Effect of different vitamin E levels on lipid peroxidation in streptozotocin-diabetic rats.

Administration of streptozotocin is used to induce diabetes in experimental models, causing a selective destruction of pancreatic beta islet cells associated with generation of free radicals. Supplementation with antioxidant vitamins such as vitamin E is a protective factor against free radicals. The objective of this study was to determine the effect of administration of a diet supplemented with, or deficient in vitamin E to streptozotocin diabetic rats, controlled or not with insulin, on plasma glucose, hepatic vitamin E and hepatic thiobarbituric acid reactive substance (TBARS) levels before streptozotocin and 24 hours and one and two weeks after drug administration. Deficiency of vitamin E alone increased TBARS levels, and streptozotocin elevated TBARS two times in deficient groups, regardless of insulin control. In rats supplemented with vitamin E, a reduction of plasma glucose and liver vitamin E was observed two weeks after streptozotocin administration (p < 0.05). In conclusion, vitamin E supplementation probably protected against lipoperoxidation and contributed to the absence of elevation of plasma glucose levels, and vitamin E deficiency produced an increase in hepatic TBARS levels in streptozotocin diabetic rats.     

Lipid peroxidation and glutathione peroxidase activity in the liver of cholesterol-fed rats.

The effects of cholesterol feeding on lipid peroxidation and on glutathione peroxidase activity in the liver of rats were examined. Cholesterol (1 or 1.5%) was added to two basal diets containing either 10% soy oil (diet 1) or 15% soy oil plus 100 IU of alpha-tocopherol/kg of diet (diet 2). The rate of lipid peroxidation in the liver was determined in vitro by the thiobarbituric acid test and by conjugated diene measurement (234 nm). Cholesterol feeding elevated the rate of lipid peroxidation in the liver of rats fed diet 1 or 2. The rate of lipid peroxidation in rats fed diet 2 increased with duration of feeding suggesting an increased need for antioxidant as the levels of cholesterol or other lipids in the liver elevated. Cholesterol feeding also decreased the activity of liver glutathione peroxidase and pentose phosphate pathway dehydrogenases. Glutathione peroxidase activities increased with the duration of feeding in rats fed basal diet 2, but they remained unchanged in rats fed the same diet supplemented with cholesterol. The study suggests that cholesterol feeding in rats can increase the susceptibility of the tissue to lipid peroxidation and also can lead to a depression in the activity of glutathione peroxidase.     

Lipid peroxidation in relation to vitamin C and vitamin E levels

Oxidative stress plays an important contributory role in the pathogenesis of age-related chronic diseases. Increased lipid peroxidation process is caused by an enhanced free radical formation together with a higher supply of substrates and by an insufficient defense by antioxidants as well. Levels of malondialdehyde to content of lipid peroxidation substrates (polyunsaturated fatty acids), promoters (homocysteine--hydroxyl radical producer) and inhibitors (essential vitamins C and E) were estimated in a group (n=92) of subjective healthy adults randomly selected from general population. The relationship of malondialdehyde levels to values of peroxidisability index of fatty acids as well as to levels of homocysteine is significantly positive linear A significant inverse linear correlation between malondialdehyde levels and natural antioxidant levels (vitamin C, vitamin E) was recorded. Lipid peroxidation products (conjugated dienes of fatty acids--initial, malondialdehyde--secondary) are significantly increased in groups of subjects with deficient levels of vitamin C (below the limit from antioxidative point of view), vitamin E and both vitamins, if compared to group with normal vitamin levels (over limit in accordance with antioxidative criterion). The results document that the deficiency in two key antioxidants for lipid peroxidation inhibition means the insufficient defense against free radicals and the increased lipid peroxidation.     

维生素E对二硫化碳致雄性大鼠睾丸组织脂质过氧化的拮抗作用

目的探讨二硫化碳(CS2)对雄性大鼠睾丸组织氧自由基及抗氧化水平的影响,同时观察维生素E(VE)对其的拮抗作用。方法取健康Wistar雄性大鼠36只随机分为6组,以不同浓度CS2(0、50、250、1250mgm3)静式吸入染毒,共10周,另设1250mgm3(CS2)加VE(250mgkg)组和单纯VE(250mgkg)组,VE拌入饲料中,染毒结束后,处死动物取出睾丸制备组织匀浆,分别测定各组SOD、MDA、GST、GSH、GSHpx、NO、总NOS和iNOS水平,同时检测VE对其的拮抗水平。结果睾丸组织中SOD活力下降,MDA含量上升,与对照组比较有显著差异(P<0.05);GSH含量、GST、GSHpx活力总体趋势下降,与对照组比较有显著差异(P<0.05或P<0.01);NO含量及总NOS、iNOS活力均下降,有随染毒浓度增加而降低的趋势,与对照组比较有显著差异(P<0.05或P<0.01)。但用VE干预后,SOD、GST、GSHpx、总NOS、iNOS活力均有不同程度上升,GSH、NO含量亦是如此,而MDA含量则下降。结论VE对CS2致睾丸组织脂质过氧化有拮抗作用。     

Protective effects of antioxidants against endrin-induced lipid peroxidation,glutathione depletion,and lethality in rats

Endrin depletes glutathione levels and induces lipid peroxidation in various species of animals. We have, therefore, examined the effect of antioxidants on these parameters in endrin-treated rats. Butylated hydroxyanisole (BHA), vitamin E, vitamin C, and the glutathione precursor cysteine significantly inhibited hepatic glutathione depletion and lipid peroxidation induced by 4 mg endrin/kg body weight. Furthermore, these antioxidants provided partial protection against lethality produced by 8 mg endrin/kg body weight. These results suggest but do not prove that free radical-mediated lipid peroxidation and glutathione depletion may be involved in the toxic manifestations of endrin.     

Effect of vitamin E,selenium and age on lipid peroxidation events in rat cerebrum

The effect of 8 and 20 weeks of dietary vitamin E (200 IU/kg diet) and/or selenium (0.2 ppm) supplementation or deficiency on oxidative processes in cerebrum of 1 and 15 month old male F344 rats was examined. After 8 weeks of treatment a 32-fold difference in plasma and a 3-fold difference in cerebrum alpha-tocopherol (a-T) level was found between vitamin E supplemented and deficient young rats. These differences were 1.8- and 1.5-fold, respectively, in old rats and increased to 8- and 2-fold differences, respectively, after an additional 12 weeks of treatment. Selenium deficiency had a significant effect on plasma glutathione peroxidase activity and a slight sparing effect on plasma a-T content. Endogenous lipid peroxides (thiobarbituric acid reactants present without incubation) in cerebrum were not correlated with a-T concentration or age. However, incubation of cerebrum homogenates with or without the addition of 0.1 mM Fe²⁺, 0.25 mM ascorbic acid, or 100 mg % acetaldehyde revealed that dietary vitamin E has a major role and selenium has a minor role in the protection against ex-vivo and possibly in vivo lipid peroxidation in cerebrum.     

Influence of amla (Emblica officinalis Gaertn.) on hypercholesterolemia and lipid peroxidation in cholesterol-fed rats

The effects of amla on low-density lipoprotein (LDL) oxidation and cholesterol levels were investigated in vitro and in vivo using Cu(2+)-induced LDL oxidation and cholesterol-fed rats. SunAmla and ethyl acetate (EtOAc) extract of amla significantly inhibited thiobarbituric acid (TBA)-reactive substance level in the Cu(2+)-induced LDL oxidation and the effects were stronger than those of probucol. In addition, the administration of SunAmla (at a dose of 20 or 40 mg/kg body weight/d) or EtOAc extract of amla (at a dose of 10 or 20 mg/kg body weight/d) for 20 d to rats fed 1% cholesterol diet significantly reduced total, free and LDL-cholesterol levels in a dose-dependent manner, and EtOAc extract of amla exhibited more potent serum cholesterol-lowering effect than SunAmla in the same amount. Furthermore, the oxidized LDL level in serum was markedly elevated in cholesterol-fed control rats as compared with normal rats, while it was significantly decreased by the administration of SunAmla or EtOAc extract of amla. Moreover, the serum TBA-reactive substance level was also significantly decreased after oral administration of SunAmla or EtOAc extract of amla. These results suggest that amla may be effective for hypercholesterolemia and prevention of atherosclerosis.     

Effect of the joint administration of selenium and vitamin E in combination with regular aerobic exercise on markers of lipid peroxidation and glutathione peroxidase in diabetic rats

We investigated the effect of long-term treatment (6 wk) with selenium and vitamin E, in combination with aerobic exercise training, on malondialdehyde (MDA), oxidized low-density lipoprotein (ox-LDL), and glutathione peroxidase (GPx) in STZ-induced diabetic rats. The rats were assigned randomly to one of three treatment groups (n = 12 per group); 1) exercise group (EX), 2) selenium/vitamin E/exercise group (SVE), and 3) selenium/vitamin E group (SV). To estimate the acute effect of exercise, a 30-min endurance exercise was used. The MDA concentration was significantly lower in the SVE. The ox-LDL was significantly lower in the SVE and SV. The hepatic concentrations of selenium and vitamin E were significantly higher in the SVE. These results indicate that the increase in MDA is mildly attenuated in rats that were aerobically trained. Moreover, the joint administration of selenium and vitamin E with or without exercise training reduces the levels of ox-LDL.     

Vitamin E reduces lipid peroxidation in experimental hepatotoxicity in rats

Background and aims Lipid peroxidation is believed to be involved in the pathophysiology of a number of diseases and in the process of aging. This study investigates the effects of dietary supplementation with vitamin E (20 g/kg diet of all-rac-α-tocopheryl succinate for 3 weeks) on both non-enzymatic and enzymatic lipid peroxidation in experimental rats with carbon tetrachloride (CCl₄)-induced hepatotoxicity (2.5 mL/kg body). Methods Plasma, urine and liver samples from control rats (n = 6), CCl₄-treated rats (n = 6), and rats supplemented with vitamin E prior to CCl₄ treatment (n = 8) were collected. Non-enzymatic lipid peroxidation induced by free radicals was investigated by measurement of a major F₂-iso-prostane, 8-iso-prostaglandin F_2α (8-iso-PGF_2α). Cyclooxygenase-catalyzed enzymatic lipid peroxidation was measured with a major PGF_2α metabolite, 15-kto-13,14-dihydro-prostaglandin F_2α (15-K-DH-PGF_2α). Malondialdehyde and antioxidants in plasma were also quantified. Results CCl₄ treatment alone resulted in significantly higher levels of plasma, urinary and liver 8-iso-PGF_2α, and of plasma and urinary 15-K-DH-PGF_2α compared to controls. Rats supplemented with vitamin E prior to CCl₄ treatment had significantly lower levels of urinary and liver 8-iso-PGF_2α, urinary 15-K-DH-PGF_2α, and plasma malondialdehyde than rats treated with CCl₄ alone. However, plasma 8-iso-PGF_2α and plasma 15-K-DH-PGF_2α were not affected by vitamin E supplementation. Conclusion Thus, both non-enzymatic and enzymatic lipid peroxidation during experimental hepatic oxidative injury were suppressed by dietary vitamin E supplementation in rats. Received: 29 May 2000, Accepted: 16 November 2000     

Endotoxin and lipid peroxidation in vivo in selenium- and vitamin E-deficient and -adequate rats

The effect of Salmonella typhimurium endotoxin injected intraperitoneally (0.5 mg/kg body weight) on lipid peroxidation in vivo was assessed. Peroxidation was monitored by measuring ethane production, an autoxidation product of (n-3) unsaturated fatty acids. Weanling rats were fed a selenium- and vitamin E-deficient basal diet or one supplemented with 0.2 mg Se/kg and/or 200 mg vitamin E/kg. After 11 to 13 wk of feeding, ethane production was tripled in LPS-treated Se- and vitamin E-deficient rats compared to saline-treated deficient rats. In both doubly deficient and adequate rats, LPS increased ethane production, but it did so to a greater extent in Se- and vitamin E-deficient rats. Dietary Se or vitamin E supplementation alone significantly reduced ethane production from LPS-treated rats. Vitamin E was more protective than Se against LPS-induced lipid peroxidation. Escherichia coli and Salmonella minnesota LPS also increased ethane production in Se- and vitamin E-deficient rats. These results show that low doses of LPS stimulate lipid peroxidation in vivo in Se- and vitamin E-deficient rats.     

Interactive effect of hesperidin and vitamin E supplements on cholesterol metabolism in high cholesterol-fed rats

Certain bioflavonoids are potent antioxidants and have pharmacologic effects similar to those of vitamin E. Accordingly, the interactive effect of hesperidin and vitamin E was studied with respect to cholesterol metabolism and the antioxidant status. Hesperidin supplement (0.1%, wt/wt) with comparable levels of vitamin E was provided with a high-cholesterol (1%, wt/wt) diet to rats for 5 weeks. The amount of vitamin E included in the hesperidin-free and hesperidin diets was either a low (low-E) or a normal (normal-E) level. The hesperidin supplement and different levels of dietary vitamin E did not significantly alter the concentrations of plasma triglycerides. However, the inclusion of hesperidin significantly lowered the concentration of plasma cholesterol in both the low-vitamin E group and the normal-vitamin E group compared to the hesperidin-free groups (p < 0.05). The hepatic triglyceride content was significantly lowered by the hesperidin supplement, as opposed to the plasma triglyceride content, regardless of the vitamin E level in the diet. The hepatic HMG-CoA reductase activity was significantly lowered by the hesperidin supplement with both the low-vitamin E and the normal-vitamin E compared to the hesperidin-free groups (p < 0.05). The hepatic HMG-CoA reductase activity was also significantly lowered with an increase in the dietary vitamin E within the hesperidin and hesperidin-free groups. The excretion of fecal neutral sterol and acidic sterols tended to be lower with the hesperidin supplement. Neither dietary hesperidin nor vitamin E significantly changed the hepatic antioxidant enzyme activity. This data indicates that hesperidin lowers the concentration of plasma cholesterol and the hepatic triglyceride content regardless of the dietary vitamin E level. However, the concentration of plasma cholesterol in the hesperidin-free groups was dependent on the dietary vitamin E level. This information may contribute to understanding the interactive effect of hesperidin and vitamin E on cholesterol biosynthesis in high cholesterol-fed rats.     

实验性高脂血症大鼠的血硒、维生素E、GSH－Px及脂质过氧化物的改变

采用幼年ＳＤ雄性大鼠３０只，随机分成３组，分别饲喂基础饲料，猪油饲料（１０％猪油和１．５％胆固醇）和玉米油饲料（１０％玉米油和１．５％胆固醇）。９周后，玉米油组和猪油组的大鼠形成高脂高胆固醇血症，第１０周处死动物，取血测定全血硒（Ｓｅ），谷胱甘肽过氧化物酶（６ＧＳＨ－Ｐｘ），血清维生素Ｅ（ＶＥ）和脂质过氧化物（ＬＰＯ）含量。结果由猪油和玉米油诱导的高血脂大鼠血Ｓｅ水平低于基础饲料组的大鼠，基础组、猪油组和玉米油组的血Ｓｅ值分别为０．０９６、０．０８１和０．０８０ｍｇ／Ｌ，而且随着饲养时间的延长，血Ｓｅ趋于下降，但各组间的差异无显著性意义。基础组和猪油组大鼠的ＧＳＨ－Ｐｘ活性分别为２０．０４和２１．０１ｍｍｏｌ／（ｍｉｎ．Ｌ），而玉米油组最低，仅为１１．０８ｍｍｏｌ／（ｍｉｎ．Ｌ），玉米油组与基础组和猪油组之间呈极显著差异（Ｐ＜０．０１）。血清ＬＰＯ含量在各组之间未观察到显著性差异（基础组１７．５８，猪油组１７．４４，玉米油组１７．７３μｍｏｌ／Ｌ）。但值得注意的是玉米油组的ＧＳＨ－Ｐｘ／ＬＰＯ比值为０．６３，明显低于基础组（１．１３）和猪油组（１．１９），说明玉米油组大鼠体内抗氧化能力减弱。猪油组血清ＶＥ浓?     

维生素C和维生素E对糖尿病大鼠非酶糖化和过氧化反应的影响

以链脲佐菌素腹腔注射ＳＤ大鼠建立糖尿病动物模型，在纯营养素饲料配方中补充维生素Ｃ和／或维生素Ｅ，喂饲周，观察单独或联合补充维生素Ｃ、维生素Ｅ对糖尿病非酶糖化及过氧化的干预作用。结果显示维生素Ｃ和Ｅ联合补充可显著减少糖尿病大鼠血红蛋白、低「密度脂蛋白及肾脏皮质的糖化终产物（ＡＧＥｓ）含量，同时显著降低脂质过氧化产物丙二醛（ＭＤＡ）水平，单独补充维生素Ｃ或维生素Ｅ能显著降低糖尿病鼠血清及肾脏ＭＤＡ含量     

Effects of vitamin E-enriched egg yolk on lipid peroxidation, hemolysis and serum lipid concentration in young and old rats

Effects of a diet containing different amount of vitamin E-enriched egg yolk powder on lipid peroxidation, hemolysis, and serum lipid concentration were examined in young and old rats. Young and old rats were fed experimental diets containing 5.6% or 22.5% of normal egg yolk powder, and 5.6% or 22.5% of vitamin E-enriched egg yolk powder. When young rats were fed these diets, their tocopherol concentrations in testes, heart, kidneys, and retroperitoneum fat pads increased according to the diet tocopherol contents. Lipid peroxide levels in these tissues were inversely proportional to the tocopherol concentrations. The liver and serum, however, did not show the above relationship. In the rats fed vitamin E-enriched egg yolk diets hemolysis did not increase, in contrast to those fed normal egg yolk diets. The rats fed a 5.6% vitamin E-enriched egg yolk diet had a lower serum cholesterol level than those fed a normal egg yolk diet. In old rats, one control group was used to determine initial tocopherol concentration and two other groups were fed 5.6% normal and vitamin E-enriched egg yolk diets. The vitamin E-enriched egg yolk rats showed lower weights of the body, liver, and retroperitoneum fat pads at the end of the experiment. The normal egg yolk group had atrophied testes. The tissue and serum tocopherol concentrations were increased in the vitamin E-enriched egg yolk group, whereas they were decreased in the normal egg yolk group. In the vitamin E-enriched egg yolk group, lipid peroxide, hemolysis and serum cholesterol, especially HDL-cholesterol, did not increase. These results indicate that egg yolk tocopherol was absorbed and prevented lipid peroxidation and hemolysis in young and old rats, and testes atrophy in old rats.     

Hypocholesterolemic effect of vitamin E on cholesterol-fed rabbit

Serum cholesterol level increased sharply in rabbits fed an atherosclerosis-promoting diet containing 0.25% or 0.5% cholesterol. Oral supplementation with 2100 IU of vitamin E per week manifested a hypocholesterolemic effect only after four weeks, with 50% reduction attained on the 8th week. Changes in low density and very low density lipoprotein cholesterol levels paralleled those in the serum. Liver total cholesterol level and the ratio of free to ester forms were not different between vitamin E-supplemented and nonsupplemented rabbits, whereas a 4-5 fold increase in hepatic cholesterol-7 alpha-hydroxylase activity, elevation of bile salt concentration and improvement in bile lithogenic index were observed in the vitamin E-supplemented groups.     

Effect of vitamin E on lipid parameters in ovariectomized rats

The risk of cardiovascular disease drastically increases at the onset of menopause, in part, because of rise in blood cholesterol and unfavorable changes in lipid profile. This study was designed to investigate the dose-dependent effects of vitamin E supplementation on lipid parameters in ovariectomized (ovx) rats. Sixty 12-month-old female Sprague-Dawley rats were either sham-operated (sham; one group) or ovx (four groups). All rats were maintained on a semipurified caseinbased diet (AIN-93M; 75 IU vitamin E/kg of diet) for a period of 120 days. Thereafter, ovx rats were placed on one of four doses of vitamin E treatment (75, 300, 525, or 750 IU vitamin E/kg of diet), while the sham group was continued on 75 IU vitamin E/kg of diet for 100 days. Ovariectomy tended to increase (by 24%, P = 0.1) serum non?high-density lipoprotein (HDL) cholesterol and decrease (by 14%, P = 0.1) HDL cholesterol. Vitamin E did not have any significant effects on serum lipid parameters. Liver total lipids were notably increased (P < .001) in ovx animals, and supplementation with vitamin E at 525 IU/kg of diet was able to significantly reduce liver total lipids by 13%. Additionally, ovariectomy caused an increase in serum glucose and liver C18:1 fatty acid concentrations along with decreases in C18:0, C20:4, and C22:6 fatty acid concentrations. These alterations on liver fatty acid profiles were unaffected by vitamin E. The findings of this study suggest that vitamin E supplementation moderately improves lipid parameters in ovarian hormone-deficient rats.