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PubMed1988

The metabolism of acetaldehyde and not acetaldehyde itself is responsible for in vivo ethanol-induced lipid peroxidation in rats.

A single oral administration of ethanol (5 g/kg) to rats induced a marked increase in lipid peroxidation, in the liver and kidney within 9 hr, as assessed by malondialdehyde accumulation. The pretreatment with alcohol dehydrogenase (ADH) inhibitor, 4-methylpyrazole (1 mmol/kg) caused approximately 50% inhibition of the hepatic ADH activity and abolished this ethanol-induced lipid peroxidation. The disulfiram treatment (100 mg/kg) significantly inhibited 63% of the hepatic low Km aldehyde dehydrogenase (ALDH) but not the high Km ALDH. The cyanamide treatment (15 mg/kg) effectively decreased 83% of the low Km and 70% of the high Km ALDH in the liver. Although there was more than a 20-fold elevation of acetaldehyde levels by the inhibition of acetaldehyde metabolism with disulfiram or cyanamide, the ethanol-induced lipid peroxidation was significantly suppressed by pretreatment with these drugs. More than 90% inhibition of xanthine oxidase and dehydrogenase by the pretreatment with allopurinol (100 mg/kg), with no effect on the hepatic ADH and ALDH activities, did not alter the enhancement of lipid peroxidation following ethanol administration. We propose that the metabolism of acetaldehyde (probably via the low Km ALDH) and not acetaldehyde itself is responsible for the ethanol-induced lipid peroxidation in vivo and that the contribution of xanthine oxidase, as an initiator of lipid peroxidation through acetaldehyde oxidation is minute during acute intoxication.

Acetaldehyde↗
PubMed1988

Lipid peroxidation as a possible cause of ochratoxin A toxicity.

Addition of the mycotoxin ochratoxin A (OA), a nephrotoxic carcinogen, to rat liver microsomes greatly enhanced the rate of NADPH or ascorbate-dependent lipid peroxidation as measured by malondialdehyde formation. NADPH-dependent lipid peroxidation in kidney microsomes was similarly enhanced by OA. The process required the presence of trace amounts of iron but cytochrome P-450 and free active oxygen species appeared not to be involved. The efficiency of several ochratoxins (ochratoxins A, B, C, alpha and O-methyl-ochratoxin C) to enhance lipid peroxidation was related to the presence and reactivity of the phenolic hydroxyl group. Furthermore, the ability of these ochratoxins to enhance lipid peroxidation in microsomes correlated precisely with their known toxicities in chicks. Administration of ochratoxin A to rats also resulted in enhanced lipid peroxidation in vivo as evidenced by a seven-fold increase in the rate of ethane exhalation. These results suggest that lipid peroxidation may play a role in the observed toxicity of ochratoxin A in animals; a mechanism is proposed. (Formula: see text). Ochratoxin A: X = Cl; R1 = R2 = R3 = R4 = H Ochratoxin B: X = H; R1 = R2 = R3 = R4 = H Ochratoxin C: X = Cl; R1 = R2 = R3 = H; = R4 = CH3 O-Methyl-ochratoxin C: X = Cl; R2 = R3 = H; R1 = R4 = CH3 (4R)-4-hydroxyochratoxin A: X = Cl; R1 = R3 = R4 = H; R2 = OH (4S)-4-hydroxyochratoxin A: X = Cl; R1 = R2 = R4 = H; R3 = OH Fig. 1. Chemical structures of the various ochratoxins.

Animals↗
PubMed1989

Rat liver microsomal NADPH-supported oxidase activity and lipid peroxidation dependent on ethanol-inducible cytochrome P-450 (P-450IIE1).

The liver microsomal ethanol-inducible cytochrome P-450 (P-450IIE1) form is known to exhibit a high rate of oxidase activity in the absence of substrate and it was therefore of interest to evaluate whether this form of P-450 could contribute to microsomal and liposomal NADPH-dependent oxidase activity and lipid peroxidation. The rate of microsomal NADPH-consumption, O2--formation, H2O2-production and generation of thiobarbituric acid (TBA) reactive substances correlated to the amount of P-450IIE1 in 28 microsomal samples from variously treated rats. Anti-P-450IIE1 IgG inhibited, compared to control IgG, microsomal H2O2-formation by 45% in microsomes from acetone-treated rats and by 22% in control microsomes. NADPH-dependent generation of TBA-reactive products was completely inhibited by these antibodies, whereas preimmune IgG was essentially without effect. Liposomes containing reductase and P-450IIE1 were peroxidized in a superoxide dismutase (SOD) sensitive reaction at a 5-10-fold higher rate than membranes containing 3 other forms of cytochrome P-450. Lipid peroxidation in reconstituted vesicles dependent on the presence of P-450IIB1 was by contrast not inhibited by SOD. Microsomal peroxidase activities, using 15-(S)-hydroperoxy-5-cis-8,11,13-trans-eicosatetraenoic acid as a substrate were high in microsomes from phenobarbital- or ethanol-treated rats but low in membranes from isoniazid-treated rats, having the highest relative level of P-450IIE1. It is suggested that the oxidase activity of P-450IIE1 contributes to microsomal NADPH-dependent lipid peroxidation. The combined action of the oxidase activity by P-450IIE1 and the peroxidase activities by P-450IIB1 and other forms of P-450 may be important for the high rate of lipid peroxidation observed in e.g. microsomes from ethanol- or acetone-treated rats. The possible importance of cytochrome P-450IIE1-dependent lipid peroxidation in vivo after ethanol abuse is discussed.

Animals↗
PubMed1989

Allyl alcohol-induced hemolysis and its relation to iron release and lipid peroxidation.

Allyl alcohol administration to starved mice produced, along with liver necrosis, a high incidence (about 50%) of hemolysis. A marked decrease in erythrocyte glutathione (GSH) was seen in all the intoxicated animals. Such a decrease was significantly higher in the animals showing hemolysis. In these animals a substantial amount of malonic dialdehyde (MDA) was detected in plasma and a marked decrease in arachidonic and docosahexaenoic acids was found in erythrocyte phospholipids. These data suggest that the allyl alcohol-induced hemolysis is mediated by lipid peroxidation. In vitro studies have shown that the addition of acrolein to mouse erythrocytes produces a dramatic GSH depletion, which is followed by the appearance of lipid peroxidation and, after an additional 30 min of incubation, by the development of hemolysis. Prevention of lipid peroxidation by an antioxidant (Trolox C) or an iron chelator (desferrioxamine, DFO), prevented hemolysis even if the erythrocyte GSH level was dramatically decreased. In vitro, allyl alcohol and acrylic acid were ineffective in inducing GSH depletion, lipid peroxidation and hemolysis. Studies of possible induction of lipid peroxidation in erythrocytes showed that a progressive increase in "free" (desferal chelatable) iron occurs in the erythrocytes during the incubation with acrolein. It seems, therefore, that a release of iron from iron-containing complexes occurs in acrolein-treated erythrocytes and that such "free" iron promotes lipid peroxidation.

1-Propanol↗
PubMed1990

Lipid peroxidation and antioxidant systems in the liver injury produced by glutathione depleting agents.

The mechanisms of the liver damage produced by three glutathione (GSH) depleting agents, bromobenzene, allyl alcohol and diethylmaleate, was investigated. The change in the antioxidant systems represented by alpha-tocopherol (vitamin E) and ascorbic acid were studied under conditions of severe GSH depletion. With each toxin liver necrosis was accompanied by lipid peroxidation that developed only after severe depletion of GSH. The hepatic level of vitamin E was decreased whenever extensive lipid peroxidation developed. In the case of bromobenzene intoxication, vitamin E decreased before the onset of lipid peroxidation. Changes in levels of the ascorbic and dehydroascorbic acid indicated a redox cycling of vitamin C with the oxidative stress induced by all the three agents. Such a change of the redox state of vitamin C (increase of the oxidized over the reduced form) may be an index of oxidative stress preceding lipid peroxidation in the case of bromobenzene. In the other cases, such a change is likely to be a consequence of lipid peroxidation. Experiments carried out with vitamin E deficient or supplemented diets indicated that the pathological phenomena occurring as a consequence of GSH depletion depend on hepatic levels of vitamin E. In vitamin E deficient animals, lipid peroxidation and liver necrosis appeared earlier than in animals fed the control diet. Animals fed a vitamin E supplemented diet had an hepatic vitamin E level double that obtained with a commercial pellet diet. In such animals, bromobenzene and allyl alcohol had only limited toxicity and diethylmaleate none in spite of comparable hepatic GSH depletion. Thus, vitamin E may largely modulate the expression of the toxicity by GSH depleting agents.

1-Propanol↗
PubMed1991

Influences of Ginkgo biloba on cyclosporin A induced lipid peroxidation in human liver microsomes in comparison to vitamin E, glutathione and N-acetylcysteine.

The in vitro effect of cyclosporin A (CsA) on lipid peroxidation in human liver microsomes was investigated, and efforts were made to prevent the resulting toxic effect of CsA. Microsomes were prepared from human liver resection material and incubated with CsA (0, 10, 30, 100, 300, 1000 micrograms/mL) for one hour (pH 7.4, 37 degrees, 95% O2, 5% CO2). Subsequently the resulting concentrations of malondialdehyde equivalents (MDA) were determined, a breakdown product of lipid peroxidation. Furthermore the duration of incubation was varied (0, 15, 30, 60, 90 min) using a CsA concentration of 300 micrograms/mL. CsA was shown to stimulate MDA-formation to up to 10-fold of the control value in both a time and concentration dependent manner. The dosage dependent experiment stated above was repeated, adding alpha-tocopherol (vitamin E, 1 mM), reduced glutathione (GSH, 1 mM), N-acetylcysteine (0.1, 0.3, 1, 3 mM), and Ginkgo biloba extract (Gbe, 15, 50, 150 micrograms/mL), respectively, to the medium of incubation. Vitamin E, a potent radical scavenger, proved to inhibit lipid peroxidation almost totally. Both GSH and N-acetylcysteine were also able to prevent lipid peroxidation, suggesting that the antioxidant effect of GSH might be caused by its thiol group and does not depend on the integrity of the whole molecule. Gbe inhibited CsA induced lipid peroxidation in a concentration dependent manner. This effect of Gbe was diminished yet not totally abolished when FeCl3 was added to the medium of incubation, whereas N-acetylcysteine even slightly enhanced CsA stimulated lipid peroxidation in the presence of iron. These results suggest that Gbe might be able to prevent radical mediated damage to human membranes caused by CsA.

Acetylcysteine↗
PubMed1992

Protective action of seven natural phenolic compounds against peroxidative damage to biomembranes.

The effects of seven phenolic compounds isolated from Salvia miltiorrhiza on peroxidative damage to liver microsomes, hepatocytes and erythrocytes of rats were studied. The results show that the seven compounds inhibited lipid peroxidation of rat liver microsomes induced by iron/cysteine and Vitamin C/NADPH. The hemolysis of rat erythrocytes induced by hydrogen peroxide was also inhibited. The degree of inhibition varied with different compounds. Among the seven compounds, the action of salvianolic acid A (Sai A) was the most potent. Therefore, the protective action of Sai A against peroxidative damage to isolated rat hepatocytes and their plasma membranes was evaluated further. Malondialdehyde (MDA) production and bleb of the surfaces of rat hepatocytes induced by iron/cysteine were prevented by Sai A. The production of MDA and the consumption of NADPH of the plasma membrane during lipid peroxidation initiated by iron/cysteine and Vitamin C/NADPH were also inhibited. The results strongly suggest that several phenolic compounds like Sai A have a protective action against peroxidative damage to biomembranes.

Animals↗
PubMed1992

The role of lipid peroxidation in the nephrotoxicity of cisplatin.

The possible role of lipid peroxidation in the nephrotoxicity of the antitumour drug cisplatin was studied in vitro. In contrast to Adriamycin, cisplatin did not induce lipid peroxidation in rat kidney microsomes containing a NADPH-generating system. Pretreatment of rat kidney microsomes with cisplatin did not reduce the activity of a microsomal glutathione (GSH)-dependent protective factor against lipid peroxidation induced by Fe(2+)-ascorbate. However, pretreatment of rat kidney microsomes with 0.1 mM N-ethyl maleimide (NEM) did reduce this GSH-dependent protection. Cisplatin also did not reduce the activity of a cytosolic GSH-dependent protective factor against Fe(2+)-ascorbate-induced lipid peroxidation. The results of our experiments indicate that, in contrast to Adriamycin, cisplatin does not induce lipid peroxidation in vitro in various test systems. It also does not destroy microsomal and cytosolic GSH-dependent protective factors against lipid peroxidation.

Animals↗
PubMed1994

Effect of oxygen tension on the generation of F2-isoprostanes and malondialdehyde in peroxidizing rat liver microsomes.

Although numerous methods have been developed for the detection of lipid peroxidation, it is generally recognized that most of these lack specificity and/or sensitivity, particularly when applied to in vivo situations. We have reported recently that a series of prostaglandin F2-like compounds, termed F2-isoprostanes, are formed in vivo from the free radical catalyzed peroxidation of arachidonic acid and appear to be a useful marker of oxidant stress. Because of formation of other products of lipid peroxidation, such as alkanes and malondialdehyde (MDA), are affected by oxygen tension, which may influence their usefulness as markers of oxidant stress, we carried out a systematic study of the generation of F2-isoprostanes at various oxygen concentrations and compared these changes with the generation of MDA. The disappearance of the F2-isoprostane precursor, arachidonic acid, was used as a reference measure. Rat liver microsomes were peroxidized using an iron-ascorbate system. The incubations were carried out in sealed flasks at 37 degrees under N2 and various concentrations of O2 up to 100%. F2-isoprostanes were quantified by mass spectrometry and MDA by the thiobarbituric acid reaction. Microsomal fatty acids were measured by gas chromatography. Both MDA and F2-isoprostane formation increased in a time-dependent manner up to 15 min. Their formation correlated with a loss of polyunsaturated fatty acid and with an increase in O2 tension up to 21% O2. At oxygen tensions above 21%, MDA generation continued to increase, while F2-isoprostane generation and arachidonic acid loss did not. Levels of MDA and F2-isoprostanes increased a maximum of 65 and 9.4 times baseline values, respectively. These studies, therefore, define factors that influence the formation of F2-isoprostanes in an in vitro model of lipid peroxidation. Further, they demonstrate that higher O2 tensions do not block formation of F2-isoprostanes and validate their usefulness for assessing lipid peroxidation under high, as well as low, oxygen tension.

Animals↗
PubMed1995

Differential effects of in vitro peroxidation on peripheral- and central-type benzodiazepine receptors. Protection by diverse antioxidants.

The influence of various concentrations of ferrous iron and ascorbate on in vitro peroxidation and drug binding of diverse membrane preparations (cerebral cortex and liver) was studied. Peroxidation was not simply dose-related to ascorbate and ferrous iron, but a complex relationship between iron and ascorbate when added in association was established. Under our conditions 0.01 mM Fe2+ and 0.5 mM ascorbate was the most peroxidative combination for cerebral and liver membranes. Under the same conditions, cerebral membranes were more peroxidated than liver membranes. Considering the consequences of drug binding, peripheral-type benzodiazepine receptors (PBRs) of liver were more affected by peroxidative events than central-type benzodiazepine receptors (CBRs) of the cerebral cortex. The degree of binding disturbance was generally inversely correlated to the degree of peroxidation and this was more significant for liver PBRs than for cerebral CBRs. The liver membrane model was retained for testing in vitro protection by diverse putative antioxidants. Under our conditions desferrioxamine, ethylene diamine tetra acetate (EDTA), trolox, and rutin were good protective antioxidants, whereas phenyl-butyl-nitrone (PBN) and tocopherol were not effective.

Animals↗
PubMed1993

Membrane lipid peroxidation induces changes in gamma-[3H]aminobutyric acid transport and calcium uptake by synaptosomes.

In the present study, we analyze the effect of Fe2+/ascorbate-induced lipid peroxidation on Ca(2+)-dependent and Ca(2+)-independent release and on the uptake of gamma-[3H]aminobutyric acid (GABA) by sheep brain synaptosomes. In addition, we study the effect of lipid peroxidation on the levels of cytosolic calcium and on the uptake of calcium (45Ca2+). After membrane lipid peroxidation, a decrease in the uptake of GABA is observed. After ascorbate/Fe(2+)-induced membrane lipid peroxidation, a significant decrease in [3H]GABA release in response to K(+)-depolarization occurs, in the absence and in the presence of Ca2+. The influx of 45Ca2+ induced by K(+)-depolarization is significantly depressed under peroxidative conditions, while basal calcium uptake is inhibited to a much lesser degree. The levels of free ionic calcium [Ca2+]i, as determined by the fluorescent dye Indo-1, are increased after synaptosomes were submitted to the ascorbate/Fe2+ oxidative stress. It is concluded that membrane lipid peroxidation induces a decrease in Ca(2+)-dependent and Ca(2+)-independent efflux of accumulated [3H]GABA in response to elevated K+ pulses (60 mM) and in the depolarization-induced calcium influx, while free ionic calcium levels increase. The Ca(2+)-dependent efflux is interpreted to reflect stimulus-secretion coupling process and the Ca(2+)-independent efflux may reflect membrane transport processes. Thus, the results suggest a possible relationship between a reduced calcium movement across the membrane, the decrease in neurotransmitters uptake and release and oxidative stress.

Animals↗
PubMed1987

The oxidation of benzo[a]pyrene-7,8-dihydrodiol mediated by lipid peroxidation in the rat intestine and the effect of dietary lipids.

This study has demonstrated that the microsomal fraction of the rat small intestinal mucosa has the capacity to catalyse the oxidation of benzo[a]pyrene(BP)-7,8-diol to BP-diol-epoxides (BPDEs) both by a mechanism involving the mixed-function oxidase system (NADPH-dependent) and as a result of the initiation of peroxidation of the membrane phospholipids by ferrous ions, ascorbate and ADP. The NADPH-dependent reaction was fastest in the proximal part of the intestine and resulted in the formation of approximately equal amounts of BPDE I and BPDE II. The lipid peroxidation-catalysed reaction favoured the production of BPDE I and was maximal in the middle region of the intestine, closely paralleling the rate of lipid peroxidation in the intestinal sections. Feeding rats on a cod liver oil diet, rich in C20:5 and C22:6, significantly increased the incorporation of these fatty acids into the microsomal fractions. This resulted in a greatly increased rate of lipid peroxidation in vitro and a significantly higher rate of lipid peroxidation-catalysed BP-7,8-diol oxidation compared to rats fed fat-free, mono-unsaturated lard or corn oil (58% C18:2) diets. Thus the rate of conversion of BP-7,8-diol to its ultimate carcinogenic forms during lipid peroxidation in the intestinal fractions of rats fed a polyunsaturated fat was quantitatively more important than the NADPH-catalysed reaction as measured in vitro.

Animals↗
PubMed1992

NADH-dependent reductive stress and ferritin-bound iron in allyl alcohol-induced lipid peroxidation in vivo: the protective effect of vitamin E.

The role of iron in allyl alcohol-induced lipid peroxidation and hepatic necrosis was investigated in male NMRI mice in vivo. Ferrous sulfate (0.36 mmol/kg) or a low dose of ally alcohol (0.6 mmol/kg) itself caused only minor lipid peroxidation and injury to the liver within 1 h. When FeSO4 was administered before allyl alcohol, lipid peroxidation and liver injury were potentiated 50-100-fold. Pretreatment with DL-tocopherol acetate 5 h before allyl alcohol protected dose-dependently against allyl alcohol-induced lipid peroxidation and liver injury in vivo. Products of allyl alcohol metabolism, i.e. NADH and acrolein, both mobilized trace amounts of iron from ferritin in vitro. Catalytic concentrations of FMN greatly facilitated the NADH-induced reductive release of ferritin-bound iron. NADH effectively reduced ferric iron in solution. Consequently, a mixture of NADH and Fe3+ or NADH and ferritin induced lipid peroxidation in mouse liver microsomes in vitro. Our results suggest that the reductive stress (excessive NADH formation) during allyl alcohol metabolism can release ferrous iron from ferritin and can reduce chelated ferric iron. These findings provide a rationale for the strict iron-dependency of allyl alcohol-induced lipid peroxidation and hepatotoxicity in mice in vivo and document iron mobilization and reduction as one of several essential steps in the pathogenesis.

1-Propanol↗
PubMedDate not supplied

The role of physiological oxygen partial pressures in lipid peroxidation. Theoretical considerations and experimental evidence.

The oxidative breakdown of membrane lipids, i.e. lipid peroxidation, is considered to be decisively involved in a number of toxicological and pathological processes including liver injury caused by iron overload and halogenated alkanes such as CCl4. Within the physiological oxygen partial pressure (PO2) range, i.e. at PO2 between 1 and 100 mmHg, lipid peroxidation depends on O2 in a complex manner. For instance, CCl4-induced lipid peroxidation exhibits a distinct maximum at PO2 of around 7 mmHg, and iron-induced lipid peroxidation shows marked differences in its O2 dependence between an early lag phase and a later phase of self-accelerating propagation. The O2 dependence of lipid peroxidation is either determined by the O2 dependence of initiation or the O2 dependence of propagation. Factors decisive for this are presented and the underlying alterations in the pattern of the peroxidation-related reactions delineated.

Animals↗
PubMedDate not supplied

Lipid peroxidation and associated hepatic organelle dysfunction in iron overload.

Iron overload can have serious health consequences. Since humans lack an effective means to excrete excess iron, overload can result from an increased absorption of dietary iron or from parenteral administration of iron. When the iron burden exceeds the body's capacity for safe storage, the result is widespread damage to the liver, heart and joints, and the pancreas and other endocrine organs. Clear evidence is now available that iron overload leads to lipid peroxidation in experimental animals, if sufficiently high levels of iron are achieved. In contrast, there is a paucity of data regarding lipid peroxidation in patients with iron overload. Data from experiments using an animal model of dietary iron overload support the concept that iron overload results in an increase in an hepatic cytosolic pool of low molecular weight iron which is catalytically active in stimulating lipid peroxidation. Lipid peroxidation is associated with hepatic mitochondrial and microsomal dysfunction in experimental iron overload, and lipid peroxidation may underlie the increased lysosomal fragility that has been detected in homogenates of liver samples from both iron-loaded human subjects and experimental animals. Some current hypotheses focus on the possibility that the demonstrated functional abnormalities in organelles of the iron-loaded liver may play a pathogenic role in hepatocellular injury and eventual fibrosis. The recent demonstration that hepatic fibrosis is produced in animals with long-term dietary iron overload will allow this model to be used to further investigate the relationship between lipid peroxidation and hepatic injury in iron overload.

Animals↗
PubMedDate not supplied

Lipid peroxides and human diseases.

Development of a simple and reliable method to determine the lipid peroxide level in human serum or plasma has made it possible to survey the levels in human diseases. Since in some human diseases lipid peroxides are increased in various organs or tissues and leak into the bloodstream, the increased lipid peroxide level in the blood aids the diagnosis of such diseases. Furthermore, determination of the level provides useful information as to their prognosis, since the increased lipid peroxides in the blood primarily attack the endothelial cells of vessels and then intact organs or tissues as well. The present paper describes a method to determine the lipid peroxide level in human serum or plasma and its profile of change in several human diseases. Intervention of lipid peroxides in the pathogenesis of certain diseases is also mentioned.

Disease↗
PubMed1990

The cooperative action of vitamins E and C in the protection against peroxidation of parinaric acid in human erythrocyte membranes.

The influence of vitamins E and C on the initial stages of lipid peroxidation in human erythrocyte membranes was assessed with the fluorescent polyunsaturated fatty acid, parinaric acid, as probe molecule. Cumene hydroperoxide was used as initiator with either haemin-Fe3+ or Cu2+ as metal ion cofactor. The effect of vitamin C (pro- or antioxidant) appeared to be determined by the localisation of the metal ions, either in the water phase or in the membrane. Vitamin C is only able to reduce metal ions in the water phase, which results in acceleration of radical generation and subsequent enhancement of parinaric acid peroxidation. Thus, interaction of vitamin C with Cu2+ in the water phase led to drastically enhanced peroxidation of parinaric acid. In contrast, when only membrane-associated haemin-Fe3+ was present, vitamin C functioned as an antioxidant at all concentrations tested (0-10 microM). In a system with haemin-Fe3+ equilibrated between the water phase and the membranes, less than 5 microM vitamin C produced an overall prooxidant, and greater than 15 microM vitamin C an overall antioxidant effect. At vitamin C concentrations of 5-15 microM, continuous measurement of parinaric acid fluorescence revealed a shift in the vitamin C effect from antioxidant to prooxidant within the time-course of an assay. Vitamin E exhibited a protective effect on peroxidation initiated by cumene (per)oxyl radicals with haemin-Fe3+ as cofactor, by inducing a concentration-dependent extension of the lag-phase in parinaric acid peroxidation. Vitamin E appeared to be much more effective compared with vitamin C in scavenging radicals in this system. This indicates that vitamin C has only a limited ability to react with cumene (per)oxyl radicals in the membrane. The combination of vitamins E and C produced a protective effect on parinaric acid peroxidation exceeding the sum of their individual contributions. Moreover, the rate of vitamin E consumption was drastically lowered in the presence of vitamin C, whereas the rate of vitamin C consumption hardly decreased in the presence of vitamin E. The results are discussed in terms of a reaction scheme where the relative contributions of a number of reactions are considered to determine the total effect of added vitamin C or E. Vitamin E radicals constitute an additional substrate for vitamin C, resulting in a more than additive shift in the overall effect to the antioxidant side.

Animals↗
PubMed1981

Serum vitamin E, lipid peroxide and glutathione peroxidase in patients with chronic pancreatitis.

It has been reported that lipid peroxidation increases in patients with antioxidant deficiencies, such as vitamin E and glutathione peroxidase. The relationships between serum lipid peroxide and vitamin E on the one hand and glutathione peroxidase on the other were examined in 22 patients with chronic pancreatitis, often accompanied by malabsorption of fats and fat-soluble vitamins due to the impaired exocrine pancreatic function. Both serum vitamin E concentrations and glutathione peroxidase activities were depressed, especially in patients with chronic calcifying pancreatitis. On the other hand, serum lipid peroxide levels were elevated. A significant negative correlation was found between the serum lipid peroxide levels and vitamin E concentration. These findings suggest than an elevation of the serum lipid peroxide level may be due to the lack of an antioxidative defense mechanism, such as vitamin E, against lipid peroxide.

Chronic Disease↗