Investigations into combined dietary deficiencies of copper,selenium, and vitamin E in the rat

Interactions between dietary Cu, Se, and vitamin E in ascorbate-induced hemolysis of erythrocytes obtained from rats fed diets deficient or adequate in these elements were investigated. Hemolysis was affected by all three dietary factors, through closely interrelated but distinct mechanisms. In vitamin E-deficient cells, hemolysis was increased and the amount of hemolysis was directly related to the amount of hemoglobin breakdown. Deficiency of Cu or Se decreased hemolysis, but only in vitamin E-deficient cells. Vitamin E did not affect the breakdown of hemoglobin, but Cu and Se did. Hemolysis and hemoglobin breakdown were decreased by the addition of glucose, through mechanisms independent of that involving reduced glutathione metabolism. These results suggest that vitamin E acts within erythrocyte membranes to prevent products of hemoglobin breakdown from initiating peroxidation and subsequent hemolysis. Effects of Cu and Se are linked with that of vitamin E by the involvement of glutathione peroxidase and Cu superoxide dismutase in the cytoplasmic breakdown of hemoglobin, rather than by a direct effect of these enzymes on lipid peroxidation. It is concluded that the erythrocyte, because of its high heme content, probably represents a special system in terms of peroxidative pathways, and these findings may not be directly applicable to other tissues.     

Influence of dietary selenium and vitamin E on the levels of fatty acids in brain and liver tissues of lambs

In this study, the effects of dietary vitamin E, selenium, and their combination on the levels of fatty acid composition of the brain and liver tissues were examined. In brain tissue, the amounts of most fatty acids increased in vitamin E, combination and selenium groups compared with control group values. While the proportions of myristic, pentadecanoic, palmitic, linoleic, and total saturated fatty acids were decreased in vitamin E, Se and combination groups, eicosapentaenoic, total unsaturated and MUFA were increased in the same groups. In addition, the proportions arachidonic, eicosapentaenoic, total unsaturated, ω6 and MUFA in the combination group were higher than in the control group. In liver tissue, the amounts of myristic, pentadecanoic, palmitic, eicosedienoic, eicosapentaenoic, docosahexaenoic, ω3 and PUFA were higher in the combination group than in the control group. Also the proportions of eicosapentaenoic, docosahexaenoic acids in supplemented groups were higher than those in the control group. We conclude that dietary vitamin E and selenium have an influence on the levels of fatty acids in the brain and liver. Copyright © 1999 John Wiley & Sons, Ltd.     

Protective role of supplemental vitamin E and selenium on lipid peroxidation, vitamin E, vitamin A, and some mineral concentrations of Japanese quails reared under heat stress

This study was conducted to determine the effects of vitamin E and selenium (Se) on lipid peroxidation (MDA), serum and liver concentration of antioxidant vitamins, and some minerals of Japanese quails reared under heat stress (34°C). One hundred twenty 10-d-old Japanese qualis (60 males, 60 females) were randomly assigned to 4 treatment groups, 3 replicates of 10 birds each. The experiment was designed in a 2×2 factorial arrangement using two levels of vitamin E (125 and 250 mg/kg of diet) and two levels of selenium (0.1 and 0.2 mg/kg of diet). Greater dietary vitamin E and selenium inclusions resulted in a greater (p=0.001) serum vitamin E and vitamin A, but lower (p=0.001) MDA concentrations. Liver vitamin E and vitamin A concentrations increased (p=0.001) and MDA concentrations decreased (p=0.001) when both dietary vitamin E and selenium increased. No interactions between vitamin E and selenium were detected (p≥0.11) for any parameters. Increasing both dietary vitamin E and selenium caused an increase in serum concentrations of Fe and Zn (p=0.001), but a decrease in serum concentration of Cu (p=0.001). Results of the present study showed that dietary vitamin E and selenium have synergistic effects and that supplementing a combination of dietary vitamin E (250 mg/kg of diet) and selenium (0.2 mg/kg of diet) offers a good management practice to reduce heat stress-related depression in performance of Japanese quails.     

Effect of vitamin E and selenium supplementation of cockerel diets on glutathione peroxidase activity and lipid peroxidation susceptibility in sperm, testes, and liver

The phospholipids of avian spermatozoa are characterized by high proportions of arachidonic (20:4n-6) and docosatetraenoic (22:4n-6) fatty acids and are therefore sensitive to lipid peroxidation. α-Tocopherol and glutathione peroxidase [GSH-Px] are believed to be the primary components of the antioxidant system of the spermatozoa. The present study evaluates the effect of vitamin E and vitamin E plus Se supplementation of the cockerel diet on GSH-Px activity, vitamin E accumulation, and lipid peroxidation in the spermatozoa, testes, and liver. At the beginning of the experiment 75 Rhode Island Red cockerels were divided into five groups, kept in individual cages, and fed a wheat-barley-based ration balanced in all nutrients. Supplements fed to the different groups were as follows: vitamin E, 0, 20, 200, 20, and 200 mg/kg to groups 1–5, respectively, with groups 4 and 5 also receiving 0. 3 mg Se/kg. The vitamin E supplementation produced increased levels of α-tocopherol in semen, testes, and liver. The inclusion of the Se into the cock diet had a significant (P < 0.01) stimulating effect on GSH-Px activity in seminal plasma, spermatozoa, testes, and liver. The increased vitamin E concentration in the spermatozoa was associated with a reduction in their susceptibility to lipid peroxidation. Similarly, the increased GSH-Px activity provided enhanced protection against lipid peroxidation.     

Effects of high-fat,low-cholesterol diets on hepatic lipid peroxidation and antioxidants in apolipoprotein E-deficient mice

The present study describes the effects of several high-fat low-cholesterol antiatherogenic diets on the hepatic lipid peroxidation and hepatic antioxidant systems in apolipoprotein E-deficient mice. Eighty mice were distributed into five groups and fed with regular mouse chow or chow supplemented with coconut, palm, olive and sunflower seed oils. After ten weeks, they were sacrificed and the livers were removed so that lipid peroxidation and -tocopherol concentrations, and superoxide dismutase, glutathione peroxidase and glutathione reductase activities could be measured. The size of the atherosclerotic lesions in the aortas was also measured. Results showed that the diets supplemented with olive oil, palm oil or sunflower seed oil significantly decreased the size of the lesion. However, there was an association between those mice that were on diets supplemented with palm or coconut oils and a significant increase in hepatic lipid peroxidation. This association was not found in animals fed with olive or sunflower seed oils, the diets with the highest content of vitamin E. The dietary content of vitamin E was significantly correlated (r = 0.98; p < 0.05) with the hepatic concentration of this compound. Our study suggests that the high content of vitamin E in olive oil or sunflower seed oil may protect from the undesirable hepatotoxic effects of high-fat diets in apo E-deficient mice and that this should be taken into account when these diets are used to prevent atherosclerosis.     

Protective role of intraperitoneally administered vitamin E and selenium in rats anesthetized with enflurane

The aim of this investigation was to determine levels of liver vitamins A and E and blood biochemical and hematological parameters in the enflurane anesthesia of rats. Fifty adult male Wistar rats were used in this study. All rats were randomly divided into five groups. The first and second groups were used as the control and anesthesia control groups, respectively, and only the placebo was intraperitoneally injected. The third group was intraperitoneally administered with vitamin E (dl/-α-tocopheryl acetate, 100 mg/kg body weight), the fourth group with Se (Na₂SeO₃ 1.5 mg/kg body weight), and the fifth group with vitamin E and Se (dl-α-tocopheryl acetate, 100 mg/kg body weight + Na₂SeO₃ 1.5 mg/kg body weight). This administration was done for three times with overday intervals and the second, third, forth, and fifth group rats were taken to enflurane anesthetise for 2 h. The liver vitamin E level was slightly lower in the anesthesia control group than in control group. However, the liver vitamin E content was significantly (p < 0.05 andp < 0.01) increased in vitamin E, Se, and combination groups, whereas the vitamin A level in liver was not statistically different. In general, plasma levels of alanine aminotransferase, creatin kinase, total bilirubin, urea, red blood cell counts, packet cell volume, and hemoglobulin values were significantly (p < 0.05 andp < 0.001) increased during the anesthesia and returned to near control values after the vitamin E plus selenium injection. However, administration of vitamin E had less effect on the hematological and biochemical parameters compared to that of selenium and their combination with vitamin E. However, the white blood cell count and levels of alkaline phosphatase, aspartate aminotransferase, total cholesterol, triglycerides, total protein, and creatinine were not statistically influenced by the anesthesia. In conclusion, we observed that plasma levels of some enzymes and metabolites were significantly increased in the enflurane anesthesia of rats, whereas the liver vitamin E levels were slightly decreased. Therefore, we observed that vitamin E and selenium have a protective effect against anesthesia complication, but the effect of selenium appears to be much greater than the vitamin E.     

Relationship between elevated lipid peroxides,vitamin E deficiency and hypertension in preeclampsia

Preeclampsia or pregnancy-induced hypertension is a major cause of both maternal and fetal-neonatal morbidity and mortality. The deficiency of vitamin E can cause accumulation of lipid peroxidation products, which, in turn, can induce vasoconstriction. This study has examined any evidence of increased cellular lipid peroxidation and accumulation of malonydialdehyde (MDA, an end product of lipid peroxidation) in pregnancy-induced hypertension and any relationship between the elevated MDA and lower vitamin E levels with hypertension in pregnant women. EDTA-Blood was collected from pregnant women at the time of delivery. Plasma vitamin E was determined by HPLC; MDA by the thiobarbituric acid-reactivity. Subjects with diastolic blood pressure(DBP) 90 mm Hg were considered hypertensive (HT) and with <90 mm Hg normotensive (NT). Data (Mean±SE) from 49 NT and 11 HT women show that HT has significantly lower vitamin E (22±1 vs 27±1 nmole/ml, p<0.03) and elevated MDA levels (0.56±0.06 vs 0.43±0.02 nmole/ml, p<0.03) compared to NT; the ages and gestational ages of women were similar. Among all women, there was a significant positive relationship between DBP and MDA levels (r=0.27, p<0.05), and a significant negative relationship between vitamin E levels and DBP (–0.36, p<0.005), and a significant negative relationship between MDA and vitamin E levels (r=–0.27, p<0.05). Thus, HT women's plasma has significantly lower E and higher MDA levels, and DBP significantly correlates with the extent of vitamin E deficiency and increased MDA levels. This study suggests a relationship between elevated lipid peroxidation and lower vitamin E levels and hypertension in pregnancy (preeclampsia).     

Eicosanoid production in experimental alcoholic liver disease is related to vitamin E levels and lipid peroxidation

We investigated the association between vitamin E, lipid peroxidation and eicosanoid production in experimental alcoholic liver injury. We used the intragastric feeding rat model in which animals were fed corn oil and ethanol (CO+E) and corn oil and dextrose (CO+D) for 2 and 4 week periods. At sacrifice, we measured plasma levels of alpha-tocopherol, 8-isoprostane, thromboxane B₂(TXB₂) and 6-ketoprostaglandin F₁(6-KetoPGF₁). Animals fed CO+E had significantly lower concentrations of -tocopherol and higher concentrations of 8 isoprostane at both 2 and 4 weeks. a significant inverse correlation was seen between -tocopherol concentrations and the TXB₂: PGF₁ ratio (r=0.72, p<0.01). A positive correlation was seen between the TXB₂: PGF₁ ratio and 8 isoprostane levels (r=0.84, p<0.001). These results suggest that vitamin E depletion and enhanced lipid peroxidation may affect eicosanoid metabolism in experimental alcoholic liver disease in such a way so as to increase the thromboxane to prostacyclin ration.Abbreviations PGH₂ Prostaglandin H₂ - PGL₂ Prostacyclin - CO+E Corn Oil and Ethanol - CO+D Corn Oil and Dextrose - TXB₂ Thromboxane B₂ - TXA₂ Thromboxane A₂     

Effects of intraperitoneally‐administered vitamin E and selenium on the blood biochemical and haematological parameters in rats

The aim of this work was to determine the role of intraperitoneally‐administered vitamin E and selenium on the biochemical and haematological parameters in the blood of rats. Thirty‐two adult male Wistar rats were used in this study. All rats were randomly divided into four groups. The first group was used as the control. The second group was intraperitoneally administered with vitamin E (±‐α‐tocopheroryl acetate, 10 mg day⁻¹), the third group with Se (Na₂SeO₃ 0·2 mg over a day), and the fourth group with vitamin E and Se (vitamin E 10 mg + Na₂SeO₃ 0·2 mg over a day). This administration was done for 5 weeks. Blood samples were taken from animals at the end of the dosage period and biochemical parameters in serum samples and haematological parameters in total blood were determined. The levels of total cholesterol (p<0·01) and number of white blood cells (p<0·001) in blood were significantly higher in the vitamin E group than in the control group. The levels of ALP, total cholesterol (p<0·01) and number of white blood cells (p<0·01) in blood were significantly higher in the selenium group than in the controls. The levels of glucose (p<0·05), ALP (p<0·01), total cholesterol (p<0·001) and number of white blood cells (p<0·01) were higher in the vitamin E and selenium combined group than in the controls. Other parameters considered within this trial (ALT, LDH, creatinine, albumin, total protein, amylase, creatine kinase, HDL, triglycerides, total lipid, sodium, chloride, uric acids, red blood cell, haemoglobin, packed cell volume, MCV, MCH, MCHC) did not show statistically significant differences between the control and injected groups. The results indicated that blood glucose and total cholesterol levels, ALP activity and white blood cell counts were significantly increased by intraperitoneal administration of vitamin E and selenium in rats. Copyright © 1999 John Wiley & Sons, Ltd.     

Influence of dietary vitamin E (DL-alpha-tocopheryl acetate) and diludine (diethyl 1,4-dihydro-2,6-dimethyl-3,5-pyridinedicarboxylate) levels on growth and lipid peroxidation in rainbow trout,Oncorhynchus mykiss

We aimed to investigate the influence of dietary vitamin E and diludine on growth and lipid peroxidation (malondialdehyde; MDA) in rainbow trout. Fish (1.5 g) were fed different dietary levels of vitamin E (0, 50 and 100 mg/kg) and diludine (0, 0.5 and 1 g/kg) for 10 weeks. Growth performance and feed conversion ratio (FCR) were significantly affected by dietary vitamin E (p < .05) but not diludine. Fish fed 50 mg/kg dietary vitamin E with no diludine had significantly better growth and lower FCR than those fed vitamin E free diets. Liver vitamin E content was significantly influenced by dietary vitamin E and diludine (p < .05). The highest hepatic vitamin E was in fish fed the highest dietary vitamin E and diludine levels. Hepatic MDA level was significantly affected by dietary vitamin E and diludine (p < .05), decreasing with the increase in both dietary vitamin E and diludine. According to our results, diludine had no significant effect on growth; however, decreased hepatic lipid peroxidation independent of vitamin E. Our results reveal that 50 mg/kg vitamin E content is suitable for optimal growth and FCR in rainbow trout juveniles. However, dose dependent effects of dietary diludine remain uncertain and need further researches.     

Protective role of intraperitoneally administered vitamin E and selenium on the antioxidative defense mechanisms in rats with diabetes induced by streptozotocin

The aim of this work was to determine the protective effects of intraperitoneally administered vitamin E and selenium (as Na₂SeO₃, Se) on the lipid peroxidation as thiobarbituric acid reactive substances (TBARS) and vitamin E levels, glutathione peroxidase (GSH-Px), reduced glutathione (GSH) activities in the plasma, red blood cell (RBC), liver, and muscle of rats with streptozotocin-induced diabetes. Fifty adult male Wistar rats were used and all rats were randomly divided into five groups. The first group was used as a control and the second group as a diabetic control. A placebo was given to first and second groups by injection. The third group was intraperitoneally administered with vitamin E (20 mg over 24 h), the fourth group with Se (0.3 mg over 24 h), and the fifth group with vitamin E and Se combination (COM) (20 mg vitamin E + 0.3 mg Se over 24 h). This administration was done for 25 days and the TBARS, vitamin E, GSH-Px, GSH levels in the plasma, RBC, liver, and muscle samples were determined. The vitamin E level in the plasma and liver was significantly (p < 0.05) higher in the control than in the diabetic control group. Also, the TBARS levels in the RBC, liver, and muscle were significantly (p < 0.05) lower in the control than in the diabetic control group. However, GSH-Px and GSH activities in RBC, liver, and muscle were not statistically different between the control and the diabetic control groups. The vitamin E levels in plasma and liver (p < 0.01 and p < 0.001) and GSH-Px activities (p < 0.01, p < 0.001) in RBC were significantly higher in vitamin E, Se, and COM groups than in both control and diabetic control groups. However, the TBARS levels of RBC, muscle, and liver in vitamin E and Se administered groups were significantly (p < 0.05-p < 0.001, respectively) decreased. These results indicate that intraperitoneally administered vitamin E and Se have significant protective effects on the blood, liver, and muscle against oxidative damage of diabetes. The abstract of this study was presented in Physiological Research 48(Suppl. 1), S99 (1999).     

Protective role of intraperitoneally administrated vitamin E and selenium on the levels of total lipid,total cholesterol,and fatty acid composition of muscle and liver tissues in rats

The aim of this work was to determine the protective effects of intraperitoneally administrated vitamin E and Se on total lipid, total cholesterol, and fatty acid composition of rat liver and muscle tissues. Total lipid content of muscle tissue in Se and combination groups decreased as compared to the control group. However, the level of total lipid in the liver tissues was seen to decrease only in the combination group (P < 0.05). While the amount of total cholesterol in liver tissue was lower (P < 0.05) in the vitamin E and combination groups, the amount of total cholesterol in muscle tissue decreased (P < 0.05) in the combination group. The amount of linoleic acid in muscle tissue slightly decreased (P < 0.05), whereas the eicosenoic and eicosatrienoic acid amounts significantly increased (P < 0.01, P < 0.001) in the vitamin E group as compared to the control group. The amounts of most fatty acid decreased (P < 0.05) in the combination group. The proportions of eicosenoic, eicosatrienoic, and total polyunsaturated fatty acid (PUFA) within the total fatty acid were higher (P < 0.05) in vitamin E group, whereas these fatty acids proportions were lower (P < 0.05) in the Se group. Although the proportions of palmitic, linolenic, and total saturated fatty acids were low (P < 0.05), oleic and total unsaturated fatty acid proportions were higher (P < 0.05) in the combination group than in the control group. The amount of palmitic acid and total saturated fatty acid in liver tissue decreased (P < 0.01 and P < 0.05, respectively) in the vitamin E and combination groups. However, the amount of linoleic acid only decreased (P < 0.05) in the combination group. The amount of PUFA was slightly higher (P < 0.05) in vitamin E. The proportions of stearic acid and linoleic acid decreased (P < 0.05) both in the Se and combination groups. However, the proportions of eicosatrienoic, ω 6, and PUFA were slightly higher (P < 0.05) in the vitamin E group, but total saturated fatty acid proportion significantly decreased (P < 0.01) in both the vitamin E and combination groups. In conclusion, the level of total lipid and cholesterol in muscle and liver tissues were reduced by administrating vitamin E and Se together. Additionally, the fatty acid synthesis in the muscle and liver tissues was decreased by this process. However, it was observed that the protective effect of intraperitoneally administrated vitamin E was higher than Se on fatty acid composition in muscle and liver tissues. J. Cell. Biochem. 64:233–241. © 1997 Wiley-Liss, Inc.     

Ascorbate-Fe2+ lipid-peroxidation of rat liver microsomes: Effect of vitamin E and cytosolic proteins

In the present study, we examined the effect of the intraperitoneal administration of vitamin E (100 mg/kg weight/24 h) on ascorbate (0.4 mM) induced lipid peroxidation of rat liver microsomes . We also analyzed the effect of hepatic cytosolic proteins on this process. The results indicate that the ascorbate induced light emission was 76% lower in microsomes (1 mg protein) obtained from vitamin E treated animals when compared with controls. In the presence of cytosolic protein (1 mg) the chemiluminescence of control microsomes diminished 55.8 and 59.5% when cytosol from controls and treated animals was used, respectively. The chemiluminescence of vitamin E microsomes diminished 25.03 and 22.08% when both types of cytosol were added to the medium. Dialyzed or treated at 70°C cytosol was also able to inhibit the lipid peroxidation of either control or vitamin E rat liver microsomes. By means of gas chromatography we analyzed the fatty acid composition of native and peroxidated microsomes from both animal groups. The peroxidation affected principally arachidonic acid and its diminution was more evident in the control microsomes than in the microsomes from the vitamin E treated group. By HPLC we analyzed the vitamin E content in all subcellular fractions employed. In microsomes from the vitamin E-group, the content of vitamin was 11 times higher than in the control ones (0.678 ± 0.1038 vs. 0.062 ± 0.0045 g -tocopherol/mg protein, respectively), while levels in the cytosol from the vitamin E-group were only 2 times higher than in the control cytosol (0.057 ± 0.0051 vs. 0.025 ± 0.0015 g -tocopherol/mg protein, respectively).     

The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat heart and ameliorating role of vitamin E and vitamin C

Diazinon is one of the most widely used organophosphate insecticides (OPIs) in agriculture and public health programs. Reactive oxygen species (ROS) caused by OPIs may be involved in the toxicity of various pesticides. The aim of this study was to investigate how diazinon affects lipid peroxidation (LPO) and the antioxidant defense system in vivo and the possible ameliorating role of vitamins E and C. For this purpose, experiments were done to study the effects of DI on LPO and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in adult rat heart. Experimental groups were: (1) control group, (2) diazinon treated (DI) group, (3) DI+vitamins E and C-treated (DI+Vit) group. The levels of malondialdehyde (MDA) and the activities of SOD and CAT increased significantly in the DI group compared with the control group. The activity of SOD and the levels of MDA decreased significantly in the DI+Vit group compared with the DI group. The differences between the DI+Vit and control groups according to the MDA levels and the activities of both SOD and CAT were statistically significant. These results suggest that treating rats with a single dose of diazinon increases LPO and some antioxidant enzyme activities in the rat myocardium and, in addition, that single-dose treatment with a combination of vitamins E and C after the administration of diazinon can reduce LPO caused by diazinon, though this treatment was not sufficiently effective to reduce the values to those in control group.     

A comparative study on effect of dietary selenium and vitamin E on some antioxidant enzyme activities of liver and brain tissues

Since selenium and vitamin E have been increasingly recognized as an essential element in biology and medicine, current research activities in the field of human medicine and nutrition are devoted to the possibilities of using these antioxidants for the prevention or treatment of many diseases. The present study was aimed at investigating and comparing the effects of dietary antioxidants on glutathione reductase and glutathione peroxidase activities as well as free and protein-bound sulfhydryl contents of rat liver and brain tissues. For 12–14 wk, both sex of weanling rats were fed a standardized selenium-deficient and vitamin E-deficient diet, a selenium-excess diet, or a control diet. It is observed that glutathione reductase and glutathione peroxidase activities of both tissues of the rats fed with a selenium-deficient or excess diet were significantly lower than the values of the control group. It is also shown that free and bound sulfhydryl concentrations of these tissues of both experimental groups were significantly lower than the control group. The percentage of glutathione reductase and glutathione peroxidase activities of the deficient group with respect to the control were 50% and 47% in liver and 66% and 61% in the brain, respectively; while these values in excess group were 51% and 69% in liver and 55% and 80% in brain, respectively. Free sulfhydryl contents of the tissues in both experimental groups showed a parallel decrease. Furthermore, the decrease in protein-bound sulfhydryl values of brain tissues were more pronounced than the values found for liver. It seems that not only liver but also the brain is an important target organ to the alteration in antioxidant system through either a deficiency of both selenium and vitamin E or an excess of selenium alone in the diet.     

The effect of selenium and vitamin E on microvascular permeability of rat organs

The effects of dietary sodium selenite and vitamin E on the microvascular permeability of rat organs such as heart, brain, kidney, liver and eye were investigated by using the Evans blue leakage method. Combined deficiency of selenium and vitamin E caused an increase in the permeability of the heart and eye with respect to their controls while it had no considerable effect on the permeability of other organs. On the other hand, toxic levels of selenium (4.2 mg/kg) in diet decreased the permeabilities in kidney, liver, and eye whereas this parameter of brain increased in the same animal group. These results suggested that low or high sodium selenite and vitamin E contents in diet could alter the microvascular permeability of different organs in different manners. It might be important to give reasonable explanations for the pathophysiology of some diseases that are characterized with organ damage and /or disfunction originated from selenium deficiency or toxicity.     

Effects of dietary vitamin E and selenium on antioxidative defense mechanisms in the liver of rats treated with high doses of glucocorticoid

The aim of this work was to determine the effects of dietary intake vitamin E and selenium (Se) on lipid peroxidation as thiobarbituric acid reactive substances (TBARS) and on the antioxidative defense mechanisms in the liver of rats treated with high doses of prednisolone. Two hundred fifty adult male Wistar rats were randomly divided into five groups. The rats were fed a normal diet, but groups 3, 4, and 5 received a daily supplement in their drinking water of 20 mg vitamin E, 0.3 mg Se, and a combination of vitamin E and Se, respectively, for 30 d. For 3 d subsequently, the control group (group 1) was treated with a placebo, and the remaining four groups were injected intramuscularly with 100 mg/kg body weight (BW) prednisolone. After the last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48 h and the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) enzymes and the levels of glutathione (GSH) and TBARS in their livers were measured. GSH-Px, SOD, and CAT enzyme activities and GSH levels in prednisolone-treatment group (group 2) began to decrease gradually at 4 h, falling respectively to 38%, 55%, and 40% of the control levels by 24 h, and recovering to the control levels at 48 h. In contrast, prednisolone administration caused an increase in the hepatic TBARS, reaching up to four times the levels of the control at 24 h. However, supplementation with vitamin E and Se had a preventive effect on the elevation of the hepatic TBARS and improved the diminished activities of the antioxidative enzymes and the levels of GSH. Therefore, the present study demonstrates the effectiveness of vitamin E and Se in reducing hepatic damage in glucocorticoid-treated rats and suggests that reductions in increased TBARS as a result of prednisolone may be an important factor in the action of vitamin E and Se.     

Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E

Vitamin E and selenium (Se) interact synergistically as an important antioxidant defense mechanism. Se, an essential component of glutathione peroxidase (GSH-Px) and vitamin E decompose fatty acid hydroperoxides and hydrogen peroxides generated by free radical reactions. Vitamin E and GSH-Px may modulate arachidonic acid metabolism and the activity of cyclooxygenase enzymes by affecting peroxide concentration. The balance between arterial wall prostacyclin (PGI₂) production and platelet thromboxane (TX)A₂ directly influences platelet activity. In order to elucidate the differential role of dietary vitamin E and Se in aortic PGI₂ and platelet TXA₂ synthesis, 1-mo-old F344 rats were fed semipurified diets containing different levels of vitamin E (0, 30, 200 ppm) and Se (0, 0.1, 0.2 ppm) for 2 mo. Thromboxane B₂ (TXB₂) and 6-keto-PGF₁α, were measured by radioimmunoassay (RIA) after incubation of whole blood and aortic rings at 37°C for 10 and 30 min, respectively. Vitamin E deficiency reduced plasma vitamin E to 5–17% of control-fed rats, and supplementation increased it to 53% of the control-fed rats. Se supplementation in vitamin E-supplemented animals increased plasma GSH-Px by 17%, compared to vitamin E-deficient rats. Se and vitamin E supplementation did not have a similar effect on TXB₂ and PGI₂ synthesis. Se deficiency did not alter platelet TXB₂ synthesis, but significantly decreased aortic PGI₂ synthesis. It was necessary to supplement with both antioxidants in order to increase, PGI₂ synthesis. Se and vitamin E deficient groups had a higher TXB₂/PGI₂ ratio (0.17±0.08) compared to Se- and vitamin E-supplemented groups (0.03±0.01). These results confirm previous reports in humans and animals and are in accordance with epidemiological data indicating an inverse relationship between plasma Se and platelet aggregation. Thus, further suggesting that vitamin E and Se may have a specific role in controlling TXA₂ and PGI₂ synthesis.     

维生素E和硒水平对肉鸡不同自由基代谢的影响

选用200羽14日龄健康AA肉鸡,以电子自旋共振(ESR)捕集法和生物化学法对肉仔鸡血液和组织器官的不同自由基进行直接或间接测定,探讨VE和Se对肉鸡不同自由基代谢的作用及其动态变化.结果表明:组织一氧化氮(NO)自由基水平随日粮VE含量升高而降低,二者呈负相关关系,日粮高水平Se有诱导产生NO自由基的倾向;高VE和Se日粮显著提高血清和肝脏中SOD和GSH-Px的活性,但随处理时间的延长,组织SOD活性逐渐降低,而GSH-Px活性逐渐升高,说明日粮VE和/或Se不足均会诱导机体产生O.2-、H2O2自由基,且O2.-自由基会持续大量产生,而H2O2自由基仅在缺乏初期大量产生,而后趋于缓和;低VE和/或低Se均显著提高组织MDA含量,且低Se比低VE更为显著.VE和Se对肉鸡NO、O.2-和H2O2自由基代谢的作用存在协同效应.     

Antioxidant effect of conjugated linoleic acid and vitamin A during non enzymatic lipid peroxidation of rat liver microsomes and mitochondria

In the study reported here the effect of conjugated linoleic acid (CLA) and vitamin A on the polyunsaturated fatty acid composition, chemiluminescence and peroxidizability index of microsomes and mitochondria isolated from rat liver was analyzed. The effect of CLA on the polyunsaturated fatty acid composition of native microsomes was evidenced by an statistically significant p < 0.007 decrease of linoleic acid C18:2 n6, whereas in mitochondria it was observed a decrease p < 0.0001 of arachidonic acid C20:4 n6 when compared with vitamin A and control groups. Docosahexaenoic acid C22:6 n3 in mitochondria was reduced p < 0.04 in CLA and vitamin A groups when compared with control. After incubation of microsomes or mitochondria in an ascorbate (0.4 mM)-Fe⁺⁺ (2.15 M) system (120 min at 37°C) it was observed that the total cpm/mg protein originated from light emission: chemiluminescence was lower in liver microsomes or mitochondria obtained from CLA group (received orally: 12.5 mg/daily during 10 days) than in the vitamin A group (received intraperitoneal injection: daily 0.195 g/kg during 10 days). CLA reduced significantly maximal induced chemiluminescence in microsomes relative to vitamin A and control groups, whereas in mitochondria the effect was observed relative to control group The polyunsaturated fatty acid composition of liver microsomes or mitochondria changed by CLA and vitamin A treatment. The polyunsaturated fatty acids mainly affected when microsomes native and peroxidized from control group were compared were linoleic, linolenic and arachidonic acids, while in vitamin A group linoleic and arachidonic acid were mainly peroxidized, whereas in CLA group only arachidonic acid was altered. In mitochondria obtained from the three groups arachidonic acid and docosahexaenoic acid showed a significant decrease when native and peroxidized groups were compared. As a consequence the peroxidizability index, a parameter based on the maximal rate of oxidation of fatty acids, show significant changes in the CLA group compare vitamin A and control groups. The simultaneous analysis of peroxidizability index, chemiluminescence and fatty acid composition demonstrated that CLA is more effective than vitamin A protecting microsomes or mitochondria from peroxidative damage.