Effects of aurothioglucose on iron-induced rat liver microsomal lipid peroxidation

Aurothioglucose (ATG), an inhibitor of selenium-dependent glutathione peroxidase activity, at a concentration of 100 μM, strongly increases lipid peroxidation of rat liver microsomes exposed to either ferrous ion (10 μM) or the combination of ferric ion (10 μM) and ascorbic acid (500 μM), in the presence of reduced glutathione (GSH, 800 μM). This effect was not achieved using heat-inactivated microsomes and was dependent on the presence of GSH. ATG did not affect the lag period associated with ascorbic acid/ferric ion-induced microsomal lipid peroxidation (previously attributed to an undefined GSH-dependent microsomal agent), but did increase the rate of peroxidation subsequent to the lag period. The potent GSH-dependent inhibition of microsomal lipid peroxidation by cytosol (10% of total volume) was completely reversed by ATG (100 μM). ATG similarly reversed an inhibition of phosphatidyl-choline hydroperoxide-dependent liposomal peroxidation that has been attributed to phospholipid hydroperoxide glutathione peroxidase (PHGPX), an enzyme distinct from the classical glutathione that cannot utilize intact phospholipids. ATG inhibited, in addition to the classifical selenium-dependent glutathione peroxidase, both cytosolic and microsomal (basal and N-ethyl maleimide-stimulated) glutathione S-transferase activities with greater than 80% inhibition achieved at 100 μM ATG. ATG, at concentrations up to 250 μM, did not inhibit PHGPX activity measured by the coupled-enzyme method in the presence of Triton X-100 (0.1%). These data demonstrate the potential of ATG to increase toxicity of lipid peroxidative stimuli by inhibition of microsomal and cytosolic defense mechanisms. Although ATG did not inhibit Triton-enhanced PHGPX activity, overall evidence points toward inhibition of this enzyme as the mechanism for ATG-augmented lipid peroxidation and supports the conclusion that PHGPX plays a major role in the cellular defense mechanism.     

Interplay between Vitamin E,Glutathione and Dihydrolipoic Acid in Protection against Lipid Peroxidation

Free radicals can disturb the intracellular homeostasis by either modification of essential free sulfhydryl groups or by inducing lipid peroxidation. The damage provoked by oxidation of sulfhydryl groups might be reversible but the damage induced by the process of lipid peroxidation is probably not reversible. The main protective constituents of the cell are thiols and vitamin E. Thiols, especially glutathione, protect the cytosol while vitamin E protects the lipid membranes against free radicals. In the scavenging of free radicals in the lipid membrane, vitamin E becomes oxidized. However continuous recycling of vitamin E by a reductase, with the cytosolic thiol glutathione as cofactor, will keep the vitamin E levels high enough to protect against lipid peroxidation. In the recycling glutathione is oxidized. Dihydrolipoic acid cannot provide directly reducing equivalents for the recycling of vitamin E by the free radical reductase. However indirectly, via the reduction of oxidized glutathione, dihydrolipoic acid can mediate the regeneration of vitamin E. One of the secondary mechanisms that mediates free radical induced damage is the rise in intracellular free Ca²⁺-concentration caused by inactivation of the endoplasmic reticulum ca²⁺-ATPase. The Ca²⁺-ATPase can be inactivated either by sulfhydryl alkylation or by lipid peroxidation. The authors used the thiol-alkylating agent N-ethylmaleimide, cystamine and ebselen. Dithiothreitol reversed the inhibition caused by all the three agents, while dihydrolipoic acid reversed the inhibition caused by ebselen. Glutathione was not able to reverse the effects of the sulfhydryl reactive agents. The reactivation of the microsomal Ca²⁺-ATPase by dihydrolipoic acid, may – besides the reduction of oxidized glutathione – contribute to the protective effect of dihydrolipoic acid on lipid peroxidation.     

The effects of vitamin E and selenium intake on oxidative stress and plasma lipids in hamsters fed fish oil

The aim of the present work was to test the effects of large-dose supplementation of vitamin E (Vit E) and selenium (Se), either singly or in combination, on fish oil (FO)-induced tissue lipid peroxidation and hyperlipidemia. The supplementation of Se has been shown to lower blood cholesterol and increase tissue concentrations of the antioxidant glutathione (GSH); however, the effects of Se supplementation, either alone or in combination with supplemental Vit E, on FO-induced oxidative stress and hyperlipidemia have not been studied. Male Syrian hamsters received FO-based diets that contained 14.3 wt% fat and 0.46 wt% cholesterol supplemented with Vit E (129 IU d-α-tocopheryl acetate/kg diet) and/or Se (3.4 ppm as sodium selenate) or that contained basal requirements of both nutrients. The cardiac tissue of hamsters fed supplemental Se showed increased concentrations of lipid hydroperoxides (LPO) but decreased oxidized glutathione (GSSG) concentrations. The higher concentrations of LPO in the hearts of Se-supplemented hamsters were not lowered with concurrent Vit E supplementation. In the liver, Se supplementation was associated with higher Se-dependent glutathione peroxidase activity and an increase in the GSH/GSSG ratio, whereas a lower hepatic non-Se-dependent glutathione peroxidase activity was seen with Vit E supplementation. Supplemental intake of Se was associated with lower plasma concentrations of total cholesterol and low density lipoprotein cholesterol plus very low density lipoprotein cholesterol. In view of the pro-oxidative effects of Se supplementation on cardiac tissue, a cautionary approach needs to be taken regarding the plasma lipid-lowering properties of supplemental Se.     

Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes

Rat lung and liver microsomes were used to examine the effects of dietary vitamin E deficiency on membrane lipid peroxidation. Microsomes from vitamin-E-deficient rats displayed increased lipid peroxidation in comparison to microsomes from vitamin-E-supplemented controls. The extent of lipid peroxidation, as determined by measurement of thiobarbituric acid reacting materials, was enhanced by addition of reduced iron and ascorbate (or NADPH). Rats fed a vitamin-E-supplemented diet and exposed to 3 ppm NO₂ for 7 days did not exhibit increases in microsomal lipid peroxidation compared to air-breathing controls. However, increases were found in microsomes prepared from rats fed a vitamin-E-deficient diet and exposed to NO₂. Lung microsomes from vitamin-E-fed rats contained almost 10 times as much vitamin E as liver microsomes when expressed in terms of polyunsaturated fatty acid content. The extent of lipid peroxidation was, in turn, considerably less in lung than in liver microsomes. Lipid peroxidation in lung microsomes from vitamin-E-deficient rats was comparable to liver microsomes from vitamin-E-supplemented rats as was the content of vitamin E in these respective microsomal samples. A combination of vitamin E deficiency and NO₂ exposure resulted in the greatest increases in lung and liver microsomal lipid peroxidation with the largest relative increases occurring in lung microsomes. An inverse relationship was found between the extent of lipid peroxidation and vitamin E content. Most of the peroxidation in lung microsomes appeared to proceed nonenzymatically whereas peroxidation in liver was largely enzymatic. Vitamin E appears to be assimilated by the lung during oxidant inhalation, but with dietary vitamin E deprivation, the margin for protection in lung may be less than in liver.     

Toxikologie freier Radikale und Antioxidantien unter besonderer Berücksichtigung von Vitamin E

Toxicology of Free Radicals and Antioxidants with Specific Regards to Vitamin E By metabolic activation radicals of xenobiotics can occur in the body which may be toxic by reacting with oxygen. The oxygen radicals formed then react with cellular macromolecules. When reacting with lipids lipid peroxidation occurs. Antioxidants may either inhibit the formation of oxygen radicals or prevent lipid peroxidation. As examples carbon tetrachloride, adriamycin, paraquat and some carcinogens are dealt with. With some toxicity as well as lipid peroxidation are inhibited by vitamin E and other antioxidants. Furthermore, the toxicology of the antioxidants is discussed, because they are themselves transformed into free radicals. Whereas vitamin E has practically no toxic effects, some synthetic antioxidants show carcinogenic effects in animal experiments.     

Effect of dietary vitamin E and selenium on susceptibility of brain regions to lipid peroxidation

The effect of dietary vitamin E and/or selenium (Se) supplementation (200 IU and/or 0.2 ppm, respectively) or deficiency for two months on lipid peroxidation in cerebrum, cerebellum, mid-brain, and brain stem of one-month-old male F344 rats was investigated. Dietary treatment had a minimal effect on weight gain of rats for the period tested. Plasma α-tocopherol (α-T) concentration and glutathione peroxidase (GSH-Px) activity were reflective of dietary treatments. Supplementation of diets with vitamin E and/or Se increased plasma α-T and/or GSH-Px activity, while diets devoid of these nutrients reduced them significantly. Increased GSH-Px activity in Sesupplemented rats was further enhanced by vitamin E supplementation. Differential concentrations of α-T among brain regions were affected by dietary vitamin E but not by Se. In vitro lipid peroxidation of brain homogenates was inhibited by dietary vitamin E supplementation and increased by deficiency. Addition of 0.25 mM ascorbic acid or 0.1 mM of Fe²⁺ to brain homogenates markedly increased in vitro lipid peroxidation. Ascorbic acid-induced lipid peroxidation was inversely correlated with dietary vitamin E and Se in cerebrum. In vitro Fe²⁺-addition induced the greatest stimulation of lipid peroxidation, with cerebellum and brain stem of vitamin E-deficient rats showing the highest response to Fe²⁺ challenge. These findings indicate that concentrations of α-T among the brain regions are different and can be altered by dietary vitamin E treatments, cerebellum and brain stem are more susceptible to in vitro challenge by peroxidative agents than other regions, and the degree of lipid peroxidation of brain regions is partially affected by dietary vitamin E but not by Se in the levels tested.     

Advances in carcinogenic metal toxicity and potential molecular markers

Metal compounds such as arsenic, cadmium, chromium, cobalt, lead, mercury, and nickel are classified as carcinogens affecting human health through occupational and environmental exposure. However, the underlying mechanisms involved in tumor formation are not well clarified. Interference of metal homeostasis may result in oxidative stress which represents an imbalance between production of free radicals and the system's ability to readily detoxify reactive intermediates. This event consequently causes DNA damage, lipid peroxidation, protein modification, and possibly symptomatic effects for various diseases including cancer. This review discusses predominant modes of action and numerous molecular markers. Attention is paid to metal-induced generation of free radicals, the phenomenon of oxidative stress, damage to DNA, lipid, and proteins, responsive signal transduction pathways with major roles in cell growth and development, and roles of antioxidant enzymatic and DNA repair systems. Interaction of non-enzymatic antioxidants (carotenoids, flavonoids, glutathione, selenium, vitamin C, vitamin E, and others) with cellular oxidative stress markers (catalase, glutathione peroxidase, and superoxide dismutase) as well as certain regulatory factors, including AP-1, NF-κB, Ref-1, and p53 is also reviewed. Dysregulation of protective pathways, including cellular antioxidant network against free radicals as well as DNA repair deficiency is related to oncogenic stimulation. These observations provide evidence that emerging oxidative stress-responsive regulatory factors and DNA repair proteins are putative predictive factors for tumor initiation and progression.     

The effect of glutathione on the vitamin E requirement for inhibition of liver microsomal lipid peroxidation

Vitamin E dependent inhibition of rat liver microsomal lipid peroxidation in an NADPH and ADP-Fe⁺³ containing system occurred at lower vitamin E concentrations in the presence of glutathione (GSH). Using microsomes from rats fed a vitamin E deficient diet, vitamin E was shown to be rquired for inhibition. Inhibition also required the presence of a storage labile microsomal component, since no inhibition was observed when using microsomes that had been stored for one moth. This observation provides evidence that direct reduction of reversibly oxidized vitamin E by GSH does not appear to contribute significantly to inhibition of peroxidation. During GSH and vitamin E dependent inhibition of lipid peroxidation, vitamin E (reduced form) concentrations remained constant, indicating that GSH maintained vitamin E concentrations. Without GSH, vitamin E concentrations dropped rapidly. By adding vitamin E to microsomes, it was found that inhibition of lipid peroxidation in the presence of GSH occurred at about five-fold less vitamin E than in the absence of GSH. Inhibition at these lower levels of vitamin E was 85–90% complete. Results indicate that GSH can be used to maintain vitamin E (reduced form) concentrations, thereby lowering the concentration of vitamin E necessary to inhibit microsomal lipid peroxidation.     

Pathophysiologic role of redox status in blood platelet activation. Influence of docosahexaenoic acid

Decrease of platelet glutathione peroxidase activity results in increased life span of lipid hydroperoxides, especially the 12-lipoxygenase product of arachidonic acid, 12-HpETE. Phospholipase A₂ activity is subsequently enhanced with the release of arachidonic acid, which results in higher thromboxane formation and platelet function. Docosahexaenoic acid may either potentiate platelet lipid peroxidation or lower it when used at high or low concentrations, respectively. In the case of slowing down lipid peroxidation, docosahexaenoic acid was specifically incorporated in plasmalogen ethanolamine phospholipids. This could have a relevant pathophysiologic role in atherothrombosis.     

Antioxidant and prooxidant effects of α‐tocopherol in a linoleic acid‐copper(II)‐ascorbate system

The peroxidation of linoleic acid (LA) in the absence and presence of either Cu(II) ions alone or Cu(II)‐ascorbate combination was investigated in aerated and incubated emulsions at 37°C and pH 7. LA peroxidation induced by either copper(II) or copper(II)‐ascorbic acid system followed pseudo‐first order kinetics with respect to primary (hydroperoxides) and secondary (aldehydes‐ and ketones‐like) oxidation products, detected by ferric‐thiocyanate and TBARS tests, respectively. α‐Tocopherol showed both antioxidant and prooxidant effects depending on concentration and also on the simultaneous presence of Cu(II) and ascorbate. Copper(II)‐ascorbate combinations generally led to distinct antioxidant behavior at low concentrations of α‐tocopherol and slight prooxidant behavior at high concentrations of α‐tocopherol, probably associated with the recycling of tocopherol by ascorbate through reaction with tocopheroxyl radical, while the scavenging effect of α‐tocopherol on lipid peroxidation was maintained as long as ascorbate was present. On the other hand, in Cu(II) solutions without ascorbate, the antioxidant behavior of tocopherol required higher concentrations of this compound because there was no ascorbate to regenerate it. Practical applications: Linoleic acid (LA) peroxidation induced by either copper(II) or copper(II)‐ascorbic acid system followed pseudo‐first order kinetics with respect to primary (hydroperoxides) and secondary (e.g., aldehydes and ketones) oxidation products. α‐Tocopherol showed both antioxidant and prooxidant effects depending on concentration and also on the simultaneous presence of Cu(II) and ascorbate. The findings of this study are believed to be useful to better understand the actual role of α‐tocopherol in the preservation of heterogenous food samples such as lipid emulsions. Since α‐tocopherol (vitamin E) is considered to be physiologically the most important lipid‐soluble chain‐breaking antioxidant of human cell membranes, the results can be extended to in vivo protection of lipid oxidation.     

Involvement of vitamin E and protein thiols in the inhibition of microsomal lipid peroxidation by glutathione

Iron-ascorbate stimulated lipid peroxidation in rat liver microsomes can be inhibited by glutathione (GSH). The role of protein thiols and vitamin E in this process was studied in liver microsomes isolated from rats fed diets either sufficient or deficient in vitamin E and incubated at 37°C unde 100% O₂. Lipid peroxidation was induced by adding 400 μM adenosine 5′-triphosphate, 2.5 to 20 μM FeCl₃, and 450 μM ascorbic acid. One mL of the incubation mixture was removed at defined intervals for the measurement of thiobarbituric acid reactive substances (TBARS), protein thiols and vitamin E. In vitamin E sufficient microsomes, the addition of GSH enhanced the lag time prior to the onset of maximal TBARS accumulation and inhibited the loss of vitamin E. Treatment of these microsomes with the protein thiol oxidant diamide resulted in a 56% loss of protein thiols, but did not significantly change vitamin E levels. However, diamide treatment abolished the GSH-mediated protection against TBARS formation and loss of vitamin E during ascorbate-induced peroxidation. Liver microsomes isolated from rats fed a vitamin E deficient diet contained 40-fold less vitamin E and generated levels of TBARS similar to vitamin E sufficient microsomes at a 4-fold lower concentration of iron. GSH did not affect the lag time prior to the onset of maximal TBARS formation in vitamin E deficient microsomes although total TBARS accumulation was inhibited. Similar to what was previously found in vitamin E sufficient microsomes [Palamanda and Kehrer, (1992)Arch. Biochem. Biophys. 293, 103–109], GSH prevented the loss of protein thiols in vitamin E deficient microsomes. However, GSH did not protect efficiently against the loss of residual vitamin E in deficient microsomes. These data provide support for the concept that GSH protects against microsomal lipid peroxidation by maintaining protein thiols, and consequently vitamin E, in the reduced state. The lack of protection in vitamin E deficient microsomes may be related to the inability of such low levels of vitamin E to inhibit peroxidation.     

Effect of dietary vitamin E levels on fatty acid profiles and nonenzymatic lipid peroxidation in the guinea pig liver

Guinea pigs were fed for five weeks with three diets containing different levels of vitamin E: LOW (but nondeficient, 15 mg of vitamin E/kg diet), MEDIUM (150 mg/kg diet), and HIGH (1,500 mg/kg diet). Dietary vitamin E supplementation did not change oxidative stress indicators in the hydrophilic compartment but increased liver α-tocopherol in a dose-dependent way and strongly decreased sensitivity to nonenzymaticin vitro liver lipid peroxidation. This last effect was already observed in group MEDIUM, and no further decrease inin vitro lipid peroxidation occurred from group MEDIUM to group HIGH. The protective effect of vitamin E againstin vitro lipid peroxidation was observed even though an optimum dietary concentration of vitamin C for this animal model was present in the three different vitamin E diets. Both HIGH and LOW vitamin E decreased percentage fatty acid unsaturation in all phospholipid fractions from membrane origin in relation to group MEDIUM. The results, together with previous information, show that both vitamin E and vitamin C at intermediate concentrations are needed for optimal protection against lipid peroxidation and loss of fatty acid unsaturation even in normal nonstressful conditions. These protective concentrations are higher than those needed to avoid deficiency syndromes.     

Urinary malondialdehyde as an indicator of lipid peroxidation in the diet and in the tissues

Although malondialdehyde (MDA) is extensively metabolized to CO₂, small amounts are nevertheless excreted in an acid-hydrolyzable form in rat urine. In this study, urinary MDA was evaluated as an indicator of lipid peroxidation in the diet and in the tissues. MDA was released from its bound form(s) in urine by acid treatment and determined as the TBA-MA derivative by HPLC. MDA excretion by the rat was found to be responsive to oral administration of the Na enol salt and to peroxidation of dietary lipids. Urinary MDA also increased in response to the increased lipid peroxidation in vivo produced by vitamin E deficiency and by administration of iron nitrilotriacetate. Chronic feeding of a diet containing cod liver oil led to increases in MDA excretion which were not completely eliminated by fasting or feeding a peroxide-free diet, indicating that there was increased lipid peroxidation in vivo. MDA excretion was not responsive to Se deficiency or CCl₄ administration. DPPD, a biologically active antioxidant, but not BHA, a non-biologically active antioxidant, prevented the increase in MDA excretion in vitamin E deficient animals. The results indicate that MDA excretion can serve as an indicator of the extent of lipid peroxidation in the diet and, under conditions which preclude a dietary effect, as an index of lipid peroxidation in vivo. Part of this research was performed in fulfillment of the requirements for the MSc degree in nutrition.     

Low doses of eicosapentaenoic acid, docosahexaenoic acid, and hypolipidemic eicosapentaenoic acid derivatives have no effect on lipid peroxidation in plasma

It was of interest to investigate the influence of both high doses of eicosapentaenoic acid (EPA) and low doses of 2-or 3-methylated EPA on the antioxidant status, as they all cause hypolipidemia, but the dose required is quite different. We fed low doses (250 mg/d/kg body wt) of different EPA derivatives or high doses (1500 mg/d/kg body wt) of EPA and DHA to rats for 5 and 7 d, respectively. The most potent hypolipidemic EPA derivative, 2,2-dimethyl-EPA, did not change the malondialdehyde content in liver or plasma. Plasma vitamin E decreased only after supplementation of those EPA derivatives that caused the greatest increase in the fatty acyl-CoA oxidase activity. Fatty acyl-CoA oxidase activity increased after administration of both EPA and DHA at high doses. High doses of EPA and DHA decreased plasma vitamin E content, whereas only DHA elevated lipid peroxidation. In liver, however, both EPA and DHA increased lipid peroxidation, but the hepatic level of vitamin E was unchanged. The glutathione-requiring enzymes and the glutathione level were unaffected, and no significant changes in the activities of xanthine oxidase and superoxide dismutase were observed in either low-or high-dose experiments. In conclusion, increased peroxisomal β-oxidation in combination with high amounts of polyunsaturated fatty acids caused elevated lipid peroxidation. At low doses of polyunsaturated fatty acids, lipid peroxidation was unchanged, in spite of increased peroxisomal β-oxidation, indicating that polyunsaturation is the most important factor for lipid peroxidation.     

Effect of vitamin E on pentane exhaled by rats treated with methyl ethyl ketone peroxide

One useful method to monitor in vivo lipid peroxidation is the measurement of volatile hydrocarbons, mainly pentane and ethane, that derive from unsaturated fatty acid hydroperoxides. Vitamin E, the biological antioxidant, inhibits lipid peroxidation and the production of pentane and ethane. The rates of pentane production by male Sprague-Dawley rats fed a diet that contained 10% vitamin E-stripped corn oil and 0, 1, 3, 5 or 10 IU dl-α-tocopherol acetate/kg were monitored over a 12-wk period. During the eleventh and twelfth weeks, the rats were injected intraperitoneally with 3.3 and 13 mg of methyl ethyl ketone peroxide (MEKP)/kg body wt, respectively. Pentane production was then measured at intervals over a 50-min period, and the total amount of pentane produced over this time interval was estimated. An asymptotic function was found to describe the relationship between exhaled pentane and the low levels of dietary vitamin E that were fed to the rats. As measured by pentane production, rats had a higher minimal vitamin E requirement after they were treated with the potent peroxidation initiator MEKP than they did prior to treatment. The level of pentane exhaled by rats injected with 13 mg MEKP/kg body wt was significantly correlated with kidney and spleen tocopherol levels.     

Oral Rg1 supplementation strengthens antioxidant defense system against exercise-induced oxidative stress in rat skeletal muscles

ABSTRACT: BACKGROUND: Previous studies reported divergent results on nutraceutical actions and free radical scavenging capability of ginseng extracts. Variations in ginsenoside profile of ginseng due to different soil and cultivating season may contribute to the inconsistency. To circumvent this drawback, we assessed the effect of major ginsenoside-Rg1 (Rg1) on skeletal muscle antioxidant defense system against exhaustive exercise-induced oxidative stress. METHODS: Forty weight-matched rats were evenly divided into control (N = 20) and Rg1 (N = 20) groups. Rg1 was orally administered at the dose of 0.1 mg/kg bodyweight per day for 10- week. After this long-term Rg1 administration, ten rats from each group performed an exhaustive swimming, and remaining rats considered as non-exercise control. Tibialis anterior (TA) muscles were surgically collected immediately after exercise along with nonexercise rats. RESULTS: Exhaustive exercise significantly (p <0.05) increased the lipid peroxidation of control group, evidenced by elevated malondialdehyde (MDA) levels. The increased oxidative stress after exercise was also confirmed by decreased reduced glutathione to oxidized glutathione ratio (GSH/GSSG ratio) in control rats. However, these changes were completely eliminated in Rg1 group. Catalase (CAT) and glutathione peroxidase (GPx) activities were significantly (p <0.05) increased by Rg1 in non-exercise rats, while no significant change after exercise. Nevertheless, glutathione reductase (GR) and glutathione S-transferase (GST) activities were significantly increased after exercise in Rg1 group. CONCLUSIONS: This study provide compelling evidences that Rg1 supplementation can strengthen antioxidant defense system in skeletal muscle and completely attenuate the membrane lipid peroxidation induced by exhaustive exercise. Our findings suggest that Rg1 can use as a nutraceutical supplement to buffer the exhaustive exercise-induced oxidative stress.     

Effect of dietary menhaden oil and vitamin E onin vivo lipid peroxidation induced by iron

Weanling rats were fed diets containing 10% menhaden oil (MO) or 10% corn oil-lard (1∶1, COL) with low (≤5 IU/kg) or supplementary (35 IU/kg) vitamin E for six weeks. The rats were killed 30 min after injection with 24 mg iron/kg as ferrous chloride because thiobarbituric acid-reactive substances (TBARS) in liver homogenates were highest at 30 min after injection of iron into rats fed a standard diet. Tissue homogenates were used either without incubation (zero-time) or after incubation at 37°C for 1 hr. In addition to TBARS and conjugated dienes, headspace hexanal and total volatiles (TOV) determined by capillary gas chromatography were useful indices of lipid peroxidation since they were decreased by vitamin E supplementation and were increased with increasing iron dose. Regardless of the dietary lipid used, vitamin E supplementation decreased headspace hexanal, TOV, TBARS and conjugated dienes in both zero-time and incubated homogenates of liver and kidney. Dietary MO increased TBARS in both zero-time and incubated homogenates of tissue from rats injected with iron. In contrast, dietary MO decreased hexanal and TOV in incubated tissue homogenates. The study demonstrated the usefulness and limitations of using hexanal and TOV as indices of lipid peroxidation.     

Relative susceptibility of microsomes from lung,heart, liver,kidney, brain and testes to lipid peroxidation: Correlation with vitamin E content

Rates of in vitro lipid peroxidation of microsomes and homogenates were found to vary widely among different tissues and species. In rats and rabbits, lung microsomes peroxidized at a 25- to 50-fold lower rate than liver, kidney, testes and brain microsomes. Heart microsomes peroxidized at a rate slightly greater than, but most similar to, lung microsomes. Comparison of tissue homogenates also revealed the unique resistance of lung and heart to lipid peroxidation. The ratio of vitamin E to peroxidizable polyunsaturated fatty acids in lung and heart microsomes was several-fold higher than in microsomes from the other tissues studied, which accounted for the relative resistance of lung and heart to lipid peroxidation. Liposomes of extracted rat lung microsomal lipid were also resistant to peroxidation and the amount of vitamin E contained in the lung lipid extract was sufficient to confer the same degree of resistance when incorported into an equivalent amount of rat liver lipid. Higher rates of peroxidation in mouse lung microsomes relative to rabbit, rat and human lung microsomes were similarly correlated with a lower ratio of vitamin E to peroxidizable fatty acids in mouse lung microsomes. These data provide strong support for the role of vitamin E as the major cellular antioxidant, especially in the highly oxygenated tissues of heart and lung, and demonstrate the utility of the microsomal system in characterizing tissue differences in susceptibility to peroxidative membrane decomposition.     

Antioxidative properties of irradiated chitosan/vitamin C complex and their use as food additive for lipid storage

Improving the antioxidant activity of chitosan was achieved by decreasing their molecular weight by γ rays followed by incorporation with vitamin C to prepare chitosan/vitamin C (CSVC) complex in the range of nanoparticles. Transmittance electron microscopy of CSVC complex showed mean diameters ranged from 23.2 to 82 nm. The antioxidant activities of CSVC complexes were examined using scavenging effect on DPPH radicals and reducing power measurements. CSVC complexes have a synergistic effect on increasing the antioxidant properties rather than their individual effects. The effect of CSVC complexes on lipid peroxidation of meat during 21 days of refrigerated storage was investigated using thiobarbituric acid reactive substance (TBARS) assay. Treatment of meat with CSVC complex reduced lipid peroxidation about 75% after 7 days of storage as a result the decrease in TBARS values. The results demonstrate promising use of CSVC complex as antioxidants for lipid storage. © 2015 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2015 , 132, 42105.     

Vitamin E Supplementation of Smokers and Non-Smokers

Twenty male smokers and 20 non-smokers took either vitamin E capsules (1000 IU/day) or placebo for 14 days. Erythrocytes from smokers showed a marked tendency to peroxidise in vitro compared with non-smokers, an effect which was abolished by vitamin E supplementation. The increased erythrocyte peroxidation may reflect a lipid hydroperoxide-induced decrease in glucose-6-phosphate dehydrogenase activity. Evidence that smokers incurred a sustained oxidant stress also included increased plasma conjugated dienes, decreased plasma vitamin C and an increase in erythrocyte glutathione. Plasma cholesterol, vitamin E and conjugated dienes increased with age in all groups. Results suggest that smokers are under a sustained oxidant stress, some indices of which can be partially ameliored by vitamin E supplementation.