MDD/782 control, SMD =0.83 [0.56–1.09], z=6.11, P<0.01, I2=84.0%) and was correlated with greater depressive symptom severity (B=0.05, df=8, P<0.01). Antidepressant treatment was associated with a reduction in lipid peroxidation in MDD patients (studies=5, N=222, SMD=0.71 [0.40–0.97], P<0.01; I2=42.5%). Limitations Lipid peroxidation markers were sampled from peripheral blood, included studies comparing MDD to controls were all cross-sectional, and only five antidepressant treatment studies were eligible for inclusion. Conclusion Increased lipid peroxidation was associated with MDD and may be normalized by antidepressants. Continued investigation of lipid peroxidation in MDD is warranted. PMID:26491326

  4. [Effect of ambroxol on lipid peroxidation in homogenates of the human placenta].

    PubMed

    Chlubek, D; Zawierta, J; Olszewska, M; Kaźmierczyk, A; Sikora, M

    2001-10-01

    Free radically induced lipid peroxidation has been suggested as a possible pathogenic factor in pregnancy complications. The placenta is a potential source of lipid peroxides, due to its high lipid concentration. Cells and tissues are protected against toxic lipid peroxides by antioxidants. Ambroxol was found to be equipotent to well-known antioxidants in protecting lipids from peroxidative attack in lungs. To date there is no information on ambroxol capacity to act as a lipid antioxidant in the human placenta. Therefore, the aim of our study was to investigate the effect of ambroxol on lipid peroxidation in homogenates of the human placenta by malondialdehyde measurements. Fourteen homogenates of placentas obtained from healthy women were incubated for 24 hours (pH = 7.4, temp. 37 degrees C) without (group II) and with (group III) ambroxol hydrochloride solutions (Boehringer Ingelheim--Germany) at concentration of 2200 ng/mL. Non-incubated homogenates were treated as a control group (group I). It was found that lipid peroxidation and malondialdehyde formation is significantly higher in group II homogenates than in the control group (p < 0.05). Incubation with ambroxol (group III) caused a non-significant increase of malondialdehyde concentration in comparison with the control group and a non-significant but distinct decrease when compared with group II (incubation without ambroxol). This investigation shows that ambroxol decreases malondialdehyde formation in homogenates of the human placenta and can be regarded as lipid antioxidant. PMID:11848017

  5. Carbon Monoxide Modulates Connexin Function through a Lipid Peroxidation-Dependent Process: A Hypothesis

    PubMed Central

    Retamal, Mauricio A.

    2016-01-01

    Hemichannels are ion channels composed of six connexins (Cxs), and they have the peculiarity to be permeable not only to ions, but also to molecules such as ATP and glutamate. Under physiological conditions they present a low open probability, which is sufficient to enable them to participate in several physiological functions. However, massive and/or prolonged hemichannel opening induces or accelerates cell death. Therefore, the study of the molecular mechanisms that control hemichannel activity appears to be essential for understanding several physiological and pathological processes. Carbon monoxide (CO) is a gaseous transmitter that modulates many cellular processes, some of them through modulation of ion channel activity. CO exerts its biological actions through the activation of guanylate cyclase and/or inducing direct carbonylation of proline, threonine, lysine, and arginine. It is well accepted that guanylate cyclase dependent pathway and direct carbonylation, are not sensitive to reducing agents. However, it is important to point out that CO—through a lipid peroxide dependent process—can also induce a secondary carbonylation in cysteine groups, which is sensitive to reducing agents. Recently, in our laboratory we demonstrated that the application of CO donors to the bath solution inhibited Cx46 hemichannel currents in Xenopus laevis oocytes, a phenomenon that was fully reverted by reducing agents. Therefore, a plausible mechanism of CO-induced Cx46 hemichannel inhibition is through Cx46-lipid oxidation. In this work, I will present current evidence and some preliminary results that support the following hypothesis: Carbon monoxide inhibits Cx46 HCs through a lipid peroxidation-dependent process. The main goal of this paper is to broaden the scientific community interest in studying the relationship between CO-Fatty acids and hemichannels, which will pave the way to more research directed to the understanding of the molecular mechanism(s) that control

  6. Carbon Monoxide Modulates Connexin Function through a Lipid Peroxidation-Dependent Process: A Hypothesis.

    PubMed

    Retamal, Mauricio A

    2016-01-01

    Hemichannels are ion channels composed of six connexins (Cxs), and they have the peculiarity to be permeable not only to ions, but also to molecules such as ATP and glutamate. Under physiological conditions they present a low open probability, which is sufficient to enable them to participate in several physiological functions. However, massive and/or prolonged hemichannel opening induces or accelerates cell death. Therefore, the study of the molecular mechanisms that control hemichannel activity appears to be essential for understanding several physiological and pathological processes. Carbon monoxide (CO) is a gaseous transmitter that modulates many cellular processes, some of them through modulation of ion channel activity. CO exerts its biological actions through the activation of guanylate cyclase and/or inducing direct carbonylation of proline, threonine, lysine, and arginine. It is well accepted that guanylate cyclase dependent pathway and direct carbonylation, are not sensitive to reducing agents. However, it is important to point out that CO-through a lipid peroxide dependent process-can also induce a secondary carbonylation in cysteine groups, which is sensitive to reducing agents. Recently, in our laboratory we demonstrated that the application of CO donors to the bath solution inhibited Cx46 hemichannel currents in Xenopus laevis oocytes, a phenomenon that was fully reverted by reducing agents. Therefore, a plausible mechanism of CO-induced Cx46 hemichannel inhibition is through Cx46-lipid oxidation. In this work, I will present current evidence and some preliminary results that support the following hypothesis: Carbon monoxide inhibits Cx46 HCs through a lipid peroxidation-dependent process. The main goal of this paper is to broaden the scientific community interest in studying the relationship between CO-Fatty acids and hemichannels, which will pave the way to more research directed to the understanding of the molecular mechanism(s) that control the

  7. Enhancement of lipid peroxidation and its amelioration by vitamin E in a subject with mutations in the SBP2 gene[S

    PubMed Central

    Saito, Yoshiro; Shichiri, Mototada; Hamajima, Takashi; Ishida, Noriko; Mita, Yuichiro; Nakao, Shohei; Hagihara, Yoshihisa; Yoshida, Yasukazu; Takahashi, Kazuhiko; Niki, Etsuo; Noguchi, Noriko

    2015-01-01

    Selenocysteine (Sec) insertion sequence-binding protein 2 (SBP2) is essential for the biosynthesis of Sec-containing proteins, termed selenoproteins. Subjects with mutations in the SBP2 gene have decreased levels of several selenoproteins, resulting in a complex phenotype. Selenoproteins play a significant role in antioxidative defense, and deficiencies in these proteins can lead to increased oxidative stress. However, lipid peroxidation and the effects of antioxidants in subjects with SBP2 gene mutations have not been studied. In the present study, we evaluated the lipid peroxidation products in the blood of a subject (the proband) with mutations in the SBP2 gene. We found that the proband had higher levels of free radical-mediated lipid peroxidation products, such as 7β-hydroxycholesterol, than the control subjects. Treatment of the proband with vitamin E (α-tocopherol acetate, 100 mg/day), a lipid-soluble antioxidant, for 2 years reduced lipid peroxidation product levels to those of control subjects. Withdrawal of vitamin E treatment for 7 months resulted in an increase in lipid peroxidation products. Collectively, these results clearly indicate that free radical-mediated oxidative stress is increased in the subject with SBP2 gene mutations and that vitamin E treatment effectively inhibits the generation of lipid peroxidation products. PMID:26411970

  8. Neurotoxic lipid peroxidation species formed by ischemic stroke increase injury

    PubMed Central

    Zeiger, Stephanie L. H.; Musiek, Erik S.; Zanoni, Giuseppe; Vidari, Giovanni; Morrow, Jason D.; Milne, Ginger J.; McLaughlin, BethAnn

    2009-01-01

    Stroke is the third leading cause of death in the United States yet no neuroprotective agents for treatment are clinically available. There is a pressing need to understand the signaling molecules which mediate ischemic cell death and identify novel neuroprotective targets. Cyclopentenone isoprostanes (IsoP), formed following free radical mediated peroxidation of arachidonic acid, are used as markers of stress but their bioactivity is poorly understood. We have recently shown that 15-A2t-Isop is a potent neurotoxin in vitro and increases the free radical burden in neurons. In this work, we demonstrate that 15-A2t-IsoP is abundantly produced in stroke infarcted human cortical tissue. Using primary neuronal cultures we found that minimally toxic exposure to 15-A2t-IsoP does not alter ATP content, but in combination with oxygen glucose deprivation resulted in a significant hyperpolarization of the mitochondrial membrane and dramatically increased neuronal cell death. In the presence of Ca2+, 15-A2t-IsoP led to a rapid induction of the permeability transition pore and release of cytochrome c. Taken with our previous work, these data support a model in which ischemia causes generation of reactive oxygen species, calcium influx, lipid peroxidation and 15-A2t-IsoP formation. These factors combine to enhance opening of the permeability transition pore leading to cell death subsequent to mitochondrial cytochrome c release. This data is the first documentation of significant 15-A2t-IsoP formation following acute ischemic stroke and suggests addition of 15-A2t-IsoP to in vitro models of ischemia may help to more fully recapitulate stroke injury. PMID:19699297

  9. Lipid peroxidation and water penetration in lipid bilayers: a W-band EPR study.

    PubMed

    Conte, Elena; Megli, Francesco Maria; Khandelia, Himanshu; Jeschke, Gunnar; Bordignon, Enrica

    2013-02-01

    Lipid peroxidation plays a key role in the alteration of cell membrane's properties. Here we used as model systems multilamellar vesicles (MLVs) made of the first two products in the oxidative cascade of linoleoyl lecithin, namely 1-palmitoyl-2-(13-hydroperoxy-9,11-octadecanedienoyl)-lecithin (HpPLPC) and 1-palmitoyl-2-(13-hydroxy-9,11-octadecanedienoyl)-lecithin (OHPLPC), exhibiting a hydroperoxide or a hydroxy group at position 13, respectively. The two oxidized lipids were used either pure or in a 1:1 molar ratio mixture with untreated 1-palmitoyl-2-linoleoyl-lecithin (PLPC). The model membranes were doped with spin-labeled lipids to study bilayer alterations by electron paramagnetic resonance (EPR) spectroscopy. Two different spin-labeled lipids were used, bearing the doxyl ring at position (n) 5 or 16: γ-palmitoyl-β-(n-doxylstearoyl)-lecithin (n-DSPPC) and n-doxylstearic acid (n-DSA). Small changes in the acyl chain order in the sub-polar region and at the methyl-terminal induced by lipid peroxidation were detected by X-band EPR. Concomitantly, the polarity and proticity of the membrane bilayer in those regions were investigated at W band in frozen samples. Analysis of the g(xx) and A(zz) parameters revealed that OHPLPC, but mostly HpPLPC, induced a measurable increase in polarity and H-bonding propensity in the central region of the bilayer. Molecular dynamics simulation performed on 16-DSA in the PLPC-HpPLPC bilayer revealed that water molecules are statistically favored with respect to the hydroperoxide groups to interact with the nitroxide at the methyl-terminal, confirming that the H-bonds experimentally observed are due to increased water penetration in the bilayer. The EPR and MD data on model membranes demonstrate that cell membrane damage by oxidative stress cause alteration of water penetration in the bilayer. PMID:23036933

  10. Loss of PLA2G6 leads to elevated mitochondrial lipid peroxidation and mitochondrial dysfunction

    PubMed Central

    Castillo-Quan, Jorge Iván; Bartolome, Fernando; Angelova, Plamena R.; Li, Li; Pope, Simon; Cochemé, Helena M.; Khan, Shabana; Asghari, Shabnam; Bhatia, Kailash P.; Hardy, John; Abramov, Andrey Y.; Partridge, Linda

    2015-01-01

    The PLA2G6 gene encodes a group VIA calcium-independent phospholipase A2 beta enzyme that selectively hydrolyses glycerophospholipids to release free fatty acids. Mutations in PLA2G6 have been associated with disorders such as infantile neuroaxonal dystrophy, neurodegeneration with brain iron accumulation type II and Karak syndrome. More recently, PLA2G6 was identified as the causative gene in a subgroup of patients with autosomal recessive early-onset dystonia-parkinsonism. Neuropathological examination revealed widespread Lewy body pathology and the accumulation of hyperphosphorylated tau, supporting a link between PLA2G6 mutations and parkinsonian disorders. Here we show that knockout of the Drosophila homologue of the PLA2G6 gene, iPLA2-VIA, results in reduced survival, locomotor deficits and organismal hypersensitivity to oxidative stress. Furthermore, we demonstrate that loss of iPLA2-VIA function leads to a number of mitochondrial abnormalities, including mitochondrial respiratory chain dysfunction, reduced ATP synthesis and abnormal mitochondrial morphology. Moreover, we show that loss of iPLA2-VIA is strongly associated with increased lipid peroxidation levels. We confirmed our findings using cultured fibroblasts taken from two patients with mutations in the PLA2G6 gene. Similar abnormalities were seen including elevated mitochondrial lipid peroxidation and mitochondrial membrane defects, as well as raised levels of cytoplasmic and mitochondrial reactive oxygen species. Finally, we demonstrated that deuterated polyunsaturated fatty acids, which inhibit lipid peroxidation, were able to partially rescue the locomotor abnormalities seen in aged flies lacking iPLA2-VIA gene function, and restore mitochondrial membrane potential in fibroblasts from patients with PLA2G6 mutations. Taken together, our findings demonstrate that loss of normal PLA2G6 gene activity leads to lipid peroxidation, mitochondrial dysfunction and subsequent mitochondrial membrane

  11. Benzoyl peroxide increases UVA-induced plasma membrane damage and lipid oxidation in murine leukemia L1210 cells.

    PubMed

    Ibbotson, S H; Lambert, C R; Moran, M N; Lynch, M C; Kochevar, I E

    1998-01-01

    Ultraviolet A radiation induces oxidative stress and cell damage. The purpose of this investigation was to examine whether ultraviolet A-induced cell injury was amplified by the presence of a non-ultraviolet A absorbing molecule capable of generating free radicals. Benzoyl peroxide was used as a lipid soluble potential radical-generating agent. Plasma membrane permeability assessed by trypan blue uptake was used to measure cell damage in murine leukemia L1210 cells. Cells were irradiated with a pulsed Nd/YAG laser at 355 nm using 0-160 J per cm2. The ratio of the fluence-response slope in the presence of 40 microM benzoyl peroxide to that of irradiated controls was 4.3 +/- 2.6. Benzoyl peroxide alone or benzoyl peroxide added after irradiation did not cause increased trypan blue uptake. The ratio of the fluence-response slopes in the presence of 40 microM benzoyl peroxide to that of irradiated controls was 4.7 +/- 1.4 when cells were irradiated (0-43 J per cm2) with a xenon lamp, filtered to remove wavelengths <320 nm. The increased trypan blue uptake in 355 nm-irradiated cells in the presence of benzoyl peroxide was inhibited in a concentration-dependent manner by butylated hydroxytoluene, vitamin E, and trolox, a water-soluble vitamin E derivative. Lipid oxidation, assessed as thiobarbituric acid reactive substances, was significantly increased in samples irradiated with ultraviolet A in the presence of benzoyl peroxide at fluences >34 J per cm2. The increased trypan blue uptake and thiobarbituric acid reactive substances were inhibited by butylated hydroxytoluene. These results suggest that agents not absorbing ultraviolet A radiation may enhance ultraviolet A-initiated oxidative stress in cells. PMID:9424093

  12. DNA-repair capacity and lipid peroxidation in chronic alcoholics.

    PubMed

    Topinka, J; Binková, B; Srám, R J; Fojtíková, I

    1991-07-01

    The possible impact of long-term overexposure to ethanol was studied in a group of chronic alcoholics in the psychiatric hospital. The level of DNA methylation and unscheduled DNA synthesis (UDS) induced by N-methyl-N-nitrosourea (MNU) in lymphocytes and lipid peroxidation (LPO) in plasma were used as markers of injury caused by alcohol abuse. The data were correlated with plasma levels of some natural antioxidants (vitamins A, C and E) and vitamin B12. The following results were obtained. The degree of DNA methylation by MNU in lymphocytes was the same in the exposed and control groups under our experimental conditions. The DNA excision-repair capacity of lymphocytes measured as UDS was decreased in alcoholics (p less than 0.01) and LPO in plasma was significantly higher (p less than 0.01) as a consequence of alcohol overconsumption. By the simple regression method, a correlation was found between LPO and vitamin C levels (LPO = -0.078 x vit. C + 1.9; p less than 0.05) and between UDS and LPO values (UDS = -0.384 x LPO + 4.1; p less than 0.05). These results support the hypothesis of a connection of cell membrane status and DNA damage and repair and the possible role of active oxygen species in cell damage caused by ethanol. PMID:2067553

  13. Relationship between Active Oxygen Species, Lipid Peroxidation, Necrosis, and Phytoalexin Production Induced by Elicitins in Nicotiana.

    PubMed Central

    Rusterucci, C.; Stallaert, V.; Milat, M. L.; Pugin, A.; Ricci, P.; Blein, J. P.

    1996-01-01

    Excised leaves of Nicotiana tabacum var Xanthi and Nicotiana rustica were treated with cryptogein and capsicein, basic and acidic elicitins, respectively. Both compounds induced leaf necrosis, the intensity of which depended on concentration and duration of treatment. N. tabacum var Xanthi was the most sensitive species and cryptogein was the most active elicitin. Lipid peroxidation in elicitin-treated Nicotiana leaves was closely correlated with the appearance of necrosis. Elicitin treatments induced a rapid and transient burst of active oxygen species (AOS) in cell cultures of both Nicotiana species, with the production by Xanthi cells being 6-fold greater than that by N. rustica. Similar maximum AOS production levels were observed with both elicitins, but capsicein required 10-fold higher concentrations than those of cryptogein. Phytoalexin production was lower in response to both elicitins in N. tabacum var Xanthi cells than in N. rustica cells, and capsicein was the most efficient elicitor of this response. In cryptogein-treated cell suspensions, phytoalexin synthesis was unaffected by diphenyleneiodonium, which inhibited AOS generation, nor was it affected by tiron or catalase, which suppressed AOS accumulation in the extracellular medium. These results suggest that AOS production, lipid peroxidation, and necrosis are directly related, whereas phytoalexin production depends on neither the presence nor the intensity of these responses. PMID:12226334

  14. [The effect of transvenous laser therapy on lipid peroxidation function in patients with ischemic heart disease].

    PubMed

    Vakhliaev, V D; Smirnova, I E; Uchaĭkina, L V; Barsel', V A; Aksiutina, M S; Matveeva, S A; Paramonova, M A; Shchedrina, I S; Syrkin, A L

    1992-07-01

    The papers deals with changes in the levels of lipid peroxidation products in patients with stable angina of effort, which occurred with intravenous helium-neon blood irradiation. The therapy was highly effective in patients with lower functional classes and persons with normal circulation, resulting in a reduction in lipid peroxidation intensity. Predictors are recommended to determine the efficiency and expediency of laser therapy in patients with coronary heart disease. PMID:1487878

  15. Lipid peroxidation during n-3 fatty acid and vitamin E supplementation in humans.

    PubMed

    Allard, J P; Kurian, R; Aghdassi, E; Muggli, R; Royall, D

    1997-05-01

    The purpose of this study was to investigate in healthy humans the effect of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) intake, alone or in combination with dL-alpha-tocopherol acetate (vitamin E) supplements on lipid peroxidation. Eighty men were randomly assigned in a double-blind fashion to take daily for 6 wk either menhaden oil (6.26 g, n-3 fatty acids) or olive oil supplements with either vitamin E (900 IU) or its placebo. Antioxidant vitamins, phospholipid composition, malondialdehyde (MDA), and lipid peroxides were measured in the plasma at baseline and week 6. At the same time, breath alkane output was measured. Plasma alpha-tocopherol concentration increased in those receiving vitamin E (P < 0.0001). In those supplemented with n-3 fatty acids, EPA and DHA increased in plasma phospholipids (P < 0.0001) and plasma MDA and lipid peroxides increased (P < 0.001 and P < 0.05, respectively). Breath alkane output did not change significantly and vitamin E intake did not prevent the increase in lipid peroxidation during menhaden oil supplementation. The results demonstrate that supplementing the diet with n-3 fatty acids resulted in an increase in lipid peroxidation, as measured by plasma MDA release and lipid peroxide products, which was not suppressed by vitamin E supplementation. PMID:9168460

  16. Lipid peroxidation is an early event in necrosis of wheat hybrid.

    PubMed

    Dalal, M; Khanna-Chopra, R

    1999-08-19

    We previously reported enhanced superoxide anion generation in an F1 necrotic hybrid produced from normal parents (Khanna-Chopra et al., Biochem. Biophys. Res. Commun. (1998) 248, 712-715). Further investigation of the mechanism of necrosis shows the possibility of lipid peroxidation as an early event in the death of necrotic leaves. Lipid peroxidation resulting from the inability of free radical scavenging is often associated with cell death. In this study the accumulation of malondialdehyde, an end product of lipid peroxidation, was measured in hybrid leaves and those of the parents. Lipid peroxidation was higher in the hybrid leaves through out the leaf ontogeny. This was accompanied by increased membrane permeability. Cell viability measured by a TTC reduction test showed a significant correlation with conductivity. There was no apparent effect on photosynthetic pigments and maximum efficiency of PSII (Fv/Fm) until the appearance of necrotic lesions on the hybrid leaf. There seems to be a close relationship among lipid peroxidation, membrane permeability, and cell viability in the leaves undergoing necrosis. This suggests the possibility of a genetic mechanism whereby the scavenging of free radical is impaired, leading to enhanced lipid peroxidation and membrane permeability, resulting in necrosis and death of the hybrid leaves in wheat. PMID:10448077

  17. Mistletoe alkali inhibits peroxidation in rat liver and kidney

    PubMed Central

    Shi, Zheng-Ming; Feng, Ping; Jiang, Dong-Qiao; Wang, Xue-Jiang

    2006-01-01

    AIM: To explore the antioxidant and free radical scavenger properties of mistletoe alkali (MA). METHODS: The antioxidant effect of mistletoe alkali on the oxidative stress induced by carbon tetrachloride (CCl4) in rats was investigated. The rats were divided into four groups (n = 8): CCl4-treated group (1 mL/kg body weight), MA -treated group (90 mg/kg), CCl4+MA-treated group and normal control group. After 4 wk of treatment, the level of malondialdehyde (MDA), a lipid peroxidation product (LPO) was measured in serum and homogenates of liver and kidney. Also, the level of glutathione (GSH), and activities of glutathione reductase (GR), glutathione peroxidase (GSPx), superoxide dismutase (SOD), and glutathione-S-transferase (GST) in liver and kidney were determined. Scavenging effects on hydroxyl free radicals produced in vitro by Fenton reaction were studied by ESR methods using 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap reagent and H2O2/UV as the OH· source. Urinary 8-hydroxydeoxyguanosine (8-OHdG) was determined by competitive ELISA. RESULTS: In CCl4-treated group, the level of LPO in serum of liver and kidney was significantly increased compared to controls. The levels of GSH and enzyme activities of SOD, GSPx and GR in liver and kidney were significantly decreased in comparison with controls. In CCl4+MA-treated group, the changes in the levels of LPO in serum of liver and kidney were not statistically significant compared to controls. The levels of SOD, GSPx and GR in liver and kidney were significantly increased in comparison with controls. There was a significant difference in urinary excretion of 8-OHdG between the CCl4-treated and MA-treated groups. CONCLUSION: Oxidative stress may be a major mechanism for the toxicity of CCl4. MA has a protective effect against CCl4 toxicity by inhibiting the oxidative damage and stimulating GST activities. Thus, clinical application of MA should be considered in cases with carbon tetrachloride-induced injury

  18. A unique antioxidant activity of phosphatidylserine on iron-induced lipid peroxidation of phospholipid bilayers.

    PubMed

    Dacaranhe, C D; Terao, J

    2001-10-01

    The relationship between the antioxidant effect of acidic phospholipids, phosphatidic acid (PA), phosphatidylglycerol (PG) and phosphatidylserine (PS), on iron-induced lipid peroxidation of phospholipid bilayers and their abilities to bind iron ion was examined in egg yolk phosphatidylcholine large unilamellar vesicles (EYPC LUV). The effect of each acidic phospholipid added to the vesicles at 10 mol% was assessed by measuring phosphatidylcholine hydroperoxides (PC-OOH) and thiobarbituric acid-reactive substances. The addition of dipalmitoyl PS (DPPS) showed a significant inhibitory effect, although the other two acidic phospholipids, dipalmitoyl PA (DPPA) and dipalmitoyl PG (DPPG), did not exert the inhibition. Neither dipalmitoyl PC (DPPC) nor dipalmitoyl phophatidylethanolamine (DPPE) showed any remarkable inhibition on this system. None of the tested phospholipids affected the lipid peroxidation rate remarkably when the vesicles were exposed to a water-soluble radical generator. The iron-binding ability of each phospholipid was estimated on the basis of the amounts of iron recovered in the chloroform/methanol phase after separation of the vesicle solution to water/methanol and chloroform/methanol phases. EYPC LUV containing DPPS, DPPA, and DPPG had higher amounts of bound iron than those containing DPPC and DPPE, indicating that these three acidic phospholipids possess an iron-binding ability at a similar level. Nevertheless, only DPPS suppressed iron-dependent decomposition of PC-OOH significantly. Therefore, it is likely that these three acidic phospholipids possess a significant iron-binding ability, although this ability per se does not warrant them antioxidative activities. The ability to suppress the iron-dependent decomposition of PC-OOH may explain the unique antioxidant activity of PS. PMID:11768154

  19. Photoirradiation of dehydropyrrolizidine alkaloids--formation of reactive oxygen species and induction of lipid peroxidation.

    PubMed

    Zhao, Yuewei; Xia, Qingsu; Yin, Jun Jie; Lin, Ge; Fu, Peter P

    2011-09-10

    Pyrrolizidine alkaloid (PA)-containing plants are widespread in the world and are probably the most common poisonous plants affecting livestock, wildlife, and human. PAs require metabolic activation to generate pyrrolic metabolites (dehydro-PAs) that bind cellular protein and DNA, leading to hepatotoxicity and genotoxicity, including tumorigenicity. In this study we report that UVA photoirradiation of a series of dehydro-PAs, e.g., dehydromonocrotaline, dehydroriddelliine, dehydroretrorsine, dehydrosenecionine, dehydroseneciphylline, dehydrolasiocarpine, dehydroheliotrine, and dehydroretronecine (DHR) at 0-70 J/cm2 in the presence of a lipid, methyl linoleate, resulted in lipid peroxidation in a light dose-responsive manner. When irradiated in the presence of sodium azide, the level of lipid peroxidation decreased; lipid peroxidation was enhanced when methanol was replaced by deuterated methanol. These results suggest that singlet oxygen is a photo-induced product. When irradiated in the presence of superoxide dismutase, the level of lipid peroxidation decreased, indicating that lipid peroxidation is also mediated by superoxide. Electron spin resonance (ESR) spin trapping studies confirmed that both singlet oxygen and superoxide anion radical were formed during photoirradiation. These results indicate that UVA photoirradiation of dehydro-PAs generates reactive oxygen species (ROS) that mediated the initiation of lipid peroxidation. UVA irradiation of the parent PAs and other PA metabolites, including PA N-oxides, under similar experimental conditions did not produce lipid peroxidation. It is known that PAs induce skin cancer and are secondary (hepatogenous) photosensitization agents. Our results suggest that dehydro-PAs are the active metabolites responsible for skin cancer formation and PA-induced secondary photosensitization. PMID:21723383

  20. Antioxidant and anti-lipid peroxidation activities of Tamarindus indica seed coat in human fibroblast cells.

    PubMed

    Nakchat, Oranuch; Meksuriyen, Duangdeun; Pongsamart, Sunanta

    2014-02-01

    Antioxidant activity and total phenolic content of tamarind seed coat extracts (TSCEs) were compared between the two extracts using boiling-water (TSCE-W) and 70% ethanol (TSCE-E) for extraction. TSCE-W, consisting of the highest phenolic content, possessed 2,2-diphenyl-1 -picrylhydrazyl (DPPH) radical scavenging and anti-lipid peroxidation activities much higher than TSCE-E and Trolox. Additionally, both TSCEs also exhibited superoxide anion and hydrogen peroxide scavenging activities higher than Trolox and BHA. Anti-lipid peroxidation and cytotoxicity of TSCE-W were also studied in human foreskin fibroblast CCD-1064Sk cells. Cytotoxic effect was not observed when exposed to TSCE-W up to 1 mg/mL for 12-48 h. However, TSCE-W significantly attenuated lipid peroxidation in H202-damaged cells. HPLC analysis showed the presence of (+)-catechin, (-)-epicatechin, and procyanidin B2 in TSCE-W, which could be responsible for antioxidant and anti-lipid peroxidation activities. The results suggest that an inexpensive and simple boiling-water extraction of TSCE-W may provide a valuable natural antioxidant source having anti-lipid peroxidation for health food additives, nutraceuticals as well as cosmeceuticals. PMID:24597144

  1. Evidence for the Accumulation of Peroxidized Lipids in Membranes of Senescing Cotyledons 1

    PubMed Central

    Pauls, K. Peter; Thompson, John E.

    1984-01-01

    Fluorescent products of lipid peroxidation accumulate with age in microsomal membranes from senescing cotyledons of Phaseolus vulgaris. The temporal pattern of accumulation is closely correlated with a rise in the lipid phase transition temperature reflecting the formation of gel phase lipid. Increased levels of fluorescent peroxidation products are also detectable in total lipid extracts of senescent cotyledons. Lipoxygenase activity increases with advancing age by about 3-fold on a fresh weight basis and 4-fold on a dry weight basis indicating that the tissue acquires elevated levels of lipid hydroperoxides. As well, levels of glutathione and superoxide dismutase activity decline on a dry weight basis as the cotyledons age, rendering the tissue more susceptible to oxidative damage. Catalase activity rises initially and then declines during senescence, but peroxidase activity rises steeply. Thus, apart from this increase in peroxidase, which would scavenge H2O2 only if appropriate cosubstrates were available, the defense mechanisms for coping with activated oxygen species (O2−, H2O2, OH) are less effective in the older tissue. The observations support the contention that formation of gel phase lipid in senescing membranes is attributable to lipid peroxidation and suggest that the reactions of lipid peroxidation are utilized by the cotyledons to mediate deteriorative changes accompanying the mobilization and transport of metabolites from the storage tissue to the developing embryo. Images Fig. 10 PMID:16663749

  2. Increase in cellular pool of low-molecular-weight iron during ethanol metabolism in rat hepatocyte cultures. Relationship with lipid peroxidation.

    PubMed

    Sergent, O; Morel, I; Cogrel, P; Chevanne, M; Pasdeloup, N; Brissot, P; Lescoat, G; Cillard, P; Cillard, J

    1995-01-01

    Ethanol-induced lipid peroxidation was studied in primary rat hepatocyte cultures supplemented with ethanol at the concentration of 50 mM. Lipid peroxidation was assessed by two indices: (1) conjugated dienes by second-derivative UV spectroscopy in lipid extract of hepatocytes (intracellular content), and (2) free malondialdehyde (MDA) by HPLC-UV detection and quantitation for the incubation medium (extracellular content). In cultures supplemented with ethanol, free MDA increased significantly in culture media, whereas no elevation of conjugated diene level was observed in the corresponding hepatocytes. The cellular pool of low-mol-wt (LMW) iron was also evaluated in the hepatocytes using an electron spin resonance procedure. An early increase of intracellular LMW iron (< or = 1 hr) was observed in ethanol-supplemented cultures; it was inhibited by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase, whereas alpha-tocopherol, which prevented lipid peroxidation, did not inhibit the increase of LMW iron. Therefore, the LMW iron elevation was the result of ethanol metabolism and was not secondarily induced by lipid hydroperoxides. Thus, ethanol caused lipid peroxidation in rat hepatocytes as shown by the increase of free MDA, although no conjugated diene elevation was detected. During ethanol metabolism, an increase in cellular LMW iron was observed that could enhance conjugated diene degradation. PMID:7779546

  3. Induced lipid peroxidation in ram sperm: semen profile, DNA fragmentation and antioxidant status.

    PubMed

    Hamilton, Thais Rose dos Santos; de Castro, Letícia Signori; Delgado, Juliana de Carvalho; de Assis, Patrícia Monken; Siqueira, Adriano Felipe Perez; Mendes, Camilla Mota; Goissis, Marcelo Demarchi; Muiño-Blanco, Teresa; Cebrián-Pérez, José Álvaro; Nichi, Marcílio; Visintin, José Antonio; D'Ávila Assumpção, Mayra Elena Ortiz

    2016-04-01

    Action of reactive oxygen species, protamination failures and apoptosis are considered the most important etiologies of sperm DNA fragmentation. This study evaluated the effects of induced lipid peroxidation susceptibility on native semen profile and identified the mechanisms involved in sperm DNA fragmentation and testicular antioxidant defense on Santa Ines ram sperm samples. Semen was collected from 12 adult rams (Ovis aries) performed weekly over a 9-week period. Sperm analysis (motility, mass motility, abnormalities, membrane and acrosome status, mitochondrial potential, DNA fragmentation, lipid peroxidation and intracellular free radicals production); protamine deficiency; PRM1, TNP1 and TNP2 gene expression; and determination of glutathione peroxidase (GPx), glutathione reductase, catalase (CAT) and superoxide dismutase activity and immunodetection in seminal plasma were performed. Samples were distributed into four groups according to the sperm susceptibility to lipid peroxidation after induction with ascorbate and ferrous sulfate (low, medium, high and very high). The results were analyzed by GLM test and post hoc least significant difference. We observed an increase in native GPx activity and CAT immunodetection in groups with high susceptibility to induced lipid peroxidation. We also found an increase in total sperm defects, acrosome and membrane damages in the group with the highest susceptibility to induced lipid peroxidation. Additionally, the low mitochondrial membrane potential, susceptible to chromatin fragmentation and the PRM1 mRNA were increased in the group showing higher susceptibility to lipid peroxidation. Ram sperm susceptibility to lipid peroxidation may compromise sperm quality and interfere with the oxidative homeostasis by oxidative stress, which may be the main cause of chromatin damage in ram sperm. PMID:26811546

  4. Free radicals and lipid peroxidation mediated injury in burn trauma: the role of antioxidant therapy.

    PubMed

    Horton, Jureta W

    2003-07-15

    (ascorbic acid, glutathione, N-acetyl-L-cysteine, or vitamins A, E, and C alone or in combination) have been shown to reduce burn and burn/sepsis mediated mortality, to attenuate changes in cellular energetics, to protect microvascular circulation, reduce tissue lipid peroxidation, improve cardiac output, and to reduce the volume of required fluid resuscitation. Antioxidant vitamin therapy with fluid resuscitation has also been shown to prevent burn related cardiac NF-kappaB nuclear migration, to inhibit cardiomyocyte secretion of TNF-alpha, IL-1beta, and IL-6, and to improve cardiac contractile function. These data collectively support the hypothesis that cellular oxidative stress is a critical step in burn-mediated injury, and suggest that antioxidant strategies designed to either inhibit free radical formation or to scavage free radicals may provide organ protection in patients with burn injury. PMID:12821284

  5. Advanced lipid peroxidation end products in oxidative damage to proteins. Potential role in diseases and therapeutic prospects for the inhibitors

    PubMed Central

    Negre-Salvayre, A; Coatrieux, C; Ingueneau, C; Salvayre, R

    2007-01-01

    Reactive carbonyl compounds (RCCs) formed during lipid peroxidation and sugar glycoxidation, namely Advanced lipid peroxidation end products (ALEs) and Advanced Glycation end products (AGEs), accumulate with ageing and oxidative stress-related diseases, such as atherosclerosis, diabetes or neurodegenerative diseases. RCCs induce the ‘carbonyl stress' characterized by the formation of adducts and cross-links on proteins, which progressively leads to impaired protein function and damages in all tissues, and pathological consequences including cell dysfunction, inflammatory response and apoptosis. The prevention of carbonyl stress involves the use of free radical scavengers and antioxidants that prevent the generation of lipid peroxidation products, but are inefficient on pre-formed RCCs. Conversely, carbonyl scavengers prevent carbonyl stress by inhibiting the formation of protein cross-links. While a large variety of AGE inhibitors has been developed, only few carbonyl scavengers have been tested on ALE-mediated effects. This review summarizes the signalling properties of ALEs and ALE-precursors, their role in the pathogenesis of oxidative stress-associated diseases, and the different agents efficient in neutralizing ALEs effects in vitro and in vivo. The generation of drugs sharing both antioxidant and carbonyl scavenger properties represents a new therapeutic challenge in the treatment of carbonyl stress-associated diseases. PMID:17643134

  6. Effects of antiperoxidants on FeCl2-induced lipid peroxidation and focal edema in rat brain.

    PubMed

    Willmore, L J; Rubin, J J

    1984-01-01

    Head trauma with contusion or cortical laceration and hemorrhage causes focal edema with encephalomalacia and gliosis. Because cerebral hemorrhage ultimately results in deposition of heme compounds and iron into the neuropil, we injected an aqueous solution of iron salts to simulate the decompartmentalization of iron after trauma. We pretreated animals with saline or with 600 mg/kg alpha-tocopherol plus 5 ppm selenium added to the drinking water. Formation of lipid peroxidation products was significantly inhibited within the iron injection site in the antiperoxidant-pretreated rats at 30, 60, and 120 min after injection of iron into the isocortex. The antiperoxidants failed to prevent formation of focal brain edema at the injection site between 1 and 8 h after injection; however, significantly less edema was present in the alpha-tocopherol + selenium-pretreated animals 24 and 48 h after injection. The efficacy of antiperoxidants in preventing lipid peroxidation, and enhancing the resolution of ferrous-induced focal brain edema suggest that tocopherol + selenium administration caused free radical quenching and termination of lipid peroxidation, and increased membrane stabilization, an effect similar to the action of glucocorticoids. PMID:6690325

  7. Antioxidant properties of aqueous extracts of unripe Musa paradisiaca on sodium nitroprusside induced lipid peroxidation in rat pancreas in vitro

    PubMed Central

    Shodehinde, Sidiqat Adamson; Oboh, Ganiyu

    2013-01-01

    Objective To evaluate and compare antioxidant activities of the aqueous extracts of unripe plantain (Musa paradisiaca), assess their inhibitory action on sodium nitroprusside induced lipid peroxidation in rat pancreas in vitro and to characterize the main phenolic constituents of the plantain products using gas chromatography analysis. Methods Aqueous extracts of plantain products (raw, elastic pastry, roasted and boiled) flour of 0.1 g/mL (each) were used to determine their total phenol, total flavonoid, 1,1 diphenyl-2 picrylhydrazyl (DPPH) and hydroxyl (OH) radical scavenging ability. The inhibitory effect of the extracts on sodium nitroprusside induced lipid peroxidation was also determined. Results The results revealed that all the aqueous extracts showed antioxidant activity. The boiled flour had highest DPPH and OH radical scavenging ability while raw flour had the highest Fe2+ chelating ability, sodium nitroprusside inhibitory effect and vitamin C content. The antioxidant results showed that elastic pastry had the highest total phenol and total flavonoid content. Characterization of the unripe plantain products for polyphenol contents using gas chromatography showed varied quantity of apigenin, myricetin, luteolin, capsaicin, isorhaemnetin, caffeic acid, kampferol, quercetin, p-hydroxybenzoic acid, shogaol, glycitein and gingerol per product on the spectra. Conclusions Considering the antioxidant activities and ability to inhibit lipid peroxidation of unripe plantain, this could justify their traditional use in the management/prevention of diseases related to stress. PMID:23730557

  8. Induction of antioxidant enzyme activity and lipid peroxidation level in ion-beam-bombarded rice seeds

    NASA Astrophysics Data System (ADS)

    Semsang, Nuananong; Yu, LiangDeng

    2013-07-01

    Low-energy ion beam bombardment has been used to mutate a wide variety of plant species. To explore the indirect effects of low-energy ion beam on biological damage due to the free radical production in plant cells, the increase in antioxidant enzyme activities and lipid peroxidation level was investigated in ion-bombarded rice seeds. Local rice seeds were bombarded with nitrogen or argon ion beams at energies of 29-60 keV and ion fluences of 1 × 1016 ions cm-2. The activities of the antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), dehydroascorbate reductase (DHAR), glutathione reductase (GR), glutathione S-transferase (GST) and lipid peroxidation level were assayed in the germinated rice seeds after ion bombardment. The results showed most of the enzyme activities and lipid peroxidation levels in both the argon and nitrogen bombarded samples were higher than those in the natural control. N-ion bombardment could induce higher levels of antioxidant enzyme activities in the rice samples than the Ar-ion bombardment. Additional effects due to the vacuum condition were found to affect activities of some antioxidant enzymes and lipid peroxidation level. This study demonstrates that ion beam bombardment and vacuum condition could induce the antioxidant enzyme activity and lipid peroxidation level which might be due to free radical production in the bombarded rice seeds.

  9. Bioactive potential of Vitis labrusca L. grape juices from the Southern Region of Brazil: phenolic and elemental composition and effect on lipid peroxidation in healthy subjects.

    PubMed

    Toaldo, Isabela Maia; Cruz, Fernanda Alves; Alves, Tatiana de Lima; de Gois, Jefferson Santos; Borges, Daniel L G; Cunha, Heloisa Pamplona; da Silva, Edson Luiz; Bordignon-Luiz, Marilde T

    2015-04-15

    Grapes are rich in polyphenols with biologically active properties. Although the bioactive potential of grape constituents are frequently reported, the effects of Brazilian Vitis labrusca L. grape juices ingestion have not been demonstrated in humans. This study identified the phenolic and elemental composition of red and white grape juices and the effect of organic and conventional red grape juice consumption on lipid peroxidation in healthy individuals. Concentrations of anthocyanins, flavanols and phenolic acids and the in vitro antioxidant activity were significantly higher in the organic juice. The macro-elements K, Ca, Na and Mg were the most abundant minerals in all juices. The acute consumption of red grape juices promoted significant decrease of lipid peroxides in serum and TBARS levels in plasma. It is concluded that red V. labrusca L. grape juices produced in Southern Brazil showed lipid peroxidation inhibition abilities in healthy subjects, regardless of the cultivation system. PMID:25466055

  10. Amyloid beta-peptide impairs glucose transport in hippocampal and cortical neurons: involvement of membrane lipid peroxidation.

    PubMed

    Mark, R J; Pang, Z; Geddes, J W; Uchida, K; Mattson, M P

    1997-02-01

    A deficit in glucose uptake and a deposition of amyloid beta-peptide (A beta) each occur in vulnerable brain regions in Alzheimer's disease (AD). It is not known whether mechanistic links exist between A beta deposition and impaired glucose transport. We now report that A beta impairs glucose transport in cultured rat hippocampal and cortical neurons by a mechanism involving membrane lipid peroxidation. A beta impaired 3H-deoxy-glucose transport in a concentration-dependent manner and with a time course preceding neurodegeneration. The decrease in glucose transport was followed by a decrease in cellular ATP levels. Impairment of glucose transport, ATP depletion, and cell death were each prevented in cultures pretreated with antioxidants. Exposure to FeSO4, an established inducer of lipid peroxidation, also impaired glucose transport. Immunoprecipitation and Western blot analyses showed that exposure of cultures to A beta induced conjugation of 4-hydroxynonenal (HNE), an aldehydic product of lipid peroxidation, to the neuronal glucose transport protein GLUT3. HNE induced a concentration-dependent impairment of glucose transport and subsequent ATP depletion. Impaired glucose transport was not caused by a decreased energy demand in the neurons, because ouabain, which inhibits Na+/K(+)-ATPase activity and thereby reduces neuronal ATP hydrolysis rate, had little or no effect on glucose transport. Collectively, the data demonstrate that lipid peroxidation mediates A beta-induced impairment of glucose transport in neurons and suggest that this action of A beta may contribute to decreased glucose uptake and neuronal degeneration in AD. PMID:8994059

  11. [Immune system function and lipid peroxidation processes in protracted forms of pneumonia].

    PubMed

    Efimov, V V; Blazhko, V I; Gladchenko, A R

    1989-04-01

    The authors studied the characteristic features of cellular and humoral immunity as well as the intensity of free-radical lipid peroxidation in 74 patients with acute and protracted course of acute pneumonia. A close relationship was established between immune disorders at the level of the regulatory link and the activity of peroxidation of lipids during transformation of acute pneumonia into protracted. It is shown that the content of products of lipid peroxidation in erythrocytes during the first days of the disease may be a well-informative criterion reflecting the character of course of the inflammatory process in the lungs and adequate immune response. This may be used for the prognosis of protracted forms of pneumonia. PMID:2756694

  12. Perioperative Intravenous Acetaminophen Attenuates Lipid Peroxidation in Adults Undergoing Cardiopulmonary Bypass: A Randomized Clinical Trial

    PubMed Central

    Billings IV, Frederic T.; Petracek, Michael R.; Roberts II, L. Jackson; Pretorius, Mias

    2015-01-01

    Background Cardiopulmonary bypass (CPB) lyses erythrocytes and induces lipid peroxidation, indicated by increasing plasma concentrations of free hemoglobin, F2-isoprostanes, and isofurans. Acetaminophen attenuates hemeprotein-mediated lipid peroxidation, reduces plasma and urine concentrations of F2-isoprostanes, and preserves kidney function in an animal model of rhabdomyolysis. Acetaminophen also attenuates plasma concentrations of isofurans in children undergoing CPB. The effect of acetaminophen on lipid peroxidation in adults has not been studied. This was a pilot study designed to test the hypothesis that acetaminophen attenuates lipid peroxidation in adults undergoing CPB and to generate data for a clinical trial aimed to reduce acute kidney injury following cardiac surgery. Methods and Results In a prospective double-blind placebo-controlled clinical trial, sixty adult patients were randomized to receive intravenous acetaminophen or placebo starting prior to initiation of CPB and for every 6 hours for 4 doses. Acetaminophen concentrations measured 30 min into CPB and post-CPB were 11.9±0.6 μg/mL (78.9±3.9 μM) and 8.7±0.3 μg/mL (57.6±2.0 μM), respectively. Plasma free hemoglobin increased more than 15-fold during CPB, and haptoglobin decreased 73%, indicating hemolysis. Plasma and urinary markers of lipid peroxidation also increased during CPB but returned to baseline by the first postoperative day. Acetaminophen reduced plasma isofuran concentrations over the duration of the study (P = 0.05), and the intraoperative plasma isofuran concentrations that corresponded to peak hemolysis were attenuated in those subjects randomized to acetaminophen (P = 0.03). Perioperative acetaminophen did not affect plasma concentrations of F2-isoprostanes or urinary markers of lipid peroxidation. Conclusions Intravenous acetaminophen attenuates the increase in intraoperative plasma isofuran concentrations that occurs during CPB, while urinary markers were unaffected

  13. Continuous millimeter-wave radiation has no effect on lipid peroxidation in liposomes

    SciTech Connect

    Logani, M.K.; Ziskin, M.C.

    1996-02-01

    The effect of millimeter waves on lipid peroxidation was studied in the presence and absence of melanin. Irradiation of liposomes with continuous millimeter electromagnetic waves at frequencies of 53.6, 61.2 and 78.2 GHz and incident power densities of 10, 1 and 500 mW/cm{sup 2}, respectively, did not show an enhancement in the formation of lipid peroxides compared to unirradiated samples. Liposomes exposed to 254 nm UVC radiation at 0.32 mW/cm{sup 2} and 302 nm UVB radiation at 1.12 mW/cm{sup 2} served as positive controls. No increment in the formation of lipid peroxides was observed when irradiation of liposomes was carried out in the presence of ADP-Fe{sup +3} and EDTA-Fe{sup +3}. Direct irradiation of melanin with millimeter waves did not exhibit an increased formation of superoxide or hydrogen peroxide. The present results indicate that millimeter waves of the above frequencies and intensities do not cause lipid peroxidation in liposomal membranes. 19 refs., 2 figs., 1 tab.

  14. Molecular simulations of the effects of phospholipid and cholesterol peroxidation on lipid membrane properties.

    PubMed

    Neto, Antenor J P; Cordeiro, Rodrigo M

    2016-09-01

    Non-enzymatic lipid peroxidation may change biomembrane structure and function. Here, we employed molecular dynamics simulations to study the effects of either phospholipid or cholesterol peroxidation individually, as well as the combined peroxidation of both components. When lipids were peroxidized, the generated OOH groups migrated to the membrane surface and engaged in H-bonds with each other and the phospholipid carbonyl ester groups. It caused the sn-2 acyl chains of phospholipid hydroperoxides to bend and the whole sterol backbone of cholesterol hydroperoxides to tilt. When phospholipids were kept intact, peroxidation of the sterol backbone led to a partial degradation of its condensing and ordering properties, independently of the position and isomerism of the OOH substitution. However, even in massively peroxidized membranes in which all phospholipids and cholesterol were peroxidized, the condensing and ordering properties of the sterol backbone were still significant. The possible implications for the formation of membrane lateral domains were discussed. Cholesterol peroxyl radicals were also investigated and we found that the OO groups did not migrate to the headgroups region. PMID:27349733

  15. [Spectrofluorometric ultramicroassay for determining the plasma lipid peroxidation index by the thiobarbituric acid test].

    PubMed

    Pré, J

    1991-01-01

    A simple, inexpensive spectrofluorometric ultramicroassay for determining the plasma lipid peroxidation index is described. Plasma is incubated for 60 minutes at 95 degrees C in a thiobarbituric acetate buffer medium (pH 3,5) with butylhydroxytoluene and Fe . The chromogen is then extracted in butanol 1-pyridine and quantified by spectrofluorometry (exc.: 532 nm; em: 553 nm). The mean value of the plasma thiobarbituric lipid peroxidation index determined by this method in 101 healthy non-smokers (age 39.1 +/- 8.7 years) was found to be 1.61 +/- 0.72. PMID:2011414

  16. Genetic differences in hepatic lipid peroxidation potential and iron levels in mice.

    PubMed

    Gerhard, Glenn S; Kaufmann, Elizabeth J; Wang, Xujun; Erikson, Keith M; Abraham, Joseph; Grundy, Martin; Beard, John L; Chorney, Michael J

    2002-01-01

    Oxidative damage to macromolecules, including lipids, has been hypothesized as a mechanism of aging. One end product of lipid peroxidation, malondialdehyde (MDA), is often quantified as a measure of oxidative damage to lipids. We used a commercial colorimetric assay for MDA (Bioxytech LPO-586, Oxis International, Portland, OR) to measure lipid peroxidation potential in liver tissue from young (2 month) male mice from recombinant inbred (RI) mouse strains from the C57BL/6J (B6)xDBA/2J (D2) series (BXD). The LPO-586 assay (LPO) reliably detected significant differences (P<0.0001) in lipid peroxidation potential between the B6 and D2 parental strains, and yielded a more than two-fold variation across the BXD RI strains. In both B6 and D2 mice, LPO results were greater in old (23 month) mice, with a larger age-related increase in the D2 strain. As the level of iron can influence lipid peroxidation, we also measured hepatic non-heme iron levels in the same strains. Although iron level exhibited a slightly negative overall correlation (r(2)=0.119) with LPO results among the entire group of BXD RI strains, a sub-group with lower LPO values were highly correlated (r(2)=0.704). LPO results were also positively correlated with iron levels from a group of 8 other inbred mouse strains (r(2)=0.563). The BXD RI LPO data were statistically analyzed to nominate quantitaive trait loci (QTL). A single marker, Zfp4, which maps to 55.2 cM on chromosome 8, achieved a significance level of P<0.0006. At least two potentially relevant candidate genes reside close to this chromosomal position. Hepatic lipid peroxidation potential appears to be a strain related trait in mice that is amenable to QTL analysis. PMID:11718810

  17. Tempol inhibits neutrophil and hydrogen peroxide-mediated DNA damage.

    PubMed

    Hahn, S M; Mitchell, J B; Shacter, E

    1997-01-01

    Inflammatory conditions characterized by neutrophil activation are associated with a variety of chronic diseases. Reactive oxygen species are produced by activated neutrophils and produce DNA damage which may lead to tissue damage. Previous studies have shown that activated murine neutrophils induce DNA strand breaks in a target plasmacytoma cell, RIMPC 2394. We studied the effect of a water soluble nitroxide anti-oxidant, Tempol, on murine neutrophil induction of DNA strand breaks in this system. Murine neutrophils were isolated from the peritoneal cavity of BALB/cAn mice after an i.p. injection of pristane oil. Neutrophils were activated by the phorbol ester PMA and co-incubated with RIMPC 2394 cells. Control alkaline elution studies revealed progressive DNA strand breaks in RIMPC cells with time. The addition of Tempol to the incubation mixture prevented DNA damage in a dose dependent fashion. Five mM Tempol provided complete protection. Tempol protection against DNA strand breaks was similar for both stimulated neutrophils and exogenously added hydrogen peroxide. Measurement of hydrogen peroxide produced by stimulated neutrophils demonstrated that Tempol did not decrease hydrogen peroxide concentration. Oxidation of reduced metals, thereby interfering with the production of hydroxyl radical, is the most likely mechanism of nitroxide protection, although superoxide dismutase (SOD) like activity and scavenging of carbon-based free radicals may also account for a portion of the observed protection. The anti-oxidant activity of Tempol inhibited DNA damage by activated neutrophils. The nitroxides as a class of compounds may have a role in the investigation and modification of inflammatory conditions. PMID:9378367

  18. Hypoxia-induced lipid peroxidation in the brain during postnatal ontogenesis.

    PubMed

    Rauchová, H; Vokurková, M; Koudelová, J

    2012-01-01

    Reactive oxygen species (ROS) are common products of the physiological metabolic reactions, which are associated with cell signaling and with the pathogenesis of various nervous disorders. The brain tissue has the high rate of oxidative metabolic activity, high concentration of polyunsaturated fatty acids in membrane lipids, presence of iron ions and low capacity of antioxidant enzymes, which makes the brain very susceptible to ROS action and lipid peroxidation formation. Membranes of brain cortex show a higher production of thiobarbituric acid-reactive substances (TBARS) in prooxidant system (ADP.Fe(3+)/NADPH) than membranes from the heart or kidney. Lipid peroxidation influences numerous cellular functions through membrane-bound receptors or enzymes. The rate of brain cortex Na(+),K(+)-ATPase inhibition correlates well with the increase of TBARS or conjugated dienes and with changes of membrane fluidity. The experimental model of short-term hypoxia (simulating an altitude of 9000 m for 30 min) shows remarkable increase in TBARS in four different parts of the rat brain (cortex, subcortical structures, cerebellum and medulla oblongata) during the postnatal development of Wistar rat of both sexes. Young rats and males are more sensitive to oxygen changes than adult rats and females, respectively. Under normoxia or hypobaric hypoxia both ontogenetic aspects and sex differences play a major role in establishing the activity of erythrocyte catalase, which is an important part of the antioxidant defense of the organism. Rats pretreated with L-carnitine (and its derivatives) have lower TBARS levels after the exposure to hypobaric hypoxia. The protective effect of L-carnitine is comparable with the effect of tocopherol, well-known reactive species scavenger. Moreover, the plasma lactate increases after a short-term hypobaric hypoxia and decreases in L-carnitine pretreated rats. Acute hypobaric hypoxia and/or L-carnitine-pretreatment modify serum but not brain lactate

  19. [Lipid peroxidation and its interrelation with the personality characteristics of surgical patients].

    PubMed

    Man'kov, Iu U; Sharapov, G N; Khyshov, V B; Pal'chikov, V P; Alekseenko, G M

    1991-04-01

    The article deals with the exam results of 42 pre- and postoperative surgical patients. The reactivity of peroxide oxidation of lipids plays an important role in regulation of adaptive process of surgical patients. The authors emphasize the role of anxiety state as one of the most intimate and obligate mechanisms of psychologic stress. The anxiety rising process influences upon the formation of typical psychophysiological correlations that lead to the intensification of lipid oxidation. PMID:1887607

  20. Alterations in circadian rhythms are associated with increased lipid peroxidation in females with bipolar disorder.

    PubMed

    Cudney, Lauren E; Sassi, Roberto B; Behr, Guilherme A; Streiner, David L; Minuzzi, Luciano; Moreira, Jose C F; Frey, Benicio N

    2014-05-01

    Disturbances in both circadian rhythms and oxidative stress systems have been implicated in the pathophysiology of bipolar disorder (BD), yet no studies have investigated the relationship between these systems in BD. We studied the impact of circadian rhythm disruption on lipid damage in 52 depressed or euthymic BD females, while controlling for age, severity of depressive symptoms and number of psychotropic medications, compared to 30 healthy controls. Circadian rhythm disruption was determined by a self-report measure (Biological Rhythm Interview of Assessment in Neuropsychiatry; BRIAN), which measures behaviours such as sleep, eating patterns, social rhythms and general activity. Malondialdehyde (MDA) levels were measured as a proxy of lipid peroxidation. We also measured the activity of total and extracellular superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST). Multiple linear regressions showed that circadian rhythm disturbance was independently associated with increased lipid peroxidation in females with BD (p < 0.05). We found decreased extracellular SOD (p < 0.05), but no differences in total SOD, CAT or GST activity between bipolar females and controls. Circadian rhythms were not associated with lipid peroxidation in healthy controls, where aging was the only significant predictor. These results suggest an interaction between the circadian system and redox metabolism, in that greater disruption in daily rhythms was associated with increased lipid peroxidation in BD only. Antioxidant enzymes have been shown to follow a circadian pattern of expression, and it is possible that disturbance of sleep and daily rhythms experienced in BD may result in decreased antioxidant defence and therefore increased lipid peroxidation. This study provides a basis for further investigation of the links between oxidative stress and circadian rhythms in the neurobiology of BD. PMID:24438530

  1. Lipid-Induced Peroxidation in the Intestine Is Involved in Glucose Homeostasis Imbalance in Mice

    PubMed Central

    Marsollier, Nicolas; Masseboeuf, Myriam; Payros, Gaëlle; Kabani, Catherine; Denom, Jessica; Lacombe, Amélie; Thiers, Jean-Claude; Negre-Salvayre, Anne; Luquet, Serge; Burcelin, Rémy; Cruciani-Guglielmacci, Céline; Magnan, Christophe

    2011-01-01

    Background Daily variations in lipid concentrations in both gut lumen and blood are detected by specific sensors located in the gastrointestinal tract and in specialized central areas. Deregulation of the lipid sensors could be partly involved in the dysfunction of glucose homeostasis. The study aimed at comparing the effect of Medialipid (ML) overload on insulin secretion and sensitivity when administered either through the intestine or the carotid artery in mice. Methodology/Principal Findings An indwelling intragastric or intracarotid catheter was installed in mice and ML or an isocaloric solution was infused over 24 hours. Glucose and insulin tolerance and vagus nerve activity were assessed. Some mice were treated daily for one week with the anti-lipid peroxidation agent aminoguanidine prior to the infusions and tests. The intestinal but not the intracarotid infusion of ML led to glucose and insulin intolerance when compared with controls. The intestinal ML overload induced lipid accumulation and increased lipid peroxidation as assessed by increased malondialdehyde production within both jejunum and duodenum. These effects were associated with the concomitant deregulation of vagus nerve. Administration of aminoguanidine protected against the effects of lipid overload and normalized glucose homeostasis and vagus nerve activity. Conclusions/Significance Lipid overload within the intestine led to deregulation of gastrointestinal lipid sensing that in turn impaired glucose homeostasis through changes in autonomic nervous system activity. PMID:21698161

  2. In vivo effects of nickel and cadmium in rats on lipid peroxidation and ceruloplasmin activity

    SciTech Connect

    Sole, J.; Huguet, J.; Arola, L.; Romeu, A. )

    1990-05-01

    Before Ni(II) and Cd(II), or any other metallic ion, can interact intracellulary, it must penetrate the cell membrane. The latter, therefore, is a primary target for toxic metals. Damage to cell membranes may allow a greater uptake of metal and thus injury may extend to more critical targets, although loss of plasmatic membrane functionality may be a crucial factor to explain the interactions of these metals with cellular components. In this sense the present study has been carried out. Factors that have been investigated in order to prove the membrane response of nickel and cadmium toxicity include lipid peroxidation, since divalent ions of transition metals can promote lipid peroxidation and this evidently contributes to the toxicity of certain metals and to metal interaction with ceruloplasmin, as its ferroxidase and scavenger of superoxide radicals activities are important protective mechanisms in vivo against peroxidative damage.

  3. Increased lipid peroxidation in tissues of nickel chloride-treated rats

    SciTech Connect

    Sunderman, F.W. Jr.; Marzouk, A.; Hopfer, S.M.; Zaharia, O.; Reid, M.C.

    1985-01-01

    Parenteral administration of nickel chloride (NiCl/sub 2/) to rats enhanced lipid peroxidation in liver, kidney, and lung as measured by the thiobarbituric acid reaction for malondialdehyde (MDA) and related chromogens in fresh tissue homogenates. After sc injection of NiCl/sub 2/ (0.75 mmol per kg body wt), MDA concentrations in liver and kidney became significantly increased by nine h and reached peak values at 48 h. For example, in nine rats killed 48 h after the NiCl/sub 2/ injection, hepatic MDA concentrations averaged 2.5 +/- 1.0 ..mu.. mol per g dry wt (P < 0.001 versus 0.5 +/- 0.3 ..mu.. mol per g in 30 controls). Dose-effect relationships for lipid peroxidation in liver and kidney were observed with NiCl/sub 2/ dosages ranging from 0.12 to 0.75 mmol per kg, sc. Intrarenal administration of a carcinogenic nickel compound, nickel subsulfide (Ni/sub 3/S/sub 2/, 0.36 mmol per kg body wt), did not affect MDA concentrations in the injected kidneys of rats killed one to 20 days post-injection. The results of this study implicate lipid peroxidation as a molecular mechanism for cell injury in acute NiCl/sub 2/ poisoning, but they do not furnish any evidence that lipid peroxidation is involved in the initiation of nickel carcinogenesis. 46 references, 4 tables.

  4. Blueberries reduce lipid peroxidation and boost antioxidant enzymes in apoe knockout mice

    Technology Transfer Automated Retrieval System (TEKTRAN)

    ApoE knockout (ApoE-/-) mice fed AIN-93G diet (CD) formulated to contain 1 % freeze-dried whole wild blueberries (CD1 percent BB) were found to have significantly less atherosclerotic lesions in aorta. Biomarkers of lipid peroxidation, including F2-isoprostanes, hydroxyoctadecadienoic acids (HODEs) ...

  5. Clinical implications of lipid peroxidation in acne vulgaris: old wine in new bottles

    PubMed Central

    2010-01-01

    Acne vulgaris is a common dermatological disorder, one that is frequently associated with depression, anxiety and other psychological sequelae. In recent years there has been an increasing focus on the extent to which oxidative stress is involved in the pathophysiology of acne. Emerging studies have shown that patients with acne are under increased cutaneous and systemic oxidative stress. Indeed, there are indications that lipid peroxidation itself is a match that lights an inflammatory cascade in acne. The notion that lipid peroxidation is a 'starter gun' in acne is not a new one; here we review the nearly 50-year-old lipid peroxidation theory and provide a historical perspective to the contemporary investigations and clinical implications. In addition, we present a novel hypothesis in which lipid peroxidation may be priming an increased susceptibility to co-morbid depression and anxiety in those with acne. The emerging research on the systemic burden of oxidative stress in acne sheds further light on the brain-skin axis. The recent findings also suggest potential avenues of approach for the treatment of acne via specific nutrients, dietary modifications, oral and topical interventions. PMID:21143923

  6. Sex-related differences in lipid peroxidation and photoprotection in Pistacia lentiscus.

    PubMed

    Juvany, Marta; Müller, Maren; Pintó-Marijuan, Marta; Munné-Bosch, Sergi

    2014-03-01

    Sex-related differences in the response of dioecious plants to abiotic stress have been poorly studied to date. This work explored to what extent sex may affect plant stress responses in Pistacia lentiscus L. (Anacardiaceae), a tree well adapted to Mediterranean climatic conditions. It was hypothesized that a greater reproductive effort in females may increase oxidative stress in leaves, particularly when plants are exposed to abiotic stress. Measurements of oxidative stress markers throughout the year revealed increased lipid peroxidation in females, but only during the winter. Enhanced lipid peroxidation in females was associated with reduced photoprotection, as indicated by reduced tocopherol levels and nonphotochemical quenching (NPQ) of chlorophyll fluorescence. Enhanced lipid peroxidation in females was also observed at predawn, which was associated with increased lipoxygenase activity and reduced cytokinin levels. An analysis of the differences between reproductive (R) and nonreproductive (NR) shoots showed an enhanced photoprotective capacity in R shoots compared to NR shoots in females. This capacity was characterized by an increased NPQ and a better antioxidant protection (increased carotenoid and tocopherol levels per unit of chlorophyll) in R compared to NR shoots. It is concluded that (i) females exhibit higher lipid peroxidation in leaves than males, but only during the winter (when sex-related differences in reproductive effort are the highest), (ii) this is associated with a lower photoprotective capacity at midday, as well as enhanced lipoxygenase activity and reduced cytokinin levels at predawn, and (iii) photoprotection capacity is higher in R relative to NR shoots in females. PMID:24378602

  7. Polyphenols from Berries of Aronia melanocarpa Reduce the Plasma Lipid Peroxidation Induced by Ziprasidone

    PubMed Central

    Dietrich-Muszalska, Anna; Kopka, Justyna

    2014-01-01

    Background. Oxidative stress in schizophrenia may be caused partially by the treatment of patients with antipsychotics. The aim of the study was to establish the effects of polyphenol compounds derived from berries of Aronia melanocarpa (Aronox) on the plasma lipid peroxidation induced by ziprasidone in vitro. Methods. Lipid peroxidation was measured by the level of thiobarbituric acid reactive species (TBARS). The samples of plasma from healthy subjects were incubated with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) alone and with Aronox (5 ug/ml; 50 ug/ml). Results. We observed a statistically significant increase of TBARS level after incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) (after 24 h incubation: P = 7.0 × 10−4, P = 1.6 × 10−3, and P = 2.7 × 10−3, resp.) and Aronox lipid peroxidation caused by ziprasidone was significantly reduced. After 24-hour incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) in the presence of 50 ug/ml Aronox, the level of TBARS was significantly decreased: P = 6.5 × 10−8, P = 7.0 × 10−6, and P = 3.0 × 10−5, respectively. Conclusion. Aronox causes a distinct reduction of lipid peroxidation induced by ziprasidone. PMID:25061527

  8. Polyphenols from Berries of Aronia melanocarpa Reduce the Plasma Lipid Peroxidation Induced by Ziprasidone.

    PubMed

    Dietrich-Muszalska, Anna; Kopka, Justyna; Kontek, Bogdan

    2014-01-01

    Background. Oxidative stress in schizophrenia may be caused partially by the treatment of patients with antipsychotics. The aim of the study was to establish the effects of polyphenol compounds derived from berries of Aronia melanocarpa (Aronox) on the plasma lipid peroxidation induced by ziprasidone in vitro. Methods. Lipid peroxidation was measured by the level of thiobarbituric acid reactive species (TBARS). The samples of plasma from healthy subjects were incubated with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) alone and with Aronox (5 ug/ml; 50 ug/ml). Results. We observed a statistically significant increase of TBARS level after incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) (after 24 h incubation: P = 7.0 × 10(-4), P = 1.6 × 10(-3), and P = 2.7 × 10(-3), resp.) and Aronox lipid peroxidation caused by ziprasidone was significantly reduced. After 24-hour incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) in the presence of 50 ug/ml Aronox, the level of TBARS was significantly decreased: P = 6.5 × 10(-8), P = 7.0 × 10(-6), and P = 3.0 × 10(-5), respectively. Conclusion. Aronox causes a distinct reduction of lipid peroxidation induced by ziprasidone. PMID:25061527

  9. Studies of lipid peroxidation of rat blood after in vivo photodynamic treatment

    NASA Astrophysics Data System (ADS)

    Yanina, Irina Yu.; Navolokin, Nikita A.; Nikitina, Victoria V.; Bucharskaya, Alla B.; Maslyakova, Galina N.; Tuchin, Valery V.

    2011-10-01

    Lipid peroxidation (LP) of blood serum of laboratory animals after in vivo photodynamic treatment was investigated. To determine changes in LP the standard colorimetric test OXYSTAT was used. The results indicate an increase in the intensity of free radical generation in tissues induced by photodynamic treatment.

  10. Studies of lipid peroxidation of rat blood after in vivo photodynamic treatment

    NASA Astrophysics Data System (ADS)

    Yanina, Irina Yu.; Navolokin, Nikita A.; Nikitina, Victoria V.; Bucharskaya, Alla B.; Maslyakova, Galina N.; Tuchin, Valery V.

    2012-03-01

    Lipid peroxidation (LP) of blood serum of laboratory animals after in vivo photodynamic treatment was investigated. To determine changes in LP the standard colorimetric test OXYSTAT was used. The results indicate an increase in the intensity of free radical generation in tissues induced by photodynamic treatment.

  11. N-3 Polyunsaturated Fatty Acids are Selective Targets of Ethanol Withdrawal-Induced Lipid Peroxidation

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Ethanol withdrawal is a potentially life-threatening neurological syndrome owing to decreased GABA transmission and increased glutamatergic transmission resulting in a pro-excitotoxic state. Previous data indicate that ethanol withdrawal may increase CNS lipid peroxidation particularly to the n-3 fa...

  12. Real-time monitoring of endogenous lipid peroxidation by exhaled ethylene in patients undergoing cardiac surgery

    PubMed Central

    Cristescu, Simona M.; Kiss, Rudolf; te Lintel Hekkert, Sacco; Dalby, Miles; Harren, Frans J. M.; Risby, Terence H.

    2014-01-01

    Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB (n = 15) or off-pump coronary artery bypass surgery (OPCAB) (n = 7) were studied. Skin and tissue incision by diathermy caused striking (>30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (>10-fold) and decreased over time. Reperfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene. PMID:25128523

  13. Real-time monitoring of endogenous lipid peroxidation by exhaled ethylene in patients undergoing cardiac surgery.

    PubMed

    Cristescu, Simona M; Kiss, Rudolf; Hekkert, Sacco te Lintel; Dalby, Miles; Harren, Frans J M; Risby, Terence H; Marczin, Nandor

    2014-10-01

    Pulmonary and systemic organ injury produced by oxidative stress including lipid peroxidation is a fundamental tenet of ischemia-reperfusion injury, inflammatory response to cardiac surgery, and cardiopulmonary bypass (CPB) but is not routinely measured in a surgically relevant time frame. To initiate a paradigm shift toward noninvasive and real-time monitoring of endogenous lipid peroxidation, we have explored pulmonary excretion and dynamism of exhaled breath ethylene during cardiac surgery to test the hypothesis that surgical technique and ischemia-reperfusion triggers lipid peroxidation. We have employed laser photoacoustic spectroscopy to measure real-time trace concentrations of ethylene from the patient breath and from the CPB machine. Patients undergoing aortic or mitral valve surgery-requiring CPB (n = 15) or off-pump coronary artery bypass surgery (OPCAB) (n = 7) were studied. Skin and tissue incision by diathermy caused striking (> 30-fold) increases in exhaled ethylene resulting in elevated levels until CPB. Gaseous ethylene in the CPB circuit was raised upon the establishment of CPB (> 10-fold) and decreased over time. Reperfusion of myocardium and lungs did not appear to enhance ethylene levels significantly. During OPCAB surgery, we have observed increased ethylene in 16 of 30 documented reperfusion events associated with coronary and aortic anastomoses. Therefore, novel real-time monitoring of endogenous lipid peroxidation in the intraoperative setting provides unparalleled detail of endogenous and surgery-triggered production of ethylene. Diathermy and unprotected regional myocardial ischemia and reperfusion are the most significant contributors to increased ethylene. PMID:25128523

  14. Substrate-selective Inhibition of Cyclooxygeanse-2 by Fenamic Acid Derivatives Is Dependent on Peroxide Tone.

    PubMed

    Orlando, Benjamin J; Malkowski, Michael G

    2016-07-15

    Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of arachidonic acid (AA) and endocannabinoid substrates, placing the enzyme at a unique junction between the eicosanoid and endocannabinoid signaling pathways. COX-2 is a sequence homodimer, but the enzyme displays half-of-site reactivity, such that only one monomer of the dimer is active at a given time. Certain rapid reversible, competitive nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to inhibit COX-2 in a substrate-selective manner, with the binding of inhibitor to a single monomer sufficient to inhibit the oxygenation of endocannabinoids but not arachidonic acid. The underlying mechanism responsible for substrate-selective inhibition has remained elusive. We utilized structural and biophysical methods to evaluate flufenamic acid, meclofenamic acid, mefenamic acid, and tolfenamic acid for their ability to act as substrate-selective inhibitors. Crystal structures of each drug in complex with human COX-2 revealed that the inhibitor binds within the cyclooxygenase channel in an inverted orientation, with the carboxylate group interacting with Tyr-385 and Ser-530 at the top of the channel. Tryptophan fluorescence quenching, continuous-wave electron spin resonance, and UV-visible spectroscopy demonstrate that flufenamic acid, mefenamic acid, and tolfenamic acid are substrate-selective inhibitors that bind rapidly to COX-2, quench tyrosyl radicals, and reduce higher oxidation states of the heme moiety. Substrate-selective inhibition was attenuated by the addition of the lipid peroxide 15-hydroperoxyeicosatertaenoic acid. Collectively, these studies implicate peroxide tone as an important mechanistic component of substrate-selective inhibition by flufenamic acid, mefenamic acid, and tolfenamic acid. PMID:27226593

  15. Carbon tetrachloride-mediated lipid peroxidation induces early mitochondrial alterations in mouse liver.

    PubMed

    Knockaert, Laetitia; Berson, Alain; Ribault, Catherine; Prost, Pierre-Emmanuel; Fautrel, Alain; Pajaud, Julie; Lepage, Sylvie; Lucas-Clerc, Catherine; Bégué, Jean-Marc; Fromenty, Bernard; Robin, Marie-Anne

    2012-03-01

    Although carbon tetrachloride (CCl(4))-induced acute and chronic hepatotoxicity have been extensively studied, little is known about the very early in vivo effects of this organic solvent on oxidative stress and mitochondrial function. In this study, mice were treated with CCl(4) (1.5 ml/kg ie 2.38 g/kg) and parameters related to liver damage, lipid peroxidation, stress/defense and mitochondria were studied 3 h later. Some CCl(4)-intoxicated mice were also pretreated with the cytochrome P450 2E1 inhibitor diethyldithiocarbamate or the antioxidants Trolox C and dehydroepiandrosterone. CCl(4) induced a moderate elevation of aminotransferases, swelling of centrilobular hepatocytes, lipid peroxidation, reduction of cytochrome P4502E1 mRNA levels and a massive increase in mRNA expression of heme oxygenase-1 and heat shock protein 70. Moreover, CCl(4) intoxication induced a severe decrease of mitochondrial respiratory chain complex IV activity, mitochondrial DNA depletion and damage as well as ultrastructural alterations. Whereas DDTC totally or partially prevented all these hepatic toxic events, both antioxidants protected only against liver lipid peroxidation and mitochondrial damage. Taken together, our results suggest that lipid peroxidation is primarily implicated in CCl(4)-induced early mitochondrial injury. However, lipid peroxidation-independent mechanisms seem to be involved in CCl(4)-induced early hepatocyte swelling and changes in expression of stress/defense-related genes. Antioxidant therapy may not be an efficient strategy to block early liver damage after CCl(4) intoxication. PMID:22157718

  16. [Kinetics of lipid peroxidation induced by UV beta rays in human keratinocyte and fibroblast cultures].

    PubMed

    Perez, S; Sergent, O; Morel, P; Chevanne, M; Dubos, M P; Cillard, P; Cillard, J

    1995-01-01

    Lipid peroxidation has been implicated in skin damage by ultraviolet radiation. The aim of the study was to determine the kinetic of lipid peroxidation induced by ultraviolet beta (UVB) in adult keratinocytes and fibroblasts in culture. The keratinocytes were obtained from a single primary culture and the fibroblasts were in the same subculture (4 to 10 transfers). For UVB irradiation, the cells were maintained in a small volume of Hanks balanced salt solution and were irradiated (0.75, 1.5, 3 and 4.5 Jcm-2). Then cells were cultured for 3 to 48 hours. Lipid peroxidation was estimated by free MDA determination in both extracellular medium and cells using a size exclusion chromatography coupled to an HPLC procedure. In addition, LDH release in culture media was evaluated as in indice of cytotoxicity. An increase of total free MDA was observed 3 hours after cell irradiation which was dose-dependent from 0.75 to 3 Jcm-2 for keratinocytes and fibroblasts. MDA was detected both in cells and in culture media. As soon as 3 hours after irradiation 90% in total MDA was present in the culture media. Kinetic of lipid peroxidation: for 0.75 Jcm-2, an elevation of MDA was observed 12 hours after irradiation in both cultures. A further increase in MDA was noted 24 hours after fibroblasts irradiation but not in irradiated keratinocytes. LDH release in culture media increased with post irradiation time until 48 hours. The cytotoxic effect of UVB irradiation on keratinocytes and fibroblasts cultures was shown by an enhancement of lipid peroxidation which was detectable during 48 hours after irradiation. An increase of LDH release was observed simultaneously. PMID:8521093

  17. The Fungicidal Activity of Thymol against Fusarium graminearum via Inducing Lipid Peroxidation and Disrupting Ergosterol Biosynthesis.

    PubMed

    Gao, Tao; Zhou, Hao; Zhou, Wei; Hu, Liangbin; Chen, Jian; Shi, Zhiqi

    2016-01-01

    Thymol is a natural plant-derived compound that has been widely used in pharmaceutical and food preservation applications. However, the antifungal mechanism for thymol against phytopathogens remains unclear. In this study, we identified the antifungal action of thymol against Fusarium graminearum, an economically important phytopathogen showing severe resistance to traditional chemical fungicides. The sensitivity of thymol on different F. graminearum isolates was screened. The hyphal growth, as well as conidial production and germination, were quantified under thymol treatment. Histochemical, microscopic, and biochemical approaches were applied to investigate thymol-induced cell membrane damage. The average EC50 value of thymol for 59 F. graminearum isolates was 26.3 μg·mL(-1). Thymol strongly inhibited conidial production and hyphal growth. Thymol-induced cell membrane damage was indicated by propidium iodide (PI) staining, morphological observation, relative conductivity, and glycerol measurement. Thymol induced a significant increase in malondialdehyde (MDA) concentration and a remarkable decrease in ergosterol content. Taken together, thymol showed potential antifungal activity against F. graminearum due to the cell membrane damage originating from lipid peroxidation and the disturbance of ergosterol biosynthesis. These results not only shed new light on the antifungal mechanism of thymol, but also imply a promising alternative for the control of Fusarium head blight (FHB) disease caused by F. graminearum. PMID:27322238

  18. Myeloperoxidase-dependent lipid peroxidation promotes the oxidative modification of cytosolic proteins in phagocytic neutrophils.

    PubMed

    Wilkie-Grantham, Rachel P; Magon, Nicholas J; Harwood, D Tim; Kettle, Anthony J; Vissers, Margreet C; Winterbourn, Christine C; Hampton, Mark B

    2015-04-10

    Phagocytic neutrophils generate reactive oxygen species to kill microbes. Oxidant generation occurs within an intracellular phagosome, but diffusible species can react with the neutrophil and surrounding tissue. To investigate the extent of oxidative modification, we assessed the carbonylation of cytosolic proteins in phagocytic neutrophils. A 4-fold increase in protein carbonylation was measured within 15 min of initiating phagocytosis. Carbonylation was dependent on NADPH oxidase and myeloperoxidase activity and was inhibited by butylated hydroxytoluene and Trolox, indicating a role for myeloperoxidase-dependent lipid peroxidation. Proteomic analysis of target proteins revealed significant carbonylation of the S100A9 subunit of calprotectin, a truncated form of Hsp70, actin, and hemoglobin from contaminating erythrocytes. The addition of the reactive aldehyde 4-hydroxynonenal (HNE) caused carbonylation, and HNE-glutathione adducts were detected in the cytosol of phagocytic neutrophils. The post-translational modification of neutrophil proteins will influence the functioning and fate of these immune cells in the period following phagocytic activation, and provides a marker of neutrophil activation during infection and inflammation. PMID:25697357

  19. Modification and inactivation of Cu,Zn-superoxide dismutase by the lipid peroxidation product, acrolein

    PubMed Central

    Kang, Jung Hoon

    2013-01-01

    Acrolein is the most reactive aldehydic product of lipid peroxidation and is found to be elevated in the brain when oxidative stress is high. The effects of acrolein on the structure and function of human Cu,Zn-superoxide dismutase (SOD) were examined. When Cu,Zn-SOD was incubated with acrolein, the covalent crosslinking of the protein was increased, and the loss of enzymatic activity was increased in a dose-dependent manner. Reactive oxygen species (ROS) scavengers and copper chelators inhibited the acrolein-mediated Cu,Zn-SOD modification and the formation of carbonyl compound. The present study shows that ROS may play a critical role in acrolein-induced Cu,Zn-SOD modification and inactivation. When Cu,Zn-SOD that has been exposed to acrolein was subsequently analyzed by amino acid analysis, serine, histidine, arginine, threonine and lysine residues were particularly sensitive. It is suggested that the modification and inactivation of Cu,Zn-SOD by acrolein could be produced by more oxidative cell environments. [BMB Reports 2013; 46(11): 555-560] PMID:24152914

  20. Myeloperoxidase-dependent Lipid Peroxidation Promotes the Oxidative Modification of Cytosolic Proteins in Phagocytic Neutrophils*

    PubMed Central

    Wilkie-Grantham, Rachel P.; Magon, Nicholas J.; Harwood, D. Tim; Kettle, Anthony J.; Vissers, Margreet C.; Winterbourn, Christine C.; Hampton, Mark B.

    2015-01-01

    Phagocytic neutrophils generate reactive oxygen species to kill microbes. Oxidant generation occurs within an intracellular phagosome, but diffusible species can react with the neutrophil and surrounding tissue. To investigate the extent of oxidative modification, we assessed the carbonylation of cytosolic proteins in phagocytic neutrophils. A 4-fold increase in protein carbonylation was measured within 15 min of initiating phagocytosis. Carbonylation was dependent on NADPH oxidase and myeloperoxidase activity and was inhibited by butylated hydroxytoluene and Trolox, indicating a role for myeloperoxidase-dependent lipid peroxidation. Proteomic analysis of target proteins revealed significant carbonylation of the S100A9 subunit of calprotectin, a truncated form of Hsp70, actin, and hemoglobin from contaminating erythrocytes. The addition of the reactive aldehyde 4-hydroxynonenal (HNE) caused carbonylation, and HNE-glutathione adducts were detected in the cytosol of phagocytic neutrophils. The post-translational modification of neutrophil proteins will influence the functioning and fate of these immune cells in the period following phagocytic activation, and provides a marker of neutrophil activation during infection and inflammation. PMID:25697357

  1. Antioxidant depletion, lipid peroxidation, and impairment of calcium transport induced by air-blast overpressure in rat lungs.

    PubMed

    Elsayed, N M; Tyurina, Y Y; Tyurin, V A; Menshikova, E V; Kisin, E R; Kagan, V E

    1996-01-01

    Exposure to blast overpressure, or the sudden rise in atmospheric pressure after explosive detonation, results in damage mainly of the gas-filled organs. In addition to the physical damage, in the lung, injury may proceed via a hemorrhage-dependent mechanism initiating oxidative stress and accumulation of lipid peroxidation products. Massive rupture of capillaries and red blood cells, release of hemoglobin, its oxidation to met-hemoglobin and degradation sets the stage for heme-catalyzed oxidations. The authors hypothesized that lipid hydroperoxides interact with met-hemoglobin in the lungs of exposed animals to produce ferryl-hemoglobin, an extremely potent oxidant that induces oxidative damage by depleting antioxidants and initiating peroxidation reactions. Oxidation-induced disturbance of Ca2+ homeostasis facilitates further amplification of the damage. To test this hypothesis, groups of anesthetized rats (6 rats/group) were exposed to blast at 3 peak pressures: low (61.2 kPa), medium (95.2 kPa), high (136 kPa). One group served as an unexposed control. Immediately after exposure, the rats were euthanized and the lungs were analyzed for biochemical parameters. Blast overpressure caused: (1) depletion of total and water-soluble pulmonary antioxidant reserves and individual antioxidants (ascorbate, vitamin E, GSH), (2) accumulation of lipid peroxidation products (conjugated dienes, TBARS), and (3) inhibition of ATP-dependent Ca2+ transport. The magnitude of these changes in the lungs was proportional to the peak blast overpressure. Inhibition of Ca2+ transport strongly correlated with both depletion of antioxidants and enhancement of lipid peroxidation. In model experiments, met-hemoglobin/H2O2 produced damage to Ca2+ transport in the lungs from control animals similar to that observed in the lungs from blast overpressure-exposed animals. Ascorbate, which is known to reduce ferryl-hemoglobin, protected against met-hemoglobin/H2O2-induced damage of Ca2+ transport

  2. Modulation of keratinocyte expression of antioxidants by 4-hydroxynonenal, a lipid peroxidation end product

    SciTech Connect

    Zheng, Ruijin; Heck, Diane E.; Mishin, Vladimir; Black, Adrienne T.; Shakarjian, Michael P.; Kong, Ah-Ng Tony; Laskin, Debra L.; Laskin, Jeffrey D.

    2014-03-01

    4-Hydroxynonenal (4-HNE) is a lipid peroxidation end product generated in response to oxidative stress in the skin. Keratinocytes contain an array of antioxidant enzymes which protect against oxidative stress. In these studies, we characterized 4-HNE-induced changes in antioxidant expression in mouse keratinocytes. Treatment of primary mouse keratinocytes and PAM 212 keratinocytes with 4-HNE increased mRNA expression for heme oxygenase-1 (HO-1), catalase, NADPH:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) A1-2, GSTA3 and GSTA4. In both cell types, HO-1 was the most sensitive, increasing 86–98 fold within 6 h. Further characterization of the effects of 4-HNE on HO-1 demonstrated concentration- and time-dependent increases in mRNA and protein expression which were maximum after 6 h with 30 μM. 4-HNE stimulated keratinocyte Erk1/2, JNK and p38 MAP kinases, as well as PI3 kinase. Inhibition of these enzymes suppressed 4-HNE-induced HO-1 mRNA and protein expression. 4-HNE also activated Nrf2 by inducing its translocation to the nucleus. 4-HNE was markedly less effective in inducing HO-1 mRNA and protein in keratinocytes from Nrf2 −/− mice, when compared to wild type mice, indicating that Nrf2 also regulates 4-HNE-induced signaling. Western blot analysis of caveolar membrane fractions isolated by sucrose density centrifugation demonstrated that 4-HNE-induced HO-1 is localized in keratinocyte caveolae. Treatment of the cells with methyl-β-cyclodextrin, which disrupts caveolar structure, suppressed 4-HNE-induced HO-1. These findings indicate that 4-HNE modulates expression of antioxidant enzymes in keratinocytes, and that this can occur by different mechanisms. Changes in expression of keratinocyte antioxidants may be important in protecting the skin from oxidative stress. - Highlights: • Lipid peroxidation generates 4-hydroxynonenal, a reactive aldehyde. • 4-HNE induces antioxidant proteins in mouse keratinocytes. • Induction of

  3. Supplementation of broccoli or Bifidobacterium longum-fermented broccoli suppresses serum lipid peroxidation and osteoclast differentiation on alveolar bone surface in rats fed a high-cholesterol diet.

    PubMed

    Tomofuji, Takaaki; Ekuni, Daisuke; Azuma, Tetsuji; Irie, Koichiro; Endo, Yasumasa; Yamamoto, Tatsuo; Ishikado, Atsushi; Sato, Takehiko; Harada, Kayo; Suido, Hirohisa; Morita, Manabu

    2012-04-01

    High-cholesterol diet enhances osteoclastic activity on alveolar bone by increasing serum lipid peroxidation. We hypothesized that supplementation with dietary antioxidants, such as found in broccoli and its fermented products, might suppress increases in serum lipid peroxidation, contributing to the inhibition of osteoclastic activity after high-cholesterol diet intake. The purpose of the present study was to investigate the effects of broccoli and fermented broccoli consumption on serum lipid peroxidation and osteoclast differentiation in alveolar bone of rats fed a high-cholesterol diet. In this 12-week study, rats were divided into 4 groups (n = 6/group): a control group (fed regular diet) and 3 experimental groups (fed a high-cholesterol [1% wt/wt] diet, or a high-cholesterol diet supplemented with either broccoli powder [5% wt/wt] or Bifidobacterium longum-fermented broccoli powder [5% wt/wt]). Serum hexanoyl-lysine (HEL) levels were measured as a parameter of lipid peroxidation. The number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts in alveolar bone was enumerated to evaluate osteoclast differentiation. When compared with regular diet, the high-cholesterol diet increased serum HEL levels and resulted in a higher number of TRAP-positive osteoclasts at 12 weeks. The high-cholesterol diet supplemented with broccoli or B. longum-fermented broccoli showed lower levels of serum HEL and fewer TRAP-positive osteoclasts than the high-cholesterol diet at 12 weeks. In conclusion, consumption of broccoli, or its fermented product, inhibited the effects of a high-cholesterol diet on osteoclast differentiation in rat alveolar bone by suppressing serum lipid peroxidation. PMID:22575044

  4. Compositional Factors that Influence Lipid Peroxidation in Beef Juice and Standard Sausages.

    PubMed

    Yi, Gu; Haug, Anna; Nordvi, Berit; Saarem, Kristin; Oostindjer, Marije; Langsrud, Øyvind; Egelandsdal, Bjørg

    2015-12-01

    In order to identify how different additives influenced lipid peroxidation formation, a sausage only using beef juice as pigment source and a standard beef-pork meat sausage were studied. The effects of different additives, including fish oil, myoglobin, nitrite, clove extract, and calcium sources on oxidation and sensory properties were examined. Both sausage systems were stored in 3 different manners prior to testing: (1) frozen immediately at -80 °C; (2) chilled stored for 2.5 weeks followed by fluorescent light illumination at 4 °C for another 2 wk; (3) frozen at -20 °C for 5 mo. The frozen group 3 showed the highest peroxide formation and thiobarbituric acid reactive substances (TBARS) for both sausage systems. Unpolar peroxides dominated in both systems. The clove extract could offset the peroxide formation from myoglobin/beef juice and/or fish oil, but the addition of clove flavor was recognized by the sensory panelists. Calcium addition reduced lipid peroxide formation. Added nitrite and fish oil seemed to interact to stimulate nitroso-myoglobin formation. Nitrite was identified to interact with clove addition and thereby, relatively speaking, increased TBARS. The 2 sausage systems generally ranked the additives similarly as pro- and antioxidants. PMID:26579877

  5. [Clinical evaluation and application of lipid peroxidation produced by tobacco smoke in the tracheal mucosa].

    PubMed

    García Callejo, F J; Velert Vila, M M; Esparcia Navarro, M; Martínez Beneito, M P; Marco Algarra, J

    1998-05-01

    The oxidative stress level produced by tobacco smoke on the respiratory system was evaluated by studying lipid peroxidation in the tracheal mucosa of samples obtained by tracheostomy from nonsmokers. Conjugated dienes, derived from fatty acids present in tissue, were measured in the sample. The absence of polymorphonuclear leukocytes and macrophages in the tracheal mucosa make it a more suitable model than lung parenchyma because it excludes the peroxidation produced by inflammatory cells. The tracheal mucosa was exposed to different numbers of smoke puffs, then submitted to recovery with humidified air for different time periods. The effect of diene production on several antioxidants--superoxide dismutase, catalase, deferroxamine--was studied. Exposure to four puffs of tobacco smoke from a cigarette was enough to produce lipid oxidation in samples. This activity was evident 15 minutes after exposure to smoke. When antioxidants were placed on sample surfaces, lipid peroxidation was abolished. We conclude that tobacco smoke has a peroxidant activity independent of that produced by inflammatory cells, but probably mediated by free radicals. Therefore, the tracheal model seems suitable for the evaluation of respiratory epithelial oxidation in response to tobacco smoke. PMID:9707733

  6. 4-Hydroxynonenal, an aldehydic product of lipid peroxidation, impairs signal transduction associated with muscarinic acetylcholine and metabotropic glutamate receptors: possible action on G alpha(q/11).

    PubMed

    Blanc, E M; Kelly, J F; Mark, R J; Waeg, G; Mattson, M P

    1997-08-01

    Considerable data indicate that oxidative stress and membrane lipid peroxidation contribute to neuronal degeneration in an array of age-related neurodegenerative disorders. In contrast, the impact of subtoxic levels of membrane lipid peroxidation on neuronal function is largely unknown. We now report that 4-hydroxynonenal (HNE), an aldehydic product of lipid peroxidation, disrupts coupling of muscarinic cholinergic receptors and metabotropic glutamate receptors to phospholipase C-linked GTP-binding proteins in cultured rat cerebrocortical neurons. At subtoxic concentrations, HNE markedly inhibited GTPase activity, inositol phosphate release, and elevation of intracellular calcium levels induced by carbachol (muscarinic agonist) and (RS)-3,5-dihydroxyphenyl glycine (metabotropic glutamate receptor agonist). Maximal impairment of agonist-induced responses occurred within 30 min of exposure to HNE. Other aldehydes, including malondialdehyde, had little effect on agonist-induced responses. Antioxidants that suppress lipid peroxidation did not prevent impairment of agonist-induced responses by HNE, whereas glutathione, which is known to bind and detoxify HNE, did prevent impairment of agonist-induced responses. HNE itself did not induce oxidative stress. Immunoprecipitation-western blot analysis using an antibody to HNE-protein conjugates showed that HNE can bind to G alpha(q/11). HNE also significantly suppressed inositol phosphate release induced by aluminum fluoride. Collectively, our data suggest that HNE plays a role in altering receptor-G protein coupling in neurons under conditions of oxidative stress that may occur both normally, and before cell degeneration and death in pathological settings. PMID:9231714

  7. Postprandial hyperglycemia impairs vascular endothelial function in healthy men by inducing lipid peroxidation and increasing asymmetric dimethylarginine:arginine.

    PubMed

    Mah, Eunice; Noh, Sang K; Ballard, Kevin D; Matos, Manuel E; Volek, Jeff S; Bruno, Richard S

    2011-11-01

    Postprandial hyperglycemia induces vascular endothelial dysfunction (VED) and increases future cardiovascular disease risk. We hypothesized that postprandial hyperglycemia would decrease vascular function in healthy men by inducing oxidative stress and proinflammatory responses and increasing asymmetric dimethylarginine:arginine (ADMA:arginine), a biomarker that is predictive of reduced NO biosynthesis. In a randomized, cross-over design, healthy men (n = 16; 21.6 ± 0.8 y) ingested glucose or fructose (75 g) after an overnight fast. Brachial artery flow-mediated dilation (FMD), plasma glucose and insulin, antioxidants, malondialdehyde (MDA), inflammatory proteins, arginine, and ADMA were measured at regular intervals during the 3-h postprandial period. Baseline FMD did not differ between trials (P > 0.05). Postprandial FMD was reduced following the ingestion of glucose only. Postprandial MDA concentrations increased to a greater extent following the ingestion of glucose compared to fructose. Plasma arginine decreased and the ratio of ADMA:arginine increased to a greater extent following the ingestion of glucose. Inflammatory cytokines and cellular adhesion molecules were unaffected by the ingestion of either sugar. Postprandial AUC(0-3 h) for FMD and MDA were inversely related (r = -0.80; P < 0.05), suggesting that hyperglycemia-induced lipid peroxidation suppresses postprandial vascular function. Collectively, these findings suggest that postprandial hyperglycemia in healthy men reduces endothelium-dependent vasodilation by increasing lipid peroxidation independent of inflammation. Postprandial alterations in arginine and ADMA:arginine also suggest that acute hyperglycemia may induce VED by decreasing NO bioavailability through an oxidative stress-dependent mechanism. Additional work is warranted to define whether inhibiting lipid peroxidation and restoring arginine metabolism would mitigate hyperglycemia-mediated decreases in vascular function. PMID:21940510

  8. Astaxanthin Normalizes Epigenetic Modifications of Bovine Somatic Cell Cloned Embryos and Decreases the Generation of Lipid Peroxidation.

    PubMed

    Li, R; Wu, H; Zhuo, W W; Mao, Q F; Lan, H; Zhang, Y; Hua, S

    2015-10-01

    Astaxanthin is an extremely common antioxidant scavenging reactive oxygen species (ROS) and blocking lipid peroxidation. This study was conducted to investigate the effects of astaxanthin supplementation on oocyte maturation, and development of bovine somatic cell nuclear transfer (SCNT) embryos. Cumulus-oocyte complexes were cultured in maturation medium with astaxanthin (0, 0.5, 1.0, or 1.5 mg/l), respectively. We found that 0.5 mg/l astaxanthin supplementation significantly increased the proportion of oocyte maturation. Oocytes cultured in 0.5 mg/l astaxanthin supplementation were used to construct SCNT embryos and further cultured with 0, 0.5, 1.0 or 1.5 mg/l astaxanthin. The results showed that the supplementation of 0.5 mg/l astaxanthin significantly improved the proportions of cleavage and blastulation, as well as the total cell number in blastocysts compared with the control group, yet this influence was not concentration dependent. Chromosomal analyses revealed that more blastomeres showed a normal chromosomal complement in 0.5 mg/l astaxanthin treatment group, which was similar to that in IVF embryos. The methylation levels located on the exon 1 of the imprinted gene H19 and IGF2, pluripotent gene OCT4 were normalized, and global DNA methylation, H3K9 and H4K12 acetylation were also improved significantly, which was comparable to that in vitro fertilization (IVF) embryos. Moreover, we also found that astaxanthin supplementation significantly decreased the level of lipid peroxidation. Our findings showed that the supplementation of 0.5 mg/l astaxanthin to oocyte maturation medium and embryo culture medium improved oocyte maturation, SCNT embryo development, increased chromosomal stability and normalized the epigenetic modifications, as well as inhibited overproduction of lipid peroxidation. PMID:26280670

  9. UVA photoirradiation of benzo[a]pyrene metabolites: induction of cytotoxicity, reactive oxygen species, and lipid peroxidation.

    PubMed

    Xia, Qingsu; Chiang, Hsiu-Mei; Yin, Jun-Jie; Chen, Shoujun; Cai, Lining; Yu, Hongtao; Fu, Peter P

    2015-10-01

    Benzo[a]pyrene (BaP) is a prototype for studying carcinogenesis of polycyclic aromatic hydrocarbons (PAHs). We have long been interested in studying the phototoxicity of PAHs. In this study, we determined that metabolism of BaP by human skin HaCaT keratinocytes resulted in six identified phase I metabolites, for example, BaP trans-7,8-dihydrodiol (BaP t-7,8-diol), BaP t-4,5-diol, BaP t-9,10-diol, 3-hydroxybenzo[a]pyrene (3-OH-BaP), BaP (7,10/8,9)tetrol, and BaP (7/8,9,10)tetrol. The photocytotoxicity of BaP, 3-OH-BaP, BaP t-7,8-diol, BaP trans-7,8-diol-anti-9,10-epoxide (BPDE), and BaP (7,10/8,9)tetrol in the HaCaT keratinocytes was examined. When irradiated with 1.0 J/cm(2) UVA light, these compounds when tested at doses of 0.1, 0.2, and 0.5 μM, all induced photocytotoxicity in a dose-dependent manner. When photoirradiation was conducted in the presence of a lipid (methyl linoleate), BaP metabolites, BPDE, and three related PAHs, pyrene, 7,8,9,10-tetrahydro-BaP trans-7,8-diol, and 7,8,9,10-tetrahydro-BaP trans-9,10-diol, all induced lipid peroxidation. The formation of lipid peroxides by BaP t-7,8-diol was inhibited by NaN3 and enhanced by deuterated methanol, which suggests that singlet oxygen may be involved in the generation of lipid peroxides. The formation of lipid hydroperoxides was partially inhibited by superoxide dismutase (SOD). Electron spin resonance spin trapping experiments indicated that both singlet oxygen and superoxide radical anion were generated from UVA photoirradiation of BPDE in a light dose responding manner. PMID:23552265

  10. Lipid oxidation and peroxidation in CNS health and disease: from molecular mechanisms to therapeutic opportunities.

    PubMed

    Adibhatla, Rao Muralikrishna; Hatcher, James Franklin

    2010-01-01

    Reactive oxygen species (ROS) are produced at low levels in mammalian cells by various metabolic processes, such as oxidative phosphorylation by the mitochondrial respiratory chain, NAD(P)H oxidases, and arachidonic acid oxidative metabolism. To maintain physiological redox balance, cells have endogenous antioxidant defenses regulated at the transcriptional level by Nrf2/ARE. Oxidative stress results when ROS production exceeds the cell's ability to detoxify ROS. Overproduction of ROS damages cellular components, including lipids, leading to decline in physiological function and cell death. Reaction of ROS with lipids produces oxidized phospholipids, which give rise to 4-hydroxynonenal, 4-oxo-2-nonenal, and acrolein. The brain is susceptible to oxidative damage due to its high lipid content and oxygen consumption. Neurodegenerative diseases (AD, ALS, bipolar disorder, epilepsy, Friedreich's ataxia, HD, MS, NBIA, NPC, PD, peroxisomal disorders, schizophrenia, Wallerian degeneration, Zellweger syndrome) and CNS traumas (stroke, TBI, SCI) are problems of vast clinical importance. Free iron can react with H(2)O(2) via the Fenton reaction, a primary cause of lipid peroxidation, and may be of particular importance for these CNS injuries and disorders. Cholesterol is an important regulator of lipid organization and the precursor for neurosteroid biosynthesis. Atherosclerosis, the major risk factor for ischemic stroke, involves accumulation of oxidized LDL in the arteries, leading to foam cell formation and plaque development. This review will discuss the role of lipid oxidation/peroxidation in various CNS injuries/disorders. PMID:19624272

  11. Inhibitory effect of some tropical green leafy vegetables on key enzymes linked to Alzheimer's disease and some pro-oxidant induced lipid peroxidation in rats' brain.

    PubMed

    Oboh, Ganiyu; Akinyemi, Ayodele Jacobson; Ademiluyi, Adedayo Oluwaseun; Bello, Fatai Olumide

    2014-05-01

    This study sought to investigate the inhibitory effect of some commonly consumed Nigerian green leafy vegetables (raw and blanched) on acetylcholinesterase and butyrylcholinesterase (key enzyme linked to Alzheimer's disease) activities and some pro-oxidants (FeSO4, Sodium nitroprusside and Quinolinic acid) induced lipid peroxidation in rat brain in vitro. Three commonly consumed green leafy vegetables in Nigeria [Amarantus cruentus (Arowojeja), Struchium sparganophora (Ewuro-odo) and Telfairia occidentalis (Ugwu] were blanched in hot water for 10 min, and the extracts of the raw and blanched vegetables were prepared and used for subsequent analysis. The result revealed that all the vegetables inhibited acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activity as well as the pro-oxidants induced lipid peroxidation in rat brain in a dose dependent manner; however, Amarantus cruentus extract (EC50 = 97.9 μg/ml) had the highest inhibitory effect on acetylcholinesterase activity while Telfairia occidentalis extract (EC50 = 52.7 μg/ml) had the highest inhibitory effect on butyrylcholinesterase activity. However, blanching of the vegetables caused a significant (P < 0.05) decrease in the inhibitory effect of the vegetables on AChE activities while it enhanced the inhibition of the pro-oxidants induced lipid peroxidation in rat brain in vitro. Therefore, some of the possible mechanism by which green leafy vegetables exert their neuroprotective activities could be through the inhibition of acetylcholinesterase and butyrylcholinesterase activities and prevention of lipid peroxidation in the brain. However, blanching of the vegetables could reduce their ability to inhibit acetylcholinesterase and butyrylcholinesterase activity. PMID:24803694

  12. Lipid peroxidative stress and antioxidative enzymes in brains of milk-supplemented rats.

    PubMed

    Bay, B H; Lee, Y K; Tan, B K; Ling, E A

    1999-12-24

    Skim milk cultured with lactic acid bacteria has been previously reported to reduce lipid peroxidation in rat livers. In this study, the effects of skim milk and cultured milk supplementation on peroxidative stress in brains of weanling rats were investigated. We observed a reduction of brain thiobarbituric acid reacting substances (TBARS) concentration in milk-supplemented animals as compared with controls. In brains of control rats, the superoxide dismutase (SOD) enzyme levels were significantly higher than those from the milk-supplemented animals. In addition, SOD activity in control animal brains had a positive correlation with the TBARS concentration. There was no significant differences in the brain glutathione-S-transferase (GST) levels of all the three groups of animals. The results suggest that milk supplementation may be beneficial in reducing peroxidative stress in the developing rat brain. PMID:10624826

  13. Antioxidant enzymes and lipid peroxidation in endometrium of patients with polyps, myoma, hyperplasia and adenocarcinoma

    PubMed Central

    2009-01-01

    Background Oxidative stress and impaired antioxidant system have been proposed as a potential factors involved in the pathophysiology of diverse disease states, including carcinogenesis. In this study, we explored the lipid peroxidation levels and antioxidant enzyme activities in women diagnosed with different forms of gynecological diseases in order to evaluate the antioxidant status in endometrium of such patients. Methods Endometrial tissues of gynecological patients with different diagnoses were collected and subjected to assays for superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and lipid hydroperoxides. Results Superoxide dismutase activity was significantly decreased (50% in average) in hyperplastic and adenocarcinoma patients. Activities of both glutathione peroxidase and glutathione reductase were increased 60% and 100% on average, in hyperplastic patients, while in adenocarcinoma patients only glutathione reductase activity was elevated 100%. Catalase activity was significantly decreased in adenocarcinoma patients (47%). Lipid hydroperoxides level was negatively correlated to superoxide dismutase and catalase activities, and positively correlated to glutathione peroxidase and glutathione reductase activities. Conclusions This study provided the first comparison of antioxidant status and lipid peroxidation in endometrial tissues of patients with polyps, myoma, hyperplasia and adenocarcinoma. The results showed that patients with premalignant (hyperplastic) and malignant (adenocarcinoma) lesions had enhanced lipid peroxidation and altered uterine antioxidant enzyme activities than patients with benign uterine diseases, polyps and myoma, although the extent of disturbance varied with the diagnosis. Further investigation is needed to clarify the mechanisms responsible for the observed alterations and whether lipid hydroperoxide levels and antioxidant enzyme activities in uterus of gynecological patients might be used as

  14. Pyridine and pyrimidine analogs of acetaminophen as inhibitors of lipid peroxidation and cyclooxygenase and lipoxygenase catalysis†

    PubMed Central

    Nam, Tae-gyu; Nara, Susheel J.; Zagol-Ikapitte, Irène; Cooper, Thomas; Valgimigli, Luca; Oates, John A.; Porter, Ned A.; Boutaud, Olivier; Pratt, Derek A.

    2010-01-01

    Herein we report an investigation of the efficacy of pyridine and pyrimidine analogs of acetaminophen (ApAP) as peroxyl radical-trapping antioxidants and inhibitors of enzyme-catalyzed lipid peroxidation by cyclooxygenases (COX) and lipoxygenases (LOX). In inhibited autoxidations we find that ApAP, the common analgesic and antipyretic agent, is a very good antioxidant with a rate constant for reaction with peroxyl radicals (kinh = 5 × 105 M−1 s−1) that is higher than many widely-used phenolic antioxidants, such as the ubiquitous butylated hydroxytoluene (BHT). This reactivity is reduced substantially upon incorporation of nitrogen into the phenolic ring, owing to an increase in the O–H bond dissociation enthalpy of pyridinols and pyrimidinols with respect to phenols. Incorporation of nitrogen into the phenolic ring of ApAP was also found to decrease its efficacy as an inhibitor of prostaglandin biosynthesis by ovine COX-1 (oCOX-1). This is explained on the basis of an increase in its oxidation potential and its reduced reactivity as a reducing co-substrate of the peroxidase protoporphyrin. In contrast, the efficacy of ApAP as an inhibitor of lipid hydroperoxide biosynthesis by soybean LOX-1 (sLOX-1) increased upon incorporation of nitrogen into the ring, suggesting a different mechanism of inhibition dependent on the acidity of the phenolic O–H which may involve chelation of the catalytic non-heme iron atom. The greater stability of the 3-pyridinols and 5-pyrimidinols to air oxidation as compared to phenols allowed us to evaluate some electron-rich pyridinols and pyrimidinols as inhibitors of oCOX-1 and sLOX-1. While the pyridinols had the best combination of activities as antioxidants and inhibitors of oCOX-1 and sLOX-1, they were found to be more toxic than ApAP in preliminary assays in human hepatocellular carcinoma (HepG2) cell culture. The pyrimidinols, however, were up to 17-fold more reactive to peroxyl radicals and up to 25-fold better inhibitors

  15. Vanadium-mediated lipid peroxidation in microsomes from human term placenta

    SciTech Connect

    Byczkowski, J.Z.; Wan, B.; Kulkarni, A.P.

    1988-11-01

    Vanadium is considered an essential element present in living organisms in trace amounts but it is toxic when introduced in excessive doses to animals and humans. Vanadium compounds are extensively used in modern industry and occupational exposure to high doses of vanadium is quite common. In pregnant mice, vanadium accumulates preferentially in the placenta and to lower extent in fetal skeleton and mammary gland during exposure to radioactive vanadium. Accumulation of vanadium in fetoplacental unit may present threat to the fetus by interacting with enzymes and ion-transporting systems in membranes. It is also possible that accumulation of vanadium with its concomitant reduction to vanadyl may lead to lipid peroxidation, followed by damage to biological membranes, lysosomal enzymes release and destruction of placental tissue. To explore some of these possibilities the authors decided to examine whether vanadate can undergo redox cycling in microsomes from human term placenta (HTP) that can lead to lipid peroxidation.

  16. Potentiation of ethanol-induced lipid peroxidation of biological membranes by vitamin C

    SciTech Connect

    Ahmad, F.F.; Cowan, D.L.; Sun, A.Y.

    1988-01-01

    The hydroxyl free radical (/sup ./OH) was generated by the system of ADP-Fe/sup + +/ and H/sub 2/O/sub 2/, trapped by 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and analyzed by electron spin resonance (ESR) spectroscopy. The addition of vitamin C to the system decreased considerably the amount of hydroxyl adduct of DMPO formed. In the presence of ethanol, the ESR spectrum observed was a composite signal of the hydroxyl and hydroxyethyl (HE) adducts of DMPO. However, in the presence of vitamin C and ethanol, pure HE adduct of DMPO was detected. We also detected the increase in lipid peroxidation in the presence of ethanol and vitamin C. These data lead us to hypothesize that in the biological system, formation of these long-lived HE free radicals may result in membrane damage due to an increase in lipid peroxidation.

  17. Modulatory effect of Scoparia dulcis in oxidative stress-induced lipid peroxidation in streptozotocin diabetic rats.

    PubMed

    Latha, M; Pari, L

    2003-01-01

    In light of evidence that diabetes mellitus is associated with oxidative stress and altered antioxidant status, we investigated the effect of Scoparia dulcis plant extracts (SPEt) (aqueous, ethanolic, and chloroform) in streptozotocin diabetic rats. Significant increases in the activities of insulin, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, reduced glutathione, vitamin C, and vitamin E were observed in liver, kidney, and brain on treatment with SPEt. In addition, the treated groups also showed significant decreases in blood glucose, thiobarbituric acid-reactive substances, and hydroperoxide formation in tissues, suggesting its role in protection against lipid peroxidation-induced membrane damage. Thus, the results of the present study indicate that extracts of S. dulcis, especially the aqueous extract, showed a modulatory effect by attenuating the above lipid peroxidation in streptozotocin diabetes. PMID:14977448

  18. Responses of a tropical tree species to ozone: visible leaf injury, growth, and lipid peroxidation.

    PubMed

    Cassimiro, Jéssica C; Moraes, Regina M

    2016-04-01

    The Brazilian native tree species Astronium graveolens was indicated as sensitive to ozone in a fumigation experiment. Thus, the objective of this study was to evaluate how sensitive A. graveolens is to ozone under realistic conditions in the field. Eighteen saplings were exposed to ozone in a contaminated area and in a greenhouse with filtered air during two exposure periods of approximately 63 days each (March-May 2012 and September-October 2012). Leaf injury was analyzed by means of its incidence and severity, the leaf injury index (LII) and the progression of leaf abscission. These variables were monitored weekly, whereas growth and lipid peroxidation were monitored monthly. Plants exposed to ozone showed significant growth decrease and visible leaf injury increase, but lipid peroxidation and leaf abscission remained unchanged. These results indicated that plants subjected to ozone possibly diverted energy from growth to the production of antioxidants necessary to cope with ozone-induced oxidative stress. PMID:26780049

  19. Iron-fortified flour: can it induce lipid peroxidation?

    PubMed

    Abtahi, Mitra; Neyestani, Tirang Reza; Pouraram, Hamed; Siassi, Fereydoun; Dorosty, Ahmad Reza; Elmadfa, Ibrahim; Doustmohammadian, Aazam

    2014-08-01

    This community-based study was conducted to evaluate the effects of iron-fortified bread consumption on certain biomarkers of oxidative stress in an apparently healthy population. Evaluation of food intake, anthropometric and laboratory variables was performed in the beginning and after the 8-month intervention for all participants. There was no significant change in oxidative stress biomarkers in women following 8 months intervention. However, in men, final values of total antioxidant capacity, compared to the initial ones, showed a significant decrease in (p = 0.01) which was accompanied by a significant increase in superoxide dismutase (p = 0.002). It could be concluded that although the short-term period (8 months) of extra iron intake did not show severe effects of lipid per oxidation, significant changes of serum iron and some oxidative stress indices suggested that fortification of flour with iron among non-anemic adults in the long term was not without adverse effects. PMID:24655144

  20. Anti lipid peroxidation activity of Piper trioicum Roxb. and Physalis minima L. extracts.

    PubMed

    Dinakaran, Sathis Kumar; Saraswathi, Narasimha Raju; Nalini, Venkata Rama Rao; Srisudharson; Bodanapu, Venkat Ram Reddy; Avasarala, Harani; Banji, David

    2011-07-01

    Attempt has been made to evaluate free radical scavenging activity of ethanolic extract of Piper trioicum Roxb. and Physalis minima L. individually. In this study goat liver has been used as lipid source. This in vitro evaluation was done by measuring the malondialdehyde (MDA) of tissue homogenates. The results suggest that the ethanolic extract of the Piper trioicum Roxb. and Physalis minima L. has the ability to suppress the lipid peroxidation and it was also found that Piper trioicum Roxb. extract has more activity than Physalis minima L. extract. PMID:21715277

  1. [Effect of selenium enriched diet on lipid peroxidation in patients with diabetes mellitus type 2].

    PubMed

    Skripchenko, N D; Sharafetdinov, Kh Kh; Plotnikova, O A; Meshcheriakova, V A; Mal'tsev, G Iu

    2003-01-01

    It was investigated the influence of a diet supplemented with selenium on the clinicometabolic parameters and the activity of lipid peroxidation in 43 patients with Type 2 diabetes mellitus. It was indicated that under the influence of dietotherapy besides the decrease of glucose levels in capillary and venous blood, improvement of parameters of lipid metabolism, a reduction of malondialdehyde level and tendency to increase of glutathione peroxidase activity were observed. The results of investigations testify about sufficiently expressed efficacy of a diet supplemented with selenium in correction of oxidative stress and clinicometabolic parameters in this contingent of patients. PMID:12664692

  2. Exploration of scalp surface lipids reveals squalene peroxide as a potential actor in dandruff condition.

    PubMed

    Jourdain, Roland; Moga, Alain; Vingler, Philippe; El Rawadi, Charles; Pouradier, Florence; Souverain, Luc; Bastien, Philippe; Amalric, Nicolas; Breton, Lionel

    2016-04-01

    Dandruff is a common but complex disorder with three major contributing factors: (1) individual predisposition, (2) scalp sebum and (3) Malassezia yeast colonization. To obtain further insights into the role of sebum in dandruff biogenesis, we analyzed scalp lipid species in a cohort of ten dandruff-free (control) and ten dandruff-afflicted volunteers by gas chromatography coupled to mass spectrometry. Lipid peroxidation levels and biochemical markers of oxidative stress were also assessed. Squalene, a major sebum component, was significantly more peroxidized in dandruff-affected scalps, resulting in significantly higher ratios of squalene monohydroperoxide (SQOOH)/squalene. This was observed when comparing dandruff-affected zones of dandruff subjects to both their non-affected zones and control subjects. In addition, other biomarkers such as malondialdehyde indicated that oxidative stress levels were raised on dandruff scalps. Surprisingly, differences regarding either free or bound fatty acids were fairly rare and minor. Certain novel findings, especially squalene peroxidation levels, were then confirmed in a validation cohort of 24 dandruff-affected subjects, by comparing dandruff-affected and non-dandruff zones from the same individuals. As SQOOH can induce both keratinocyte inflammatory responses and hyperproliferation in vitro, we hypothesized that increased SQOOH could be considered as a new etiological dandruff factor via its ability to impair scalp barrier function. Our results also indicated that Malassezia could be a major source of squalene peroxidation on the scalp. PMID:26842231

  3. Oxygen radicals generated at reflow induce peroxidation of membrane lipids in reperfused hearts.

    PubMed Central

    Ambrosio, G; Flaherty, J T; Duilio, C; Tritto, I; Santoro, G; Elia, P P; Condorelli, M; Chiariello, M

    1991-01-01

    To test whether generation of oxygen radicals during postischemic reperfusion might promote peroxidation of cardiac membrane lipids, four groups of Langendorff-perfused rabbit hearts were processed at the end of (a) control perfusion, (b) 30 min of total global ischemia at 37 degrees C without reperfusion, (c) 30 min of ischemia followed by reperfusion with standard perfusate, (d) 30 min of ischemia followed by reperfusion with the oxygen radical scavenger human recombinant superoxide dismutase (h-SOD). The left ventricle was homogenized and tissue content of malonyldialdehyde (MDA), an end product of lipid peroxidation, was measured on the whole homogenate as well as on various subcellular fractions. Reperfusion was accompanied by a significant increase in MDA content of the whole homogenate and of the fraction enriched in mitochondria and lysosomes. This phenomenon was not observed in hearts subjected to ischemia but not reperfused, and was similarly absent in those hearts which received h-SOD at reflow. Reperfused hearts also had significantly greater levels of conjugated dienes (another marker of lipid peroxidation) in the mitochondrial-lysosomal fraction. Again, this phenomenon did not occur in ischemic hearts or in reperfused hearts treated with h-SOD. Unlike the effect on tissue MDA and conjugated dienes, reperfusion did not significantly stimulate release of MDA in the cardiac effluent. Treatment with h-SOD was also associated with significant improvement in the recovery of cardiac function. In conclusion, these data directly demonstrate that postischemic reperfusion results in enhanced lipid peroxidation of cardiac membranes, which can be blocked by h-SOD, and therefore is most likely secondary to oxygen radical generation at reflow. Images PMID:1645750

  4. Time course of lipolytic activity and lipid peroxidation after whole-body gamma irradiation of rats

    SciTech Connect

    Rejholcova, M.; Wilhelm, J.

    1989-01-01

    The content of fluorescing products of lipid peroxidation (LFP) and hormone-stimulated lipolytic activity were determined in rat epididymal adipose tissue during a 29-day interval after whole-body gamma irradiation. An increase in LFP was accompanied by a decrease in lipolytic activity. It is suggested that these effects are interrelated and that the decrease in lipolysis in irradiated, semi fasting rats is an additional deteriorating factor leading to death in some animals.

  5. [Effect of pantethine on post-heparin lipolytic activity and lipid peroxidation in the myocardium].

    PubMed

    Kumerova, A O; Silova, A A; Utno, L Ia

    1991-01-01

    In the present work the effect of the precursor of Co a D-bis (N- pantothenyl-beta-aminoethyl) disulfide--pantethine on post heparin lipolytic activity and the intensity of lipid peroxidation has been investigated. Pantethine in doses of 5 mg/kg enhanced post heparin lipolytic activity (60.6%) and lipoprotein lipase activity (39.9%) in plasma and reduced the amount of NEFA (35.1%) and content of MDA (57.4%) in the mitochondria. PMID:2054471

  6. The onset of lipid peroxidation in rheumatoid arthritis: consequences and monitoring.

    PubMed

    Łuczaj, Wojciech; Gindzienska-Sieskiewicz, Ewa; Jarocka-Karpowicz, Iwona; Andrisic, Luka; Sierakowski, Stanisław; Zarkovic, Neven; Waeg, Georg; Skrzydlewska, Elżbieta

    2016-01-01

    Several epidemiological studies propose the association of rheumatoid arthritis (RA) with oxidative stress. The aim of this study was to estimate the possible onset of systemic lipid peroxidation in RA patients and its relevance for pathophysiology and monitoring of RA. Seventy-three patients with RA and 73 healthy subjects were included in the study. Lipid peroxidation was estimated by the measurement of 4-hydroxynonenal (4-HNE), 4-hydroxyhexenal, malondialdehyde, acrolein, crotonaldehyde, 4-oxononenal, and isoprostanes (8-isoPGF(2α)) levels. Cytosolic phospholipase A(2) (cPLA(2)), platelet-activating factor acetylhydrolase (PAF-AH) and glutathione peroxidase (GSH-Px) activities and vitamin E levels were also determined. In parallel, the plasma levels of phospholipid arachidonic acid (AA), linoleic acid (LA), and 4-HNE-protein adducts were monitored. Plasma of RA patients had increased vitamin E levels, but decreased GSH-Px activity and phospholipid AA and LA levels when compared to levels of the healthy subjects. The levels of aldehydes were significantly increased in the plasma of the RA patients and even more in urine. Significant increases in HNE-modified protein adducts was observed for the first time in plasma of RA patients, while the activities of PAF-AH and cPLA(2) were decreased. The 8-isoPGF(2α) levels were 9-fold higher in plasma and 3-fold higher in urine of RA patients and were related to the severity of disease. The levels of lipid peroxidation products in plasma and in urine suggest the relationship between lipid peroxidation and the development of RA. Additionally, urine 8-isoPGF(2α), plasma 4-HNE and 4-HNE-protein adducts appear to be convenient biomarkers to monitor progression of this autoimmune disease. PMID:26764956

  7. Sex differences in lipid peroxidation and fatty acid levels in recent onset schizophrenia.

    PubMed

    Ramos-Loyo, Julieta; Medina-Hernández, Virginia; Estarrón-Espinosa, Mirna; Canales-Aguirre, Alejandro; Gómez-Pinedo, Ulises; Cerdán-Sánchez, Luis F

    2013-07-01

    Sex differences in the symptomatology and course of illness have been reported among schizophrenic patients. Hence, the principal objective of the present study was to investigate sex differences in the concentrations of the lipid peroxidation metabolites MDA and 4-HNE, and in the membrane phospholipid levels of ARA, EPA and DHA in patients with schizophrenia. A total of 46 paranoid schizophrenics (25 women) with short-term evolution who were in an acute psychotic stage and 40 healthy controls (23 women) participated in the study. Psychopathology was evaluated by BPRS and PANSS. Lipid peroxidation sub-products (MDA, 4-HNE) and fatty acid levels (ARA, EPA, DHA) were determined in erythrocyte membranes. The men in both groups showed higher lipid peroxidation levels and those values were higher in schizophrenic patients than controls, with only EPA fatty acid concentrations found to be lower in the former than the latter. These results suggest that men may suffer greater oxidative neuronal damage than women, and that this could worsen the course of illness and result in greater disease severity. PMID:23421976

  8. A Protocol for Quantifying Lipid Peroxidation in Cellular Systems by F2-Isoprostane Analysis

    PubMed Central

    Labuschagne, Christiaan F.; van den Broek, Niels J. F.; Postma, Pjotr; Berger, Ruud; Brenkman, Arjan B.

    2013-01-01

    Cellular systems are essential model systems to study reactive oxygen species and oxidative damage but there are widely accepted technical difficulties with available methods for quantifying endogenous oxidative damage in these systems. Here we present a stable isotope dilution UPLC-MS/MS protocol for measuring F2-isoprostanes as accurate markers for endogenous oxidative damage in cellular systems. F2-isoprostanes are chemically stable prostaglandin-like lipid peroxidation products of arachidonic acid, the predominant polyunsaturated fatty acid in mammalian cells. This approach is rapid and highly sensitive, allowing for the absolute quantification of endogenous lipid peroxidation in as little as ten thousand cells as well as damage originating from multiple ROS sources. Furthermore, differences in the endogenous cellular redox state induced by transcriptional regulation of ROS scavenging enzymes were detected by following this protocol. Finally we showed that the F2-isoprostane 5-iPF2α-VI is a metabolically stable end product, which is excreted from cells. Overall, this protocol enables accurate, specific and sensitive quantification of endogenous lipid peroxidation in cellular systems. PMID:24244726

  9. Regulation of the hepatitis C virus RNA replicase by endogenous lipid peroxidation

    PubMed Central

    Yamane, Daisuke; McGivern, David R.; Wauthier, Eliane; Yi, MinKyung; Madden, Victoria J.; Welsch, Christoph; Antes, Iris; Wen, Yahong; Chugh, Pauline E.; McGee, Charles E.; Widman, Douglas G.; Misumi, Ichiro; Bandyopadhyay, Sibali; Kim, Seungtaek; Shimakami, Tetsuro; Oikawa, Tsunekazu; Whitmire, Jason K.; Heise, Mark T.; Dittmer, Dirk P.; Kao, C. Cheng; Pitson, Stuart M; Merrill, Alfred H.; Reid, Lola M.; Lemon, Stanley M.

    2014-01-01

    Although oxidative tissue injury often accompanies viral infection, there is little understanding of how it influences virus replication. We show that multiple hepatitis C virus (HCV) genotypes are exquisitely sensitive to oxidative membrane damage, a property distinguishing them from other pathogenic RNA viruses. Lipid peroxidation, regulated in part through sphingosine kinase 2, severely restricts HCV replication in Huh-7 cells and primary human hepatoblasts. Endogenous oxidative membrane damage lowers the 50% effective concentration of direct-acting antivirals, suggesting critical regulation of the conformation of the NS3/4A protease and NS5B polymerase, membrane-bound HCV replicase components. Resistance to lipid peroxidation maps genetically to trans-membrane and membrane-proximal residues within these proteins, and is essential for robust replication in cell culture, as exemplified by the atypical JFH1 strain. Thus, the typical, wild-type HCV replicase is uniquely regulated by lipid peroxidation, providing a novel mechanism for attenuating replication in stressed tissue and possibly facilitating long-term viral persistence. PMID:25064127

  10. Implications of oxidative stress and cell membrane lipid peroxidation in human cancer (Spain).

    PubMed

    Cejas, Paloma; Casado, Enrique; Belda-Iniesta, Cristobal; De Castro, Javier; Espinosa, Enrique; Redondo, Andrés; Sereno, María; García-Cabezas, Miguel A; Vara, Juan A F; Domínguez-Cáceres, Aurora; Perona, Rosario; González-Barón, Manuel

    2004-09-01

    Reactive Oxygen Species (ROS) result from cell metabolism as well as from extracellular processes. ROS exert some functions necessary for cell homeostasis maintenance. When produced in excess they play a role in the causation of cancer. ROS mediated lipid peroxides are of critical importance because they participate in chain reactions that amplify damage to biomolecules including DNA. DNA attack gives rise to mutations that may involve tumor suppressor genes or oncogenes, and this is an oncogenic mechanism. On the other hand, ROS production is a mechanism shared by many chemotherapeutic drugs due to their implication in apoptosis control. The ROS mediated cell responses depend on the duration and intensity of the cells exposing to the increased ROS environment. Thus the status redox is of great importance for oncogenetic process activation and it is also implicated in tumor susceptibility to specific chemotherapeutic drugs. Phospholipid Hydroperoxide Glutathione Peroxidase (PH-GPx) is an antioxidant enzyme that is able to directly reduce lipid peroxides even when they are bound to cellular membranes. This article will review the relevance of oxidative stress, particularly of lipid peroxidation, in cell response with special focus in carcinogenesis and cancer therapy that suggests PH-GPx as a potentially important enzyme involved in the control of this processes. PMID:15280629

  11. Metal-catalyzed oxidation of 2-alkenals generates genotoxic 4-oxo-2-alkenals during lipid peroxidation.

    PubMed

    Nuka, Erika; Tomono, Susumu; Ishisaka, Akari; Kato, Yoji; Miyoshi, Noriyuki; Kawai, Yoshichika

    2016-10-01

    Lipid peroxidation products react with cellular molecules, such as DNA bases, to form covalent adducts, which are associated with aging and disease processes. Since lipid peroxidation is a complex process and occurs in multiple stages, there might be yet unknown reaction pathways. Here, we analyzed comprehensively 2'-deoxyguanosine (dG) adducts with oxidized arachidonic acid using liquid chromatography-tandem mass spectrometry and found the formation of 7-(2-oxo-hexyl)-etheno-dG as one of the major unidentified adducts. The formation of this adduct was reproduced in the reaction of dG with 2-octenal and predominantly with 4-oxo-2-octenal (OOE). We also found that other 2-alkenals (with five or more carbons) generate corresponding 4-oxo-2-alkenal-type adducts. Importantly, it was found that transition metals enhanced the oxidation of C4-position of 2-octenal, leading to the formation of OOE-dG adduct. These findings demonstrated a new pathway for the formation of 4-oxo-2-alkenals during lipid peroxidation and might provide a mechanism for metal-catalyzed genotoxicity. PMID:27281652

  12. IFN-γ ameliorates autoimmune encephalomyelitis by limiting myelin lipid peroxidation

    PubMed Central

    Sosa, Rebecca A.; Murphey, Cathi; Robinson, Rachel R.; Forsthuber, Thomas G.

    2015-01-01

    Evidence has suggested both a pathogenic and a protective role for the proinflammatory cytokine IFN-γ in experimental autoimmune encephalomyelitis (EAE). However, the mechanisms underlying the protective role of IFN-γ in EAE have not been fully resolved, particularly in the context of CNS antigen-presenting cells (APCs). In this study we examined the role of IFN-γ in myelin antigen uptake by CNS APCs during EAE. We found that myelin antigen colocalization with APCs was decreased substantially and that EAE was significantly more severe and showed a chronic-progressive course in IFN-γ knockout (IFN-γ−/−) or IFN-γ receptor knockout (IFN-γR−/−) mice as compared with WT animals. IFN-γ was a critical regulator of phagocytic/activating receptors on CNS APCs. Importantly, “free” myelin debris and lipid peroxidation activity at CNS lesions was increased in mice lacking IFN-γ signaling. Treatment with N-acetyl-l-cysteine, a potent antioxidant, abolished lipid peroxidation activity and ameliorated EAE in IFN-γ–signaling-deficient mice. Taken together the data suggest a protective role for IFN-γ in EAE by regulating the removal of myelin debris by CNS APCs and thereby limiting the substrate available for the generation of neurotoxic lipid peroxidation products. PMID:26305941

  13. Antioxidant properties of resveratrol and piceid on lipid peroxidation in micelles and monolamellar liposomes.

    PubMed

    Fabris, Sabrina; Momo, Federico; Ravagnan, Giampietro; Stevanato, Roberto

    2008-06-01

    The antioxidant activities of trans-resveratrol (trans-3,5,4'-trihydroxystilbene) and trans-piceid (trans-5,4'-dihydroxystilbene-3-O-beta-D-glucopyranoside), its more widespread glycosilate derivative, have been compared measuring their inhibitory action on peroxidation of linoleic acid (LA) and the radical scavenging ability towards different free radicals (such as DPPH) and radical initiators. It has been found that the two stilbenes have similar antioxidant capacity, while the comparison with BHT (2,6-di-tert-butyl-4-methylphenol) and alpha-tocopherol (vitamin E, vit. E), taken as reference, points out a slower but prolonged protective action against lipid peroxidation. Furthermore, piceid appears more efficacious than resveratrol as a consequence of the reaction of the latter with its radical form. The DSC profiles of phosphatidylcholine liposomes of various chain lengths, and EPR measurements of spin labelled liposomes demonstrated that the susceptible hydroxyl group of these compounds are located in the lipid region of the bilayer close to the double bonds of polyunsaturated fatty acids, making these stilbenes particularly suitable for the prevention and control of the lipid peroxidation of the membranes. PMID:18420333

  14. Effects of glycowithanolides on lipid peroxidation and lipofuscinogenesis in male reproductive organs of mice

    PubMed Central

    Walvekar, Madhuri; Shaikh, Nilofar; Sarvalkar, Priti

    2013-01-01

    Background: Glycowithanolides (Withaferin A), is one of the main withanolides active principle isolated from plant Withania somnifera and is claimed that it possess the aphrodisiac, sedative, rejuvenate and life prolonging properties. Objective: In the present investigation, antioxidant activity of active principles of Withania somnifera was tested against D-galactose induced oxidative stress in mouse testes, epididymis and seminal vesicle. Materials and Methods: For the present investigation Swiss male albino mice Mus musculus (Linn) were used. They were grouped in to control (I), D-galactose treated (II), protective (III) and curative groups (IV). Oxidative stress was induced in six month old mice by injecting a low dose of D-galactose. Antioxidant effect of plant extract was studied in testes, epididymis, and seminal vesicle of oxidative stressed mice on Lipid peroxidation (LPO) and fluorescence product. Results: In the present study, both total as well as mitochondrial lipid peroxidation and fluorescence product in testes, epididymis and seminal vesicle were increased in D-galactose induced mice. After the treatment of glycowithanolides there was significantly decrease in total as well as mitochondrial lipid peroxidation and fluorescence product in protective and curative groups. Conclusion: Our results indicate that Withania somnifera has a capability of preventing oxidative stress and also combating stress induced infertility. PMID:24639810

  15. Mercury induced time-dependent alterations in lipid profiles and lipid peroxidation in different body organs of cat-fish Heteropneustes fossilis

    SciTech Connect

    Bano, Y.; Hasan, M.

    1989-04-01

    The effects of mercuric chloride (HgCl/sub 2/) on lipid profiles and lipid peroxidation in different body organs of fresh water cat-fish Heteropneustes fossilis were studied. The daily exposure of HgCl/sub 2/ 0.2 mg/L for 10, 20 and 30 days depleted the total lipids in brain. But the content of phospholipids enhanced significantly at 30 days. Significant diminution in C/P ratio was discernible with 30 days of exposure following mercury toxicosis. Liver exhibited elevated levels of total lipids, phospholipids, cholesterol and C/P ratio. Interestingly kidney showed marked decrease in the concentration of total lipids, cholesterol and C/P ratio at higher exposure. However, the phospholipid values increased during the longer exposure. The content of total lipids and phospholipids was high in muscle but the level of cholesterol and C/P ratio were depleted. Significant increment in lipid peroxidation was discernible in brain, liver and muscle. In kidney the rate of lipid peroxidation was significantly reduced. The results suggest that exposure of HgCl/sub 2/ enhances the peroxidation of endogenous lipids in brain, liver and muscle. Interestingly the lipid contents are affected differently in different body organs.

  16. Hispolon Protects against Acute Liver Damage in the Rat by Inhibiting Lipid Peroxidation, Proinflammatory Cytokine, and Oxidative Stress and Downregulating the Expressions of iNOS, COX-2, and MMP-9

    PubMed Central

    Huang, Guan-Jhong; Deng, Jeng-Shyan; Chiu, Chuan-Sung; Liao, Jung-Chun; Hsieh, Wen-Tsong; Sheu, Ming-Jyh; Wu, Chieh-Hsi

    2012-01-01

    The hepatoprotective potential of hispolon against carbon tetrachloride (CCl4)-induced liver damage was evaluated in preventive models in rats. Male rats were intraperitoneally treated with hispolon or silymarin once daily for 7 consecutive days. One hour after the final hispolon or silymarin treatment, the rats were injected with CCl4. Administration with hispolon or silymarin significantly decreased the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in serum and increased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione (GSH) content and decreased the malondialdehyde (MDA) content in liver compared with CCl4-treated group. Liver histopathology also showed that hispolon reduced the incidence of liver lesions induced by CCl4. In addition, hispolon decreased nitric oxide (NO) production and tumor necrosis factor (TNF-α), inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) activation in CCl4-treated rats. We also examined the involvement of matrix metalloproteinase (MMP)-9 in the development of CCl4-induced liver damage in rats. Hispolon inhibited the expression of MMP-9 protein, indicating that MMP-9 played an important role in the development of CCl4-induced rat liver damage. Therefore, we speculate that hispolon protects rats from liver damage through their prophylactic redox balancing ability and anti-inflammation capacity. PMID:22013489

  17. Age-dependent changes in lipid peroxide levels in peripheral organs, but not in brain, in senescence-accelerated mice.

    PubMed

    Matsugo, S; Kitagawa, T; Minami, S; Esashi, Y; Oomura, Y; Tokumaru, S; Kojo, S; Matsushima, K; Sasaki, K

    2000-01-01

    The tissue concentration of lipid peroxides was determined in the brain, heart, liver, lung and kidney of accelerated senescence-prone (SAMP-8) and -resistant (SAMR-1) mice at 3, 6 and 9 months of age by a method involving chemical derivatization and high performance liquid chromatography. The level of lipid peroxides in the brain did not show an age-dependent change, but at each age the brain level of lipid peroxides was significantly higher in SAMP-8 than in SAMR-1. In contrast, the lipid peroxide levels in the peripheral organs showed increases with aging in both strains, and they were significantly higher in SAMP-8 than in SAMR-1 at both 3 and 6 months of age (except at 3 months of age in the kidney). These results suggest that increased oxidative stress in the brain and peripheral organs is a cause of the senescence-related degeneration and impairments seen in SAMP-8. PMID:10643812

  18. [Effect of biogenic stimulators--aloe extract and biotrite--on lipid peroxidation processes in saliva in inflammatory periodontal disease].

    PubMed

    volik, N A; Beloklitskaia, G F; Stefanov, A V; Makarenko

    1999-01-01

    The influence of biostimulators of vegetative origin, such as aloes and biotritis, on the process of lipid peroxidation in parodontium tissues, was studied. Biotritis has a more considerable parodontoprotective effect than aloes. PMID:10726317

  19. Shengmai San reduces hepatic lipids and lipid peroxidation in rats fed on a high-cholesterol diet.

    PubMed

    Yao, Hsien-Tsung; Chang, Yi-Wei; Chen, Chiung-Tong; Chiang, Meng-Tsan; Chang, Ling; Yeh, Teng-Kuang

    2008-02-28

    Shengmai San (SMS), which is comprised of the medicinal herbs of Panax ginseng C.A. Meyer, Schisandra chinensis Baill., and Ophiopogon japonicus Ker-Gawl (2:1:2)., is a traditional Chinese medicine being used for treating coronary heart disease. The aim of this study was to investigate the effects of SMS on the plasma and liver lipids, lipid peroxidation and antioxidant systems in liver and heart of cholesterol-fed rats. Rats were fed on a high-cholesterol (0.5%) diet (control group), high-cholesterol diet containing 2% SMS (2% SMS group) and 4% SMS (4% SMS group) for four weeks. The oxidative stress marker (thiobarbituric acid reactive substances, TBARS) and antioxidant defense systems including glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST) and superoxide dismutase (SOD) activities in rat liver and heart were evaluated. Results showed that rats fed with SMS-containing diet had reduced the H(2)O(2)-induced erythrocytes susceptibility to hemolysis, and 4% SMS feeding rats had higher plasma GSH concentration compared to the animals fed with the control diet. However, SMS had no effect on plasma lipids (total cholesterol, triglyceride and high-density lipoprotein cholesterol) and TBARS concentration. On the other hand, rats fed with the 4% SMS diet reduced the hepatic cholesterol and triglyceride contents. Fecal bile acid excretion was significantly increased in rats fed with the SMS-containing diet. Higher hepatic GSH and lower TBARS concentrations were observed in rats fed with the 4% SMS diet compared with the rats fed with the control diet. No significant difference in activities of GSH-Px, GST and SOD was found in liver and heart after the SMS treatment. Results from this study indicate that the SMS may reduce hepatic lipids and lipid peroxidation in rats. PMID:18162350

  20. Modulation of keratinocyte expression of antioxidants by 4-hydroxynonenal, a lipid peroxidation end product

    PubMed Central

    Zheng, Ruijin; Heck, Diane E.; Mishin, Vladimir; Black, Adrienne T.; Shakarjian, Michael P.; Kong, Ah-Ng Tony; Laskin, Debra L.; Laskin, Jeffrey D.

    2014-01-01

    4-Hydroxynonenal (4-HNE) is a lipid peroxidation end product generated in response to oxidative stress in the skin. Keratinocytes contain an array of antioxidant enzymes which protect against oxidative stress. In these studies, we characterized 4-HNE-induced changes in antioxidant expression in mouse keratinocytes. Treatment of primary mouse keratinocytes and PAM 212 keratinocytes with 4-HNE increased mRNA expression for heme oxygenase-1 (HO-1), catalase, NADPH:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) A1-2, GSTA3 and GSTA4. In both cell types, HO-1 was the most sensitive, increasing 86-98 fold within 6 h. Further characterization of the effects of 4-HNE on HO-1 demonstrated concentration- and time-dependent increases in mRNA and protein expression which were maximum after 6 h with 30 μM. 4-HNE stimulated keratinocyte Erk1/2, JNK and p38 MAP kinases, as well as PI3 kinase. Inhibition of these enzymes suppressed 4-HNE-induced HO-1 mRNA and protein expression. 4-HNE also activated Nrf2 by inducing its translocation to the nucleus. 4-HNE was markedly less effective in inducing HO-1 mRNA and protein in keratinocytes from Nrf2−/− mice, when compared to wild type mice, indicating that Nrf2 also regulates 4-HNE-induced signaling. Western blot analysis of caveolar membrane fractions isolated by sucrose density centrifugation demonstrated that 4-HNE-induced HO-1 is localized in keratinocyte caveolae. Treatment of the cells with methyl-β-cyclodextrin, which disrupts caveolar structure, suppressed 4-HNE-induced HO-1. These findings indicate that 4-HNE modulates expression of antioxidant enzymes in keratinocytes, and that this can occur by different mechanisms. Changes in expression of keratinocyte antioxidants may be important in protecting the skin from oxidative stress. PMID:24423726

  1. Effect of selenium deficiency and glutathione-modulating agents on diquat toxicity and lipid peroxidation in rats.

    PubMed

    Awad, J A; Burk, R F; Roberts, L J

    1994-09-01

    The dipyridyl herbicide diquat undergoes redox cycling in vivo resulting in superoxide generation. Diquat administration causes hepatic and renal toxicity in rodents. Selenium deficiency worsens this injury and lipid peroxidation is a prominent feature of the toxicity. However, there is limited data regarding the role of lipid peroxidation in diquat-induced toxicity in selenium-adequate animals. In addition, little is known about the effect of glutathione-modulating agents on diquat-induced toxicity and lipid peroxidation in vivo. F2-isoprostanes are novel prostanoids which, both free in plasma and esterified to phospholipids in tissues, are markers of lipid peroxidation in vivo. By using F2-isoprostane quantitation, we examined the effects of selenium deficiency and modulation of glutathione status with 1,3-bis (2-chloroethyl)-1-nitrosourea, phorone or buthionine sulfoximine on diquat-induced toxicity and lipid peroxidation. F2-isoprostanes increased 2- to 9-fold in plasma, liver, kidney and lung in selenium-adequate Fischer 344 rats with liver injury after receiving 100 mumol of diquat per kg. Selenium deficiency or modulation of glutathione status increased diquat toxicity. This was accompanied by 10- to 100-fold increases in plasma and kidney F2-isoprostane levels. Liver F2-isoprostanes were increased 2- to 5-fold. These studies suggest that glutathione, in addition to selenium, is an important defense against diquat-induced toxicity and lipid peroxidation. PMID:7932197

  2. Application of FTIR-ATR Spectroscopy to Determine the Extent of Lipid Peroxidation in Plasma during Haemodialysis

    PubMed Central

    Oleszko, Adam; Olsztyńska-Janus, Sylwia; Grzeszczuk-Kuć, Karolina; Bujok, Jolanta; Gałecka, Katarzyna; Czerski, Albert; Witkiewicz, Wojciech; Komorowska, Małgorzata

    2015-01-01

    During a haemodialysis (HD), because of the contact of blood with the surface of the dialyser, the immune system becomes activated and reactive oxygen species (ROS) are released into plasma. Particularly exposed to the ROS are lipids and proteins contained in plasma, which undergo peroxidation. The main breakdown product of oxidized lipids is the malondialdehyde (MDA). A common method for measuring the concentration of MDA is a thiobarbituric acid reactive substances (TBARS) method. Despite the formation of MDA in plasma during HD, its concentration decreases because it is removed from the blood in the dialyser. Therefore, this research proposes the Fourier Transform Infrared Attenuated Total Reflectance (FTIR-ATR) spectroscopy, which enables determination of primary peroxidation products. We examined the influence of the amount of hydrogen peroxide added to lipid suspension that was earlier extracted from plasma specimen on lipid peroxidation with use of TBARS and FTIR-ATR methods. Linear correlation between these methods was shown. The proposed method was effective during the evaluation of changes in the extent of lipid peroxidation in plasma during a haemodialysis in sheep. A measurement using the FTIR-ATR showed an increase in plasma lipid peroxidation after 15 and 240 minutes of treatment, while the TBARS concentration was respectively lower. PMID:25961007

  3. Relationship between hepatic lipid peroxidation and fibrogenesis in carbon tetrachloride-treated rats: effect of zinc administration.

    PubMed

    Camps, J; Bargallo, T; Gimenez, A; Alie, S; Caballeria, J; Pares, A; Joven, J; Masana, L; Rodes, J

    1992-12-01

    1. Lipid peroxidation and hepatic fibrogenesis were investigated in 25 carbon tetrachloride-treated rats and in 25 control animals. Rats were further divided into two groups to receive either a standard diet or one supplemented with zinc. From each group, animals were killed at weeks 3 and 18 of the experiment for histological and biochemical assessments which included hepatic lipid peroxide and collagen concentrations and plasma zinc concentration as well as the hepatic activities of proline hydroxylase and collagenase. 2. Results indicated that oral zinc supplementation was associated with a decrease in lipid peroxidation (mean 51%; P < 0.05), collagen deposition (mean 32%; P < 0.001) and proline hydroxylase activity (mean 30%; P < 0.05) at week 18, together with an increase in collagenase activity (mean 208%; P < 0.01) at week 3, in carbon tetrachloride-treated rats. 3. There was a significant direct correlation between lipid peroxidation and proline hydroxylase activity in carbon tetrachloride-treated rats (r = 0.52; P < 0.01) and also a significant inverse correlation between lipid peroxidation and plasma zinc concentration in these animals (r = -0.62; P < 0.001). 4. These findings are consistent with the hypothesis that hepatic lipid peroxidation plays an important role in the aetiology of hepatic fibrogenesis and that zinc mitigates the process. PMID:1336440

  4. UVA Photoirradiation of Nitro-Polycyclic Aromatic Hydrocarbons—Induction of Reactive Oxygen Species and Formation of Lipid Peroxides

    PubMed Central

    Xia, Qingsu; Yin, Jun J.; Zhao, Yuewei; Wu, Yuh-Sen; Wang, Yu-Qui; Ma, Liang; Chen, Shoujun; Sun, Xin; Fu, Peter P.; Yu, Hongtao

    2013-01-01

    Nitro-polycyclic aromatic hydrocarbons (nitro-PAHs) are a class of genotoxic environmental contaminants. We have long been interested in determining the mechanisms by which nitro-PAHs induce genotoxicity. Although the metabolic activation of nitro-PAHs leading to toxicological activities has been well studied, the photo-induced activation of nitro-PAHs has seldom been reported. In this paper, we report photo-induced lipid peroxidation by 19 nitro-PAHs. The results indicated that all but two of the nitro-PAHs can induce lipid peroxidation. Mechanistic studies suggest that lipid peroxidation by nitro-PAHs is mediated by free radicals generated in the reaction. There was no structural correlation between the nitro-PAHs and their ability to induce lipid peroxidation upon UVA irradiation, or between the HOMO-LUMO gap and the ability to cause lipid peroxidation. Most of the nitro-PAHs are less potent in terms of causing lipid peroxidation than their parent PAHs. The lack of correlation is attributed to the complex photophysics and photochemistry of the nitro-PAHs and the yield of reactive oxygen species (ROS) and other factors. PMID:23493032

  5. [Effect of Salvia miltiorrhiza on serum lipid peroxide, superoxide dismutase of the patients with coronary heart disease].

    PubMed

    Xing, Z Q; Zeng, X C; Yi, C T

    1996-05-01

    Twenty-four patients of coronary heart disease(CHD) were treated with Salvia miltiorrhiza (SM) and the change of SM on serum lipid peroxide (LPO), superoxide dismutase (SOD) after treatment were observed. The results were compared with that of control group consisted of 20 healthy persons, it showed that before treatment, the serum LPO of patient was significantly higher than that of control group and the SOD of patient was lower than that of healthy subjects (P < 0.01). After treated with SM, the LPO level decreased and SOD activity increased significantly. The mechanism might be correlated with the effect of SM in inhibiting platelets aggregation, reducing blood viscosity, improving myocardial ischemia and protecting cytomembrane. It suggested that SM could be regarded as a good exogenous scavenger of oxygen free radical. PMID:9387721

  6. Effect of inorganic phosphate concentration on the nature of inner mitochondrial membrane alterations mediated by Ca2+ ions. A proposed model for phosphate-stimulated lipid peroxidation.

    PubMed

    Kowaltowski, A J; Castilho, R F; Grijalba, M T; Bechara, E J; Vercesi, A E

    1996-02-01

    Addition of high concentrations (>1 mm) of inorganic phosphate (Pi) or arsenate to Ca2+-loaded mitochondria was followed by increased rates of H2O2 production, membrane lipid peroxidation, and swelling. Mitochondrial swelling was only partially prevented either by butylhydroxytoluene, an inhibitor of lipid peroxidation, or cyclosporin A, an inhibitor of the mitochondrial permeability transition pore. This swelling was totally prevented by the simultaneous presence of these compounds. At lower Pi concentrations (1 mm), mitochondrial swelling is reversible and prevented by cyclosporin A, but not by butylhydroxytoluene. In any case (low or high phosphate concentration) exogenous catalase prevented mitochondrial swelling, suggesting that reactive oxygen species (ROS) participate in these mechanisms. Altogether, the data suggest that, at low Pi concentrations, membrane permeabilization is reversible and mediated by opening of the mitochondrial permeability transition pore, whereas at high Pi concentrations, membrane permeabilization is irreversible because lipid peroxidation also takes place. Under these conditions, lipid peroxidation is strongly inhibited by sorbate, a putative quencher of triplet carbonyl species. This suggests that high Pi or arsenate concentrations stimulate propagation of the peroxidative reactions initiated by mitochondrial-generated ROS because these anions are able to catalyze Cn-aldehyde tautomerization producing enols, which can be oxidized by hemeproteins to yield the lower Cn - 1-aldehyde in the triplet state. This proposition was also supported by experiments using a model system consisting of phosphatidylcholine/dicethylphosphate liposomes and the triplet acetone-generating system isobutanal/horseradish peroxidase, where phosphate and Ca2+ cooperate to increase the yield of thiobarbituric acid-reactive substances. PMID:8621682

  7. Lipid peroxidation in various organs and tissues of albino rats with cadmium intoxication in winter and summer.

    PubMed

    Kotelnikova, S V; Sokolova, N G; Kotelnikov, A V

    2008-09-01

    The effect of cadmium chloride on lipid peroxidation in the liver, kidneys, brain, and gonads of outbred albino rats was studied in winter and summer. Cadmium chloride in a daily dose of 2 mg per 100 g body weight was administered intragastrically for 15 days. Administration of cadmium chloride was followed by an increase in peroxide radical production in the liver during the summer period. Lipid peroxidation remained unchanged in the liver, but increased in the ovaries of animals receiving the same dose of cadmium chloride during the winter period. PMID:19240842

  8. Effect of antioxidants on lipid peroxidation in iron-loaded rats.

    PubMed

    Dillard, C J; Downey, J E; Tappel, A L

    1984-02-01

    Indirect evidence has suggested that lipid peroxidation is associated with iron overload in vivo. As a measure of lipid peroxidation, pentane expired in the breath of rats loaded with an accumulated dose of either 100 mg or 186-200 mg of iron injected intraperitoneally as iron dextran was measured over a 7 to 8 week period, and the effect on pentane production of feeding antioxidant-supplemented diets was determined. By the seventh week of feeding the diets, rats fed 0.3% L-ascorbic acid produced 17% less (P = 0.03) pentane than did rats fed the basal antioxidant-deficient diet, whereas rats fed 0.004% dl-alpha-tocopherol acetate produced 92% less (P less than 0.001). After being fed the basal diet for 7 weeks, iron-loaded rats produced 76 +/- 9 pmol pentane/100 g body wt/min. When synthetic antioxidants were added to the diet at a concentration of 0.25%, the order of effectiveness in decreasing pentane production after 1 week was: N,N'-diphenyl-p-phenylenediamine greater than ethoxyquin greater than butylated hydroxyanisole greater than butylated hydroxytoluene greater than propyl gallate approximately equal to no antioxidant. After removal of either ethoxyquin or N,N'-diphenyl-p-phenylenediamine from the diets for 1 week, pentane production increased to a high level. The total amount of lipid soluble fluorophores in individual spleens of rats fed N,N'-diphenyl-p-phenylenediamine, ethoxyquin, dl-alpha- tocopherol acetate, ascorbic acid and no antioxidant were correlated significantly with the corresponding total integrated amount of pentane produced by the individual rats over the 7 to 8 week period. This study has provided some of the most direct evidence to date that lipid peroxidation is associated with iron overload in vivo. PMID:6708751

  9. [Effect of shengmaisan on serum lipid peroxidation in acute viral myocarditis].

    PubMed

    Zhao, M H; Rong, Y Z; Lu, B J

    1996-03-01

    The effect of Shengmaisan (SMS) on 62 acute viral myocarditis patients and its peroxidation damage was studied. The results revealed that the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in blood were decreased and the content of malondialdehyde (MDA) in plasma was increased in acute viral myocarditis patients in comparison with the healthy controls (P < 0.001). 62 acute viral myocarditis patients were divided into two groups: SMS group and placebo group. After treatment, both SOD and GSH-Px activities were increased and the level of MDA decreased (P < 0.001) in SMS group, while those in placebo group were not changed (P < 0.05). The results suggested that the myocardial damage of viral myocarditis is closely related with lipid peroxidation SMS acts as an effective free radical scavenger and anti-lipid peroxidation drug. SMS could prevent the damage of myocardia and might be taken as one of the effective therapeutic methods in treatment of acute viral myocarditis. PMID:9208534

  10. Effects of selenium on UVA-induced lipid peroxidation in cultured human skin fibroblasts.

    PubMed

    Moysan, A; Morlière, P; Marquis, I; Richard, A; Dubertret, L

    1995-01-01

    The effect of selenium on the lethal action of ultraviolet radiations and on the lipid peroxidation induced by exposures to ultraviolet A (320-400 nm; 360 kJ.m-2) and ultraviolet B (290-320 nm; 2 kJ.m-2) have been measured in cultured human skin fibroblasts. The experiments have been performed with either pure selenium or a spring water containing selenium and other trace elements (zinc and strontium). For cells cultured in a standard medium containing 10% fetal calf serum, no effect of selenium or spring water addition to the culture medium was observed on the lethality or on the peroxidative process induced by ultraviolet A and B radiations. Concurrently, there was no detectable increase of the seleno-dependent glutathione peroxidase activity. For cells previously depleted in selenium by a culture in a medium containing only 2% serum, a protective effect of selenium can be detected. Depending on the fibroblast donor, we observed (1) a protective effect on lethality of dividing fibroblasts induced by ultraviolet A radiations, (2) a protective effect on lipid peroxidation induced by ultraviolet A radiations on dividing or quiescent fibroblasts and (3) an increase in glutathione peroxidase activity in fibroblasts. PMID:7632435

  11. [Effect of combined exposure to ethanol and tobacco smoke on lipid peroxidation in rats].

    PubMed

    Florek, Ewa; Ignatowicz, Ewa; Nowakowska, Anna; Piekoszewski, Wojciech; Kulza, Maksymilian; Saija, Antonella; Chuchracki, Marek; Seńczuk-Przybyłowska, Monika; Kramer, Lucyna

    2009-01-01

    Usually, alcohol addicted persons smokes cigarettes. In the study, the effect of combined exposure to alcohol and tobacco smoke in alcohol addicted rats on liver peroxidation was evaluated. Alcohol abuse and its presence in blood did not influence the cotinine level, what indicates the lack of the importance of this factor in nicotine metabolism. Similarly, enzymatic markers of liver damage (AspAT, AIAT, ALP) did not change, what showed lack of hepatotoxic effect studied compounds in applied model of alcohol addiction and tobacco smoke exposure. Combined exposure to alcohol and tobacco smoke increases the level of lipid peroxidation in brain, liver and lungs however decreases in serum. In kidneys the results are not unambiguous. PMID:20301904

  12. Migratory refueling affects non-enzymatic antioxidant capacity, but does not increase lipid peroxidation.

    PubMed

    Eikenaar, Cas; Jönsson, Johanna; Fritzsch, Anna; Wang, Hong-Lei; Isaksson, Caroline

    2016-05-01

    All aerobic organisms are to some degree affected by oxidative stress, which is an imbalance between pro-oxidants and antioxidants in favor of the former. Pro-oxidants can damage DNA, proteins and lipids, and as such oxidative stress can carry considerably fitness costs. In mammals excessive calorie intake is a known cause of oxidative stress. We investigated whether in migrant birds, which typically engage in over-eating in between flights (refueling), high food intake causes oxidative stress. In an experiment we compared levels of plasmatic total non-enzymatic antioxidant capacity (AOX) and oxidative damage (lipid peroxidation) between migrants repeatedly fasted and refed (simulating the flight-refuel cycle of wild migrants), and migrants on ad libitum food. We found that refueling increased AOX, an effect mainly attributable to an increase in uric acid level, an antioxidant that is produced during protein metabolism. Accordingly, variation in AOX was mainly explained by the refueling birds' food intake. However, food intake in migrants on ad libitum food did not explain any variation in AOX. Refueling did not affect lipid peroxidation, nor were its levels explained by food intake. We propose that over-eating migrants retain uric acid, which might be a very low cost mechanism to forego oxidative damage. PMID:26921098

  13. Diazepam blocks striatal lipid peroxidation and improves stereotyped activity in a rat model of acute stress.

    PubMed

    Méndez-Cuesta, Luis A; Márquez-Valadez, Berenice; Pérez-De La Cruz, Verónica; Escobar-Briones, Carolina; Galván-Arzate, Sonia; Alvarez-Ruiz, Yarummy; Maldonado, Perla D; Santana, Ricardo A; Santamaría, Abel; Carrillo-Mora, Paul

    2011-11-01

    In this work, the effect of a single dose of diazepam was tested on different markers of oxidative damage in the striatum of rats in an acute model of immobilization (restraint) stress. In addition, the locomotor activity was measured at the end of the restraint period. Immobilization was induced to animals for 24 hr, and then, lipid peroxidation, superoxide dismutase activity and content, and mitochondrial function were all estimated in striatal tissue samples. Corticosterone levels were measured in serum. Diazepam was given to rats as a pre-treatment (1 mg/kg, i.p.) 20 min. before the initiation of stress. Our results indicate that acute stress produced enhanced striatal levels of lipid peroxidation (73% above the control), decreased superoxide dismutase activity (54% below the control), reduced levels of mitochondrial function (35% below the control) and increased corticosterone serum levels (86% above the control). Pre-treatment of stressed rats with diazepam decreased the striatal lipid peroxidation levels (68% below the stress group) and improved mitochondrial function (18% above the stress group), but only mild preservation of superoxide dismutase activity was detected (17% above the stress group). In regard to the motor assessment, only the stereotyped activity was increased in the stress group with respect to control (46% above the control), and this effect was prevented by diazepam administration (30% below the stress group). The preventive actions of diazepam in this acute model of stress suggest that drugs exhibiting anxiolytic and antioxidant properties might be useful for the design of therapies against early acute phases of physic stress. PMID:21645264

  14. Erythropoietic Protoporphyria: Lipid Peroxidation and Red Cell Membrane Damage Associated with Photohemolysis

    PubMed Central

    Goldstein, Bernard D.; Harber, Leonard C.

    1972-01-01

    The mechanism by which long wavelength ultraviolet light hemolyzes red cells obtained from patients with erythropoietic protoporphyria (EPP) was investigated. Previous studies had suggested that irradiation of these red cells with wavelengths of light capable of eliciting dermatological manifestations led to oxygen-dependent colloid osmotic hemolysis through the formation of peroxides. In the present report, lipid peroxidation during in vitro irradiation of EPP red cells with long ultraviolet light was demonstrated by: (a) the formation of 2-thiobarbituric acid reactants; (b) the presence of conjugated diene bonds in red cell lipid; and (c) the selective loss of unsaturated fatty acids proportional to the number of carbon-carbon double bonds in each. Irradiation of EPP red cells was also shown to result in the formation of hydrogen peroxide. Before photohemolysis there was a decline in cell membrane sulfhydryl groups and a loss in activity of the cell membrane enzyme acetylcholinesterase. These parameters provide further evidence suggesting that the cell membrane is a primary site of the photohemolytic effect of long ultraviolet light in EPP red cells. Further evaluation of the radiation-induced inactivation of EPP red cell acetylcholinesterase was performed by radiating mixtures containing bovine erythrocyte acetylcholinesterase and protoporphyrin IX. These studies revealed that the rate of decline in enzyme activity is accelerated by the addition of linoleic acid, an unsaturated fatty acid, but not by palmitic acid, a saturated fatty acid. Partial protection against both photohemolysis and acetylcholinesterase decline is provided by alpha-to-copherol. This lipid antioxidant loses its activity during the irradiation of EPP red cells suggesting that it is utilized in this process. PMID:5014616

  15. Daily supplementation with iron increases lipid peroxidation in young women with low iron stores.

    PubMed

    King, Sarah M; Donangelo, Carmen M; Knutson, Mitchell D; Walter, Patrick B; Ames, Bruce N; Viteri, Fernando E; King, Janet C

    2008-06-01

    The aim of this study was to determine whether women with low iron stores (plasma ferritin lipid peroxidation as measured by ethane exhalation rates and plasma malondialdehyde. The women served as their own control as pre- and post-supplementation periods were compared. Twelve women participated in the study for a 70-day period and consumed daily iron supplements (98 mg of iron as ferrous sulfate) from day 14 to day 70. Baseline blood and expired air samples were obtained on days 1 and 14; measurements during supplementation were performed on days 56 and 70, that is at 6 and 8 weeks of supplementation. Iron status improved during the iron supplementation period; biochemical indicators of lipid peroxidation also increased. After 6 wks of iron supplementation, serum ferritin almost doubled and body iron more than doubled. Hemoglobin levels increased slightly and other indicators of iron status became normal. However, plasma malondialdehyde (MDA) and breath ethane exhalation rates (BEER) increased by more than 40% between baseline and 6 wks of supplementation; these increases correlated significantly with plasma iron and ferritin levels. MDA was positively correlated with BEER. BEER increased further after 8 wks of iron supplementation. The increased indicators of lipid peroxidation with duration of supplementation and as iron status improved suggest that providing daily nearly 100 mg iron may not be a totally innocuous regimen for correcting iron depletion in women. PMID:18408148

  16. Antioxidant systems and lipid peroxidation in Bathymodiolus azoricus from Mid-Atlantic Ridge hydrothermal vent fields.

    PubMed

    Bebianno, M J; Company, R; Serafim, A; Camus, L; Cosson, R P; Fiala-Médoni, A

    2005-11-30

    Enzymatic defenses involved in protection from oxygen radical damage were determined in gills and mantle of Bathymodiolus azoricus collected from three contrasting Mid-Atlantic Ridge (MAR) hydrothermal vent fields (Menez-Gwen, Lucky Strike and Rainbow). The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GPx) (total and Se-dependent), and levels of total oxyradical scavenging capacity (TOSC), metallothioneins (MT) and lipid peroxidation (LPO) were determined in B. azoricus tissues and the impact of metal concentrations on these antioxidant systems and lipid peroxidation assessed. SOD, CAT, TOSC, MTs and LPO levels were higher in B. azoricus gills while glutathione peroxidases (total and Se-dependent) were higher in the mantle, and with the exception of CAT, were of the same order of magnitude as in other molluscs. TOSC levels from Menez-Gwen indicate that the vent environment at this site is less stressful and the formation of ROS in mussels is effectively counteracted by the antioxidant defense system. TOSC depletion indicates an elevated ROS production in molluscs at the other two vent sites. Cytosolic SOD, GPx and LPO were more relevant at Lucky Strike (Bairro Alto) where levels of essential (Cu and Zn) and toxic metals (Cd and Ag) were highest in the organisms. CAT activity and LPO were predominant at the Rainbow vent site, where an excess of Fe in mussel tissues and in vent fluids (the highest of all three vent sites) may have contributed to increased LPO. Therefore, three distinct pathways for antioxidant enzyme systems and LPO based on environmental metal speciation of MAR vent fields are proposed for Bathymodiolus gills. At Menez-Gwen, TOSC towards peroxyl and hydroxyl radicals and peroxynitrite are predominant, while at Lucky Strike cytosolic SOD activity and GPx are the main antioxidant mechanisms. Finally at Rainbow, catalase and lipid peroxidation are dominant, suggesting that resistance of mussels to metal toxicity at

  17. N,N-diethyldithiocarbamate produces copper accumulation, lipid peroxidation, and myelin injury in rat peripheral nerve.

    PubMed

    Tonkin, Elizabeth G; Valentine, Holly L; Milatovic, Dejan M; Valentine, William M

    2004-09-01

    Previous studies have demonstrated the ability of the dithiocarbamate, disulfiram, to produce a peripheral neuropathy in humans and experimental animals and have also provided evidence that N,N-diethyldithiocarbamate (DEDC) is a proximate toxic species of disulfiram. The ability of DEDC to elevate copper levels in the brain suggests that it may also elevate levels of copper in peripheral nerve, possibly leading to oxidative stress and lipid peroxidation from redox cycling of copper. The study presented here investigates the potential of DEDC to promote copper accumulation and lipid peroxidation in peripheral nerve. Rats were administered either DEDC or deionized water by ip osmotic pumps and fed a normal diet or diet containing elevated copper, and the levels of metals, isoprostanes, and the severity of lesions in peripheral nerve and brain were assessed by ICP-AES/AAS, GC/MS, and light microscopy, respectively. Copper was the only metal that demonstrated any significant compound-related elevations relative to controls, and total copper was increased in both brain and peripheral nerve in animals administered DEDC on both diets. In contrast, lesions and elevated F2-isoprostanes were significantly increased only in peripheral nerve for the rats administered DEDC on both diets. Autometallography staining of peripheral nerve was consistent with increased metal content along the myelin sheath, but in brain, focal densities were observed, and a periportal distribution occurred in liver. These data are consistent with the peripheral nervous system being more sensitive to DEDC-mediated demyelination and demonstrate the ability of DEDC to elevate copper levels in peripheral nerve. Additionally lipid peroxidation appears to either be a contributing event in the development of demyelination, possibly through an increase of redox active copper, or a consequence of the myelin injury. PMID:15187237

  18. Melatonin Attenuates Intermittent Hypoxia-Induced Lipid Peroxidation and Local Inflammation in Rat Adrenal Medulla

    PubMed Central

    Liu, Yu; Tipoe, George Lim; Fung, Man Lung

    2014-01-01

    Chronic intermittent hypoxia (CIH) induces lipid peroxidation and leads to cardiovascular dysfunction, in which impaired activities of the adrenal medulla are involved. This may be caused by CIH-induced injury in the adrenal medulla, for which the mechanism is currently undefined. We tested the hypothesis that melatonin ameliorates the CIH-induced lipid peroxidation, local inflammation and cellular injury in rat adrenal medulla. Adult Sprague–Dawley rats were exposed to air (normoxic control) or hypoxia mimicking a severe recurrent sleep apnoeic condition for 14 days. The injection of melatonin (10 mg/kg) or vehicle was given before the daily hypoxic treatment. We found that levels of malondialdehyde and nitrotyrosine were significantly increased in the vehicle-treated hypoxic group, when compared with the normoxic control or hypoxic group treated with melatonin. Also, the protein levels of antioxidant enzymes (superoxide dismutase (SOD)-1 and SOD-2) were significantly lowered in the hypoxic group treated with vehicle but not in the melatonin group. In addition, the level of macrophage infiltration and the expression of inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6) and mediators (inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2)) were elevated in the vehicle-treated hypoxic group, but were significantly ameliorated by the melatonin treatment. Moreover, the amount of apoptotic cells in the hypoxic groups was significantly less in the melatonin-treated group. In conclusion, CIH-induced lipid peroxidation causes local inflammation and cellular injury in the adrenal medulla. The antioxidant and anti-inflammatory actions of melatonin are indicative of a protective agent against adrenal damage in patients with severe obstructive sleep apnea syndrome. PMID:25314303

  19. Impact of dietary oils and fats on lipid peroxidation in liver and blood of albino rats

    PubMed Central

    Haggag, Mohammad El-Sayed Yassin El-Sayed; Elsanhoty, Rafaat Mohamed; Ramadan, Mohamed Fawzy

    2014-01-01

    Objective To investigate the effects of different dietary fat and oils (differing in their degree of saturation and unsaturation) on lipid peroxidation in liver and blood of rats. Methods The study was conducted on 50 albino rats that were randomly divided into 5 groups of 10 animals. The groups were fed on dietary butter (Group I), margarine (Group II), olive oil (Group III), sunflower oil (Group IV) and corn oil (Group V) for 7 weeks. After 12 h of diet removal, livers were excised and blood was collected to measure malondialdehyde (MDA) levels in the supernatant of liver homogenate and in blood. Blood superoxide dismutase activity (SOD), glutathione peroxidase activity (GPx), serum vitamin E and total antioxidant capacity (TAC) levels were also measured to determine the effects of fats and oils on lipid peroxidation. Results The results indicated that no significant differences were observed in SOD activity, vitamin E and TAC levels between the five groups. However, there was significant decrease of GPx activity in groups IV and V when compared with other groups. The results indicated that feeding corn oil caused significant increases in liver and blood MDA levels as compared with other oils and fats. There were positive correlations between SOD and GPx, vitamin E and TAC as well as between GPx and TAC (r: 0.743; P<0.001) and between blood MDA and liver MDA (r: 0.897; P<0.001). The results showed also negative correlations between blood MDA on one hand and SOD, GPx, vitamin E and TAC on the other hand. Conclusions The results demonstrated that feeding oils rich in polyunsaturated fatty acids (PUFA) increases lipid peroxidation significantly and may raise the susceptibility of tissues to free radical oxidative damage. PMID:24144131

  20. [Effect of five kinds of vegetable seed oil on serum lipid and lipid peroxidation in rats].

    PubMed

    Guo, Y; Cai, X; Zhao, X; Shi, R

    2001-01-01

    The effects of vegetable seed oil on hyperlipidemia induced by high lipid diet in rats. Male adult Wistar rats were fed on the test diet containing 94% high lipid diet and 6% lard pinon seed oil, perilla seed oil, blackcurrent seed oil, borage seed oil and evening primrose seed oil respectively for 3 weeks. The results showed that the vale of trilyceride(TG), total cholesterol(TC), low density lipoprotein cholesterol (LDL-C), LDL-C/HDL-C(high density lipoprotein cholesterol) ratio increased and the vale of HDL-C/TC ratio and lecithin-cholesterol acyltransferase(LCAT) activity decreased in the groups with vegetable seed oil were less than that of the control group. The results suggested that all the five kinds of vegetable seed oil had the effect of regulating lipid metabolism of hyperlipidemia rats to some extent. Pinon seed oil and borage seed oil may be well suited for the prevention of atherosclerosis. PMID:11255765

  1. Serum Copper, Zinc and Lipid Peroxidation in Pregnant Women with Preeclampsia in Gorgan

    PubMed Central

    Rafeeinia, Arash; Tabandeh, Afsaneh; Khajeniazi, Safoura; Marjani, Abdol J

    2014-01-01

    The aim of study was to assay serum copper, zinc and lipid peroxidation levels in pregnant women with and without preeclampsia. There were significant differences between systolic, diastolic blood pressures and copper, Cu/Zn ratio and malondialdehyde among two groups. There were significant differences in weight, pre-pregnancy body mass index, systolic, diastolic blood pressures and copper, Cu/Zn ratio and malondialdehyde levels when compared to healthy pregnant women with mild and severe preeclampsia patients. A positive correlation was observed between systolic and diastolic blood pressure and copper, malondialdehyde and Cu/Zn ratio. Copper and malondialdehyde may play a role in the pathophysiology of preeclampsia. PMID:25400710

  2. Routes to 4-Hydroxynonenal: Fundamental Issues in the Mechanisms of Lipid Peroxidation*S⃞

    PubMed Central

    Schneider, Claus; Porter, Ned A.; Brash, Alan R.

    2008-01-01

    Although investigation of the toxicological and physiological actions of α/β-unsaturated 4-hydroxyalkenals has made great progress over the last 2 decades, understanding of the chemical mechanism of formation of 4-hydroxynonenal and related aldehydes has advanced much less. The aim of this review is to discuss mechanistic evidence for these non-enzymatic routes, especially of the underappreciated intermolecular pathways that involve dimerized and oligomerized fatty acid derivatives as key intermediates. These cross-molecular reactions of fatty acid peroxyls have also important implications for understanding of the basic initiation and propagation steps during lipid peroxidation and the nature of the products that arise. PMID:18285327

  3. Radiosensitization by fullerene-C60 dissolved in squalene on human malignant melanoma through lipid peroxidation and enhanced mitochondrial membrane potential

    NASA Astrophysics Data System (ADS)

    Kato, Shinya; Kimura, Masatsugu; Miwa, Nobuhiko

    2014-04-01

    We examined fullerene-C60 dissolved in squalene (C60/Sqe) for the ability to potentiate the radiosensitization under X-ray irradiation on human malignant melanoma HMV-II cells, which were treated with C60/Sqe and thereafter irradiated with X-ray. The cell proliferation for C60/Sqe was inhibited more markedly than for Sqe alone. Meanwhile, cell proliferation was almost unaltered for C60/squalane (Sqa) or Sqa, a hydrogenated form of Sqe, as compared to no-additive control. Thus radiosensitization of C60/Sqe is attributed to peroxidation of unsaturated bonds of squalene by X-ray-excited C60 in contrast to squalane. The fluorescence images of HMV-II cells stained with Rhodamine123, an indicator for mitochondrial membrane potential, were monitored for 6 h after X-ray irradiation. C60/Sqe obviously exhibited more augmented fluorescence intensity on perinuclear region of HMV-II cells than Sqe alone. TBARS assay showed that the lipid peroxidation level as malondialdehyde-equivalent increased by combination of C60/Sqe and X-ray dose-dependently on X-ray doses. C60/Sqe exhibited lipid peroxidation more markedly by 1.2-fold than Sqe alone. Thus the level of lipid peroxidation of squalene was sufficiently higher in C60/Sqe than in Sqe in the absence of C60 under X-ray irradiation, suggesting the combination of C60/Sqe and X-ray irradiation induced radiosensitization on HMV-II cells by peroxidation of absorbed Sqe in mitochondrial membrane via oxidative stress mediated by fullerene-C60.

  4. Photo-irradiation of Aloe vera by UVA--formation of free radicals, singlet oxygen, superoxide, and induction of lipid peroxidation.

    PubMed

    Xia, Qingsu; Yin, Jun Jie; Fu, Peter P; Boudreau, Mary D

    2007-01-30

    Aloe vera whole leaf extracts are incorporated into a wide variety of topically applied commercial products. Aloe vera whole leaf extracts may contain anthraquinones, which have been shown to generate reactive oxygen species in the presence of ultraviolet A (UVA) light. Exposure to UVA light alone can also generate reactive oxygen species and is associated with photo-damaged and photo-aged skin in humans. This paper examines the photochemical properties of two Aloe vera whole leaf extracts that differed in their anthraquinone content. In the presence of methyl linoleate, the UVA irradiation of Aloe vera leaf extracts induced lipid peroxidation. The amounts of lipid peroxides formed were higher in the Aloe vera leaf extract that contained lower amounts of anthraquinones. Superoxide dismutase and sodium azide inhibited and deuterium oxide enhanced the formation of lipid peroxides, suggesting that singlet oxygen and superoxide were involved in the mechanism. Spin trapping electron spin resonance (ESR) spectroscopy was used to investigate the generation of free radicals by the UVA photo-irradiated Aloe vera plant extracts. ESR measurements indicated that the UVA photo-irradiation of Aloe vera plant extracts produced carbon-centered free radicals. These results suggest that humans exposed to products that contain Aloe vera whole leaf extracts may have enhanced sensitivity to ultraviolet light. PMID:17197137

  5. Potato peel extract-a natural antioxidant for retarding lipid peroxidation in radiation processed lamb meat.

    PubMed

    Kanatt, Sweetie R; Chander, Ramesh; Radhakrishna, P; Sharma, Arun

    2005-03-01

    The effective utilization of potato peel, a waste generated in large quantities by the food industry, as an antioxidant was investigated. Potato peel extract (PPE) exhibited high phenolic content (70.82 mg of catechin equivalent/100 g), chlorogenic acid (27.56 mg/100 g of sample) being the major component. The yield of total phenolics and chlorogenic acid increased by 26 and 60%, respectively, when the extract was prepared from gamma irradiated (150 Gy) potatoes. PPE showed excellent antioxidant activity as determined by beta-carotene bleaching and radical scavenging activity of 1,1-diphenyl-2-picrylhydrazyl (DPPH). The suitability of PPE for controlling lipid oxidation of radiation processed lamb meat was also investigated. PPE (0.04%) when added to meat before radiation processing was found to retard lipid peroxidation of irradiated meat as measured by TBA number and carbonyl content. The antioxidant activity of PPE was found to be comparable to butylated hydroxytoluene (BHT). PMID:15740031

  6. Histone retention, protein carbonylation, and lipid peroxidation in spermatozoa: Possible role in recurrent pregnancy loss.

    PubMed

    Mohanty, Gayatri; Swain, Nirlipta; Goswami, Chandan; Kar, Sujata; Samanta, Luna

    2016-06-01

    Contribution from a defective paternal genome has been attributed to be an important cause for spontaneous recurrent pregnancy loss (RPL). Increased oxidative stress results in decreased detoxification and is a cause for damage to chromatin, proteins, and membrane lipids. The present study aimed to explore if there is a significant relationship between retained histones due to defective packaging of DNA in spermatozoa and oxidative stress. RPL patients (n=16) with a history of ≥2 embryo losses before the 20th week of gestation and no female factor abnormality, and fertile healthy volunteers (n=20) as controls were included in the study. A significant difference in the levels of protein carbonylation and lipid peroxidation together with an increased retention of histones in the experimental groups was noticed. Histone carrying sites for oxidative modification such as arginine and lysine might be responsible for disturbing the paternal epigenomic control during early stages of embryonic differentiation leading to abortion. PMID:26980262

  7. Soybean phosphatidylcholine liposomes as model membranes to study lipid peroxidation photoinduced by pterin.

    PubMed

    Thomas, Andrés H; Catalá, Ángel; Vignoni, Mariana

    2016-01-01

    Oxidized pterins, efficient photosensitizers under UVA irradiation, accumulate in the skin of patients suffering from vitiligo, a chronic depigmentation disorder. Soybean phosphatidylcholine (SoyPC) liposomes were employed as model membranes to investigate if pterin (Ptr), the parent compound of oxidized pterins, is able to photoinduced lipid peroxidation. Size exclusion chromatography and dialysis experiments showed that Ptr is not encapsulated inside the liposomes and the lipid membrane is permeable to this compound. The formation of conjugated dienes and trienes, upon UVA irradiation, was followed by absorption at 234 and 270 nm, respectively. The photoproducts were characterized by mass spectrometry and oxygenation of SoyPC was demonstrated. In addition, analysis of MS/MS spectra suggested the formation hydroperoxides. Finally, the biological implications of the findings are discussed. PMID:26551322

  8. Rapid determination of lipid peroxidation using a novel pyridoxamine-participating ferrous oxidation-sulfosalicylic acid spectrophotometric method.

    PubMed

    Chen, Jingnan; Cai, Danqian; Zhang, Yu

    2016-11-15

    A novel method is developed to rapidly analyze lipid peroxidation in edible oils and fatty foods at room temperature, which is called the pyridoxamine-participating ferrous oxidation-sulfosalicylic acid (PFOS) method. The PFOS method evaluates the lipid peroxide value colorimetrically via detecting the pyridoxamine-mediated pigment produced by 5-sulfosalicylic acid and Fe(3+) at 500nm, while the latter is converted from Fe(2+) in the presence of lipid peroxides. The optimized formulation was ethanol (70%, v/v), Fe(2+) (4mmol/L), 5-sulfosalicylic acid (40mmol/L) and pyridoxamine (18mmol/L). The limit of quantitation is 0.087mmol Fe(3+)/L with acceptable reproducibility. In addition, current method has a significant linear correlation with both conventional thiobarbituric acid (R(2)=0.9999) and ferric thiocyanate assays (R(2)=0.9675). This method offers a rapid technique for evaluating lipid peroxidation without heating and sophisticated instrumental procedures. Besides, current method provides a new option to evaluate the lipid peroxidation state and improve the reproducibility of ferrous-oxidation. PMID:27283678

  9. [Status of the lipid peroxidation system in the tissues of rats following a 7-day flight on the Kosmos-1667 biosatellite].

    PubMed

    Delenian, N V; Markin, A A

    1989-01-01

    Rats flown for 7 days on Cosmos-1667 were for the first time used to measure antioxidative enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase, catalase), lipid peroxidation products (diene conjugates, malonic dialdehyde, Schiff bases) and tocopherol. Enhanced lipid peroxidation in the heart was completely compensated by activation of antioxidative enzymes. The content of all lipid peroxidation products measured in the liver increased; this was accompanied by a decrease of glutathione peroxidase and an increase of superoxide dismutase activities. It is suggested that lipid peroxidation was activated in response to altered gravity. PMID:2586059

  10. [Effect of mercury chloride on the level of lipids and products of their peroxidation in rat vital organs].

    PubMed

    Kaliman, P A; Oksenenko, S V

    2002-01-01

    The influence of mercury chloride on peroxidation processes of lipids and level of common lipids, phospholipids and spectrum of neutral lipids in liver, heart, lung and kidney of rats has been investigated. Administration of mercury chloride in a dose 0.7 mg/100 g of body weight to animals has invoked accumulation of lipids peroxide products in fractions of neutral lipids and phospholipids so it testifies the development of oxidative stress. Decrease of the most sensitive to oxidation fractions in the early stages of oxidative stress development and increase of free cholesterol and its ethers content in kidney and free cholesterol in the heart in more later terms as a result of mercury chloride administration have been revealed. PMID:14964870