Tocopherol Supplementation Research Articles

Effects of Various Fat Sources, α-Tocopheryl Acetate, and Ascorbic Acid Supplements on Fatty Acid Composition and α-Tocopherol Content in Raw and Vacuum-Packed, Cooked Dark Chicken Meat

A factorial design was used to study the effects of dietary fat sources (beef tallow, fresh and oxidized sunflower oils, and linseed oil), α-tocopheryl acetate (0 and 225 mg/kg), and ascorbic acid (0 and 110 mg/kg) supplementation on fatty acid composition, as well as on fat and α-tocopherol content in vacuum-packed raw and cooked meat stored at −20°C. Raw meat fatty acid composition was affected by dietary fat sources and tocopheryl acetate supplementation. After cooking, meat composition was only affected by dietary fat sources. Birds fed linseed oil yielded meat rich in n-3 fatty acids, especially linolenic acid, which provides about 20% of the adequate intake for this fatty acid. Birds fed sunflower or oxidized sunflower oil produced meat rich in n-6 fatty acids, whereas those fed beef tallow resulted in meat rich in saturated and monounsaturated fatty acids. Raw and cooked dark chicken meat α-tocopherol content was only affected by tocopherol supplementation. Supplementation with α-tocopheryl acetate led to α-tocopherol–enriched meat, which provides about 25% of the recommended dietary allowance. Moreover, this content in vacuum-packed samples was not modified even after 7 mo of storage at − 20°C.

Effects of Dietary Functional Ingredients and Packaging Methods on Sensory Characteristics and Consumer Acceptance of Irradiated Turkey Breast Meat

Raw and cooked breast patties from turkeys fed 8 different diets [control; 200 IU/kg of vitamin E (VE); 0.3 mg/kg of Se; 2.5% conjugated linoleic acids (CLA); 200 IU/kg of VE + 0.3 mg/kg of Se; 200 IU/kg of VE + 2.5% CLA; 0.3 mg/kg of Se + 2.5% CLA; and 200 IU/kg of VE + 0.3 mg/kg of Se + 2.5% CLA] were treated with 2 irradiation doses (0 and 1.5 kGy) and 2 packaging methods (vacuum and aerobic). Raw and cooked samples from 32 treatments were tested by 8 trained sensory panelists for turkey aroma and irradiation off-aroma. Based on the sensory scores, the 3 dietary treatments producing the most and the least off-aroma were selected and used for a consumer acceptance study. Sensory results of raw meat showed that turkey aroma was intense in aerobically packaged meat, whereas irradiation off-aroma was intense with vacuum packaging. Raw meats from dietary treatments containing CLA (CLA, VE + CLA, Se + CLA, VE + Se + CLA) had greater turkey aroma scores, whereas those containing VE (VE and VE + Se) had lower scores than the control. Dietary treatments containing VE (VE, VE + Se, VE + Se + CLA) significantly lowered (P < 0.05) irradiation off-aroma in raw turkey breast meat, whereas CLA increased it, especially when the meats were packaged aerobically. In cooked meat, however, irradiation and packaging had no effect on turkey meat aroma and irradiation off-aroma. Cooked meat from turkeys supplemented with VE (VE and VE + Se) had less (P < 0.05) irradiation off-odor than other dietary treatments. Dietary CLA increased the irradiation off-aroma in cooked meat, which could not be reduced, even when VE and Se were combined in the diet. Irradiation off-aroma of raw meat was not pleasant for most consumers, and dietary supplementation of VE and VE + Se improved consumer acceptance of irradiated raw meat. For cooked meat samples, consumers preferred both color and flavor of irradiated meat to nonirradiated meat.

Lipid oxidative damage and distribution of inorganic arsenic and its metabolites in the rat nervous system after arsenite exposure: Influence of alpha tocopherol supplementation

Inorganic arsenic (iAs) exposure causes peripheral neuropathy. Oxidative effects caused by iAs exposure in peripheral nerves have been incompletely characterized. This study analyzed arsenic and lipid oxidative damage in the brain, spinal cord, and sciatic and sensory sural nerves following arsenite exposure. This study also explored whether alpha tocopherol (α-TOC) administration mitigates arsenite-induced oxidative damage. Thiobarbituric acid-reactive substance (TBARS) levels and distributions of iAs and its metabolites were evaluated in male Wistar rats following 30 d of sodium arsenite exposure (10 mg/kg bodyweight (bw)/d, by gavage). A second group also received α-TOC (125 mg/kg bw/d, by gavage) during the final 20 d of arsenite administration. Arsenite exposure caused increased TBARS levels within each region of the nervous system; oxidative stress was most pronounced in the sural and sciatic nerves. In addition there was a positive quadratic relationship between TBARS levels and the concentration of arsenicals found in the nervous system ( r 2 = 0.878, p < 0.001). Dimethylarsenic was the predominant metabolite of iAs found. Animals α-TOC-treated had a 1.7–5.2-fold reduction in TBARS levels when compared with rats that received iAs alone. These results suggest that oxidative damage may be the main mechanism of toxicity induced by exposure of the peripheral nervous system to arsenite and that such damage could be attenuated by α-TOC-supplementation.

Tolcapone decreases plasma levels of S-adenosyl-L-homocysteine and homocysteine in treated Parkinson’s disease patients

Elevated plasma total homocysteine (tHcy) appeared in levodopa/dopadecarcoxylase inhibitor (DDI) treated patients with Parkinson's disease (PD). One therapeutic approach for tHcy reduction is vitamine supplementation, since folic acid and cobalamine catalyse and enhance metabolism of tHcy to methionine. A further therapeutic alternative is inhibition of catechol-O-methyltransfrase (COMT) on a regular basis, when levodopa/DDI treatment is performed. We measured the concentrations of S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), tHcy, levodopa and 3-O-methyldopa in plasma of 13 levodopa treated PD patients before first drug intake at 0600 hours. Blood samples were taken before and after 2 days of additional application of the centrally acting catechol-O-methyltransferase inhibitor tolcapone 100 mg t.i.d. Plasma levels of SAH [day 1: 48.32+/-22.52, 23.92-98.25 (mean+/-SD, range; micromol/l); day 3: 37.72+/-15.84, 23.4-61.89; p = 0.01] and tHcy (day 1: 13.88+/-5.62, 7.63-24.81; day 3: 11.38+/-4.44, 5.98-20.45; p = 0.04) significantly reduced. Plasma levels of levodopa did not significantly (p = 0.17) increase, whereas 3-OMD concentrations significantly (p = 0.0002) reduced after additional tolcapone intake. There was no significant change of SAM plasma levels (p = 0.22). Our prospective trial shows, that COMT inhibition with tolcapone lowers tHcy synthesis. Tolcapone may also possess beside its proven, occasional, hepatotoxic potency also beneficial effects via decrease of SAH and tHcy. This may hypothetically reduce homocysteine mediated progress of neuronal degeneration and the risk for onset of dementia, vascular disease and polyneuropathy in levodopa treated PD patients in the long term.

Effect of High Dose Alpha Tocopherol Therapy on Carotid Atherosclerosis, Biomarkers of Oxidative Stress and Inflammation in Patients with Coronary Artery Disease

Oxidative stress and inflammation are crucial in atherogenesis. High dose Alpha tocopherol (RRR-AT) supplementation has antioxidant and anti-inflammatory effects. Prospective studies with lower doses of AT on atherosclerosis have been equivocal. Thus, we tested the effect of RRR-AT supplementation(1200 IU/day for 2 years)on carotid atherosclerosis in a placebo-controlled, double blind study of 90 stable coronary artery disease patients. Intimal medial thickness (IMT) of both carotids, was determined by B-mode sonography at 0, 1, 1.5 and 2 yrs. At 6-month intervals blood was obtained for AT levels, C-reactive protein (CRP) and 24-hour urine for F2 -isoprostanes. AT levels significantly increased in the AT group (2.4-fold) but not in placebo. There was no significant difference in total or left carotid IMT between placebo and AT groups. There was a significant increase in IMT progression in Placebo with time for total and right CCA-IMT (p<0.05). Also, there was a significant decrease in IMT progression in the right CCA between placebo and AT groups over 2 years (p=0.017). HsCRP levels and F2-isoprostane levels significantly decreased with AT therapy compared to placebo (32% and 26%,p<0.01). Thus, high dose RRR-AT supplementation in CAD patients significantly reduced biomarkers of oxidative stress and inflammation, there was only a marginal benefit with regards to carotid atherosclerosis progression.

Alpha tocopherol supplementation elevates plasma apolipoprotein A1 isoforms in normal healthy subjects

Plasma alpha-tocopherol (AT) concentrations are inversely related to cardiovascular (CV) risk; however, intervention studies with AT have failed to show any consistent benefit against CV disease (CVD). Proteomics offers the opportunity to examine novel effects of AT supplementation on protein expression and therefore improve our understanding of the physiological roles of AT. Thus, to investigate the effects of AT supplementation on the plasma proteome of healthy subjects we have undertaken a double-blind, randomised, parallel design supplementation study in which healthy subjects (n = 32; 11 male and 21 female) consumed AT supplements (134 or 268 mg/day) or placebo capsules for up to 28 days. Plasma samples were obtained before supplementation and after 14 and 28 days of supplementation for analysis of changes in the plasma proteome using 2-DE and MALDI-MS. Using semiquantitative proteomics, we observed that proapolipoprotein A1 (identified by MS and Western blotting) was altered at least two-fold. Using quantitative ELISA techniques, we confirmed a significant increase in plasma apolipoprotein A1 concentration following supplementation with AT which was both time and dose dependent (p < 0.01 after 28 days supplementation with 268 mg AT/day). These data demonstrate the time and dose sensitivity of the plasma proteome to AT supplementation.

Vitamin-E Supplementation Ameliorates Chromium-and/or Nickel Induced Oxidative Stress in Vivo

The present study was designed to investigate the in vivo effects of nickel chloride [NiCl2; 8, and 16 mg/kg body weight (b wt)] and/or Potassium dichromate (K2Cr2O7; 5 and 10 mg/kg b wt) in the liver of adult mice. The beneficial effects of vitamin E (2 mg/kg) along with their combination were also studied. The antioxidative indices including oxidative lipid peroxidation (LPO) and antioxidative enzymes such as glutathione (GSH), total sulfhydryl (-SH) groups, total ascorbic acid (TAA), superoxide dismutase (SOD) and catalase (CAT) were evaluated in the hepatic tissue using well established techniques. Nickel and/or chromium treatments to mice revealed a significant decline in the levels of these antioxidant parameters as compared to control. Concomitantly a significant increase in lipid peroxidation was obtained. These data indicated that the treatment induced oxidative stress in the hepatic tissue of treated mice, which was more pronounced by combination of metal salts. But supplementation of vitamin E with NiCl2 + K2Cr2O7 to mice exerted no significant alterations in the liver antioxidant system as compared to control, thus indicating its ameliorative role. These findings suggest that vitamin E prevents LPO and protects the antioxidant system in the mouse liver.

Appearance of amyloid β-like substances and delayed-type apoptosis in rat hippocampus CA1 region through aging and oxidative stress

To elucidate whether oxidative stress induces cognitive deficit, and whether nerve cells in the hippocampus, which modulates learning and memory functions in the brain, are damaged by oxidative stress and during aging, the influence of hyperoxia as oxidative stress on either the cognitive function of rats or the oxidative damage of nerve cells was investigated. Young rats showed better learning ability than both old rats and vitamin E-deficient young rats. Vitamin E- supplemented young rats showed similar ability to young control rats. After they learned the location of the platform in the Morris water maze test, the young rats and vitamin E-supplemented young rats were subjected to oxidative stress for 48 h, and the old rats and vitamin E-deficient young rats were kept in normal atmosphere. The memory function of the old rats and vitamin E-deficient young rats declined even when they were not subjected to oxidative stress for 48 h. In contrast, the young rats maintained their memory function for 4 days after the oxidative stress. However, their learning abilities suddenly declined toward that of the normal old rats after 5 days. At this point, nerve cell loss and apoptosis were observed in the hippocampal CA 1 region of young rats. Vitamin E-supplementation in the young rats prevented either memory deficit or the induction of delayed-type apoptosis. The old rats and vitamin E-deficient young rats kept in normal atmosphere for 48 h also showed apoptosis in the hippocampus. Also, 10 days after oxidative stress, amyloid beta-like substances appeared in the CA-1 region of control young rats; these substances were also observed in the CA-1 region of the old rats and vitamin E- deficient young rats. These results suggest that reactive oxygen species (ROS) generated by oxidative stress induced amyloid beta-like substances and delayed-type apoptosis in the rat hippocampus, resulting in cognitive deficit. Since amyloid beta in Alzheimer's disease characterized by cognitive deficit induces neuronal cell death, it is reasonable to consider that amyloid beta deposition in the brain may be associated with memory dysfunction. The results of this study imply that age-related hippocampal neuronal damage is prevented by vitamin E supplementation due to the antioxidant effect of vitamin E.

Increase of geometrical and positional fatty acid isomers in dark meat from broilers fed heated oils

Oxidation of polyunsaturated fatty acids leads to primary and secondary oxidation products. Compounds and amounts of these products vary, depending on the oxidative conditions. Because these oxidation products have different absorption and biological effects, we performed 2 different heating treatments on sunflower oil. The first was heating the oil at 190 to 195 degrees C for 28 h (i.e., very oxidized oil), and the other was heating at 60 degrees C for 12 d (i.e., peroxidized oil). In the frame of this study, we compared the fatty acid composition of a refined sunflower oil (fresh oil), peroxidized oil, very oxidized oil, and a mixture (1:1) of fresh and very oxidized oil (i.e., oxidized oil). Oil fatty acid compositions were affected by the heating treatments. In addition, different fatty acid isomers were formed during heating at 190 to 195 degrees C, and significant differences were found between their contents in the sunflower oils. We also studied the effect of feeding broilers with these oils and Zn and tocopherol supplements on the fatty acid composition of their raw dark meat. Various trans fatty acid isomers increased in dark meat from broilers fed oxidized and very oxidized oils. In addition, discriminant analysis showed that ditrans-conjugated linoleic acid content was able to distinguish dark chicken meat from chickens fed sunflower oils heated at 190 to 195 degrees C.

Comparison of Effect of Vitamin E-Coated Dialyzer and Oral Vitamin E on Hemodialysis-Induced Cu/Zn-Superoxide Dismutase

Background: We reported earlier that production of Cu/Zn-superoxide dismutase (SOD) increases markedly in hemodialysis patients but not in non-dialyzed chronic renal failure (CRF) patients. In this study, we compared the antioxidant effects of oral vitamin E supplementation (VE-PO) and vitamin E coating of a dialyzer (VE-BMD) by measuring increased Cu/Zn-SOD in hemodialysis patients. Methods: 31 hemodialysis patients were divided into two groups: 16 hemodialysis patients underwent usual dialysis with vitamin E supplementation 600 mg/day while 15 others were dialyzed using vitamin E-coated membrane for 6 months. Total plasma SOD activity was determined by NBT method, plasma Cu/Zn-SOD contents by ELISA and Cu/Zn-SOD mRNA in leukocytes by RT-PCR. Results: VE-PO and VE-BMD showed almost comparable effects on Cu/Zn-SOD contents and its mRNA levels in hemodialysis patients. VE-PO resulted in a progressive decrease of Cu/Zn-SOD content (p < 0.001). A comparable progressive decrease was observed also in VE-BMD (p < 0.0001). Both VE-PO and VE-BMD resulted in a progressive decrease of Cu/Zn-SOD mRNA (p < 0.01), which reached the level of non-dialyzed CRF patients.

Colour stability, under simulated retail display conditions, of M. longissimus dorsi and M. semimembranosus from steers given long-term daily exercise and supplemented with vitamin E

The objective was to determine if exercise has a negative impact on the colour stability of beef and if dietary vitamin E (VE) supplementation could counteract any negative effect. Steers were not exercised or were walked 4.41 km/day for 18 weeks. Within exercise treatment animals consumed, on average, either 450 or 1050 IU/day of VE. Muscle α-tocopherol increased ( P = 0.004) from 2.35 to 3.15 μg/g with VE supplementation. Following ageing M. longissimus dorsi (LD) and M. semimembranosus (SM) steaks were packaged under 80%O 2:20%CO 2 and stored at 4 °C. The LD of exercised steers was more red and more saturated (both P < 0.05) after 0 and 2 days of storage than LD of unexercised steers. While redness of both muscles decreased over the display period, LD retained a higher redness than SM from day 2 to 7 ( P < 0.05). Colour shelf-life of LD was extended by 0.75 days, to 3.25 days, due to VE supplementation.

Effects of Dietary Combinations of Vitamin A, E and Methionine on Growth Performance, Meat Quality and Immunity in Commercial Broilers

The experiment was conducted to study the effect of dietary combinations of vitamin A (VA), vitamin E (VE) and methionine (Met) on growth performance, meat quality and immunity in commercial broilers. Ross chicks (n=3,630) were allocated to five experimental treatments with three replicates per diet. The dietary treatments were: VA 8,000 IU, VE 10 IU (diet 1); VA 12,000 IU, VE 10 IU (diet 2); VA 8,000 IU, VE 100 IU (diet 3); VA 12,000 IU, VE 100 IU (diet 4) and; VA 12,000 IU, VE 100 IU/kg diet and 20% Met higher than other groups (diet 5). The Met content in diet 1 to diet 4 were as per the requirement suggested by NRC. Separate vitamin premixes were prepared for each treatment diet as per the requirement of study. The 35 d study revealed significantly (p<0.0001) higher weight gains in broilers fed diet 3 and diet 5, than in the rest of the groups during starter phase (0-3 weeks) only. The feed intake did not vary significantly at all phases of study, but feed efficiency was significantly (p<0.05) lower in diet 1 during starter and overall phase (4-5 weeks). The bone strength and bone composition, except bone calcium, remained unaffected due to experimental diets studied after 35 d of experimental feeding. The thio-barbituric acid reactive substances (TBARS) were significantly (p=0.0013) lower in the breast meat in group 5, followed by group 3, than in the rest of the groups. The immune studies conducted, antibody titers to sheep red blood cells, thickness index to phytohaemagglutinin-P, and heterophil: lymphocyte ratio, did not show any significant difference among treatments. It could be concluded that supplementation of VA, VE and Met at higher levels could be beneficial to broilers only during the starter phase. (Asian-Aust. J. Anim. Sci. 2005. Vol 18, No. 4 : 516-523)

Effect of Tocotrienol on Lipid Peroxidation in Experimental Gastritis Induced by Restraint Stress

Damage to gastric mucosa caused by restraint stress has been attributed to impaired blood flow that resulted in ischemia followed by reperfusion, a process that generates free radicals. Therefore oxygen radicals may mediate the lesions produced in restraint stress. To test this hypothesis, we studied the effect of free radical scavengers on restraint-induced lesions in rats. Forty rats were divided in to four groups of 10 rats. Two control groups was fed with a normal rat diet and two treatment groups fed with a vitamin E deficient diet with either tocopherol or tocotrienol, which serves as free radical scavengers. The two forms of vitamin E were administered orally at 60mg/kg body weight for 28 days. After 28 days, rats from one control group and the two treated groups were subjected to restraint stress 2 hours daily for 4 consecutive days. The rats were killed after the fourth exposure, their stomach isolated and examined for lesions, and gastric malondialdehyde (MOA) content and the gastric reduced glutathione level were measured as an index to reflect the scavenging abilities of tocopherol and tocotrienol. Both the regimes significantly attenuated the total lesion area in the stomach compared to the control. The MOA content was also significantly lower in the rats given tocopherol and tocotrienol supplementation compared to the control and the reduced glutathione levels were preserved in rats supplemented with both tocopherol and tocotrienol. We conclude that it is indeed probable that oxygen radical is involved in the pathogenesis of restraint stress-induced lesions thus supplementation with antioxidant such as vitamin E may be able to reduce or inhibit the formation of these lesions.

Vitamin E Supplementation Reverses the Age‐Associated Decrease in Effective Immune Synapse Formation in CD4+ T Cells

Aging is associated with impairment of T cell function. We demonstrate here that age-associated declines in T cell signaling are due to the inability to form effective immune synapses at the site of the T cell receptor and antigen interaction. On the basis of our previous research with vitamin E (VE), we hypothesized that VE supplementation of old CD4(+) T cells enhances effective immune synapse formation through increased translocation of signaling proteins. Using confocal microscopy, we found that when exposed to antigen-presenting cells, CD4(+) T cells from old mice have a lower percentage of effective immune synapses compared to those from young mice. Furthermore, we show that in vitro and in vivo VE supplementation increases the percentage of old CD4(+) T cells capable of forming a functional immune synapse. Further studies are under way to determine the mechanisms of age and VE-induced enhancement of effective immune synapse formation.

Modulation of Hepatic Gene Expression by α‐Tocopherol in Cultured Cells and in Vivo

To obtain a comprehensive understanding of the molecular mechanisms of action of vitamin E (VE), global gene expression profiles using DNA arrays in rat liver and hepatocellular liver carcinoma cells (HepG2) were obtained. For the analysis of short-term (49 days) and long-term (290 days) VE deficiency, rats were fed semisynthetic diets either supplemented with or deficient in VE. In addition, HepG2 cells were treated with VE concentrations comparable to those that were achieved in the in vivo experiment. Differential gene expression in rat liver and that in HepG2 cells were measured by DNA arrays comprising up to 7,000 genes. Dietary VE deficiency over a 7-week period did not induce any significant changes in the expression profile among the genes evaluated. However, long-term VE deficiency upregulated coagulation factor IX (FIX), 5-alpha-steroid reductase type 1, and CD36 mRNA levels. Furthermore, VE deficiency resulted in a significant downregulation of hepatic gamma-glutamyl-cysteinyl synthetase, the rate-limiting enzyme of glutathione synthesis. According to the rat experiment, VE supplementation changed coagulation factor IX and CD36 expression in HepG2 cells; thus, in vivo data could be partly confirmed with the in vitro model. Overall, the current studies reveal that dietary VE has important long-term effects on liver gene expression with potential downstream effects on extrahepatic tissues.

Influence of dietary vitamin E on phagocytic functions of macrophages in broilers

Vitamin E (VE) is known for its antioxidant properties and has been shown to modulate immune system functions in various species. This study examined the influence of different levels of dietary VE (α-tocopherol acetate) on phagocytic functions of macrophages (abdominal exudate cells) in broiler chickens at 3, 5, and 7 wk. Birds were fed commercial diets containing 16 (control), 110, or 220 mg of VE/kg of feed. Macrophages were elicited into the abdominal cavity by injecting a 3% Sephadex solution prepared in PBS (G50-50, 1 mL/100 g of BW) 42 h prior to harvest. The percentage of phagocytically active macrophages and the number of SRBC phagocytosed per macrophage for unopsonized and antibody-opsonized SRBC were determined. These aspects of macrophage function were assessed based on 900 macrophages per sample. When unopsonized SRBC were used, dietary VE supplementation above control level did not affect phagocytic function of macrophages at wk 3, 5, or 7. With antibody-opsonized SRBC, the percentage of phagocytically active macrophages and the number of SRBC phagocytosed per macrophage were higher (P = 0.08 and P = 0.01, respectively) in 3-wk-old birds fed 110 and 220 mg of VE/kg of feed compared with age-matched controls. This enhancing effect of VE supplementation on macrophage function was not observed in 5- and 7-wk-old broilers. It appears from this study that supplemental VE enhances Fc-receptor-mediated macrophage phagocytic activity at early stages of broiler growth.

Postintervention effect of alpha tocopherol and beta carotene on different strokes: a 6-year follow-up of the Alpha Tocopherol, Beta Carotene Cancer Prevention Study.

In the Alpha Tocopherol, Beta Carotene Cancer Prevention Study, alpha tocopherol supplementation decreased risk of cerebral infarction by 14% (95% CI, -25% to -1%), and beta carotene increased risk of intracerebral hemorrhage by 62% (95% CI, 10% to 132%). We report here the 6-year postintervention effects of alpha tocopherol and beta carotene supplementation on stroke and its subtypes. A total of 29,133 male smokers, aged 50 to 69 years, were randomized to receive 50 mg of alpha tocopherol, 20 mg of beta carotene, both, or placebo daily for 5 to 8 years. At the beginning of the post-trial follow-up, 24 382 men were still at risk for first-ever stroke. During the post-trial follow-up, 1327 men experienced a stroke: 1087 cerebral infarctions, 148 intracerebral hemorrhages, 64 subarachnoid hemorrhages, and 28 unspecified strokes. Post-trial risk for cerebral infarction was elevated among those who had received alpha tocopherol compared with those who had not (relative risk [RR], 1.13; 95% CI, 1.00 to 1.27), whereas beta carotene had no effect (RR, 0.97; 95% CI, 0.86 to 1.09). Alpha tocopherol supplementation was associated with a postintervention RR of 1.01 (95% CI, 0.73 to 1.39) for intracerebral hemorrhage and 1.38 (95% CI, 0.84 to 2.26) for subarachnoid hemorrhage. The corresponding RRs associated with beta carotene supplementation were 1.38 (95% CI, 0.99 to 1.91) and 1.09 (95% CI, 0.67 to 1.77), respectively. Neither alpha tocopherol nor beta carotene supplementation had any postintervention preventive effects on stroke. The post-trial increase in cerebral infarction risk among recipients of alpha tocopherol may present a rebound of the reduced risk of cerebral infarction during the intervention.

Identification of hepatic molecular mechanisms of action of alpha-tocopherol using global gene expression profile analysis in rats

The recent discovery that vitamin E (VE) regulates gene activity at the transcriptional level indicates that VE may exert part of its biological effects by mechanisms which may be independent of its well-recognised antioxidant function. The objective of this study was the identification of hepatic vitamin E-sensitive genes and examination of the effects of VE on their corresponding biological endpoints. Two groups of male rats were randomly assigned to either a VE-sufficient diet or to a control diet deficient in VE for 290 days. High-density oligonucleotide microarrays comprising over 7000 genes were used to assess the transcriptional response of the liver. Differential gene expression was monitored over a period of 9 months, at four different time-points, and rats were individually profiled. This experimental strategy identified several VE-sensitive genes, which were chronically altered by dietary VE. VE supplementation down-regulated scavenger receptor CD36, coagulation factor IX and 5-α-steroid reductase type 1 mRNA levels while hepatic gamma glutamyl-cysteinyl synthetase was significantly up-regulated. Measurement of the corresponding biological endpoints such as activated partial thromboplastin time, plasma dihydrotestosterone and hepatic glutathione substantiated the gene chip data which indicated that dietary VE plays an important role in a range of metabolic processes within the liver.

Effect of dietary tocopherols and tocotrienols on the antioxidant status and lipid stability of chicken

We determined the effect of dietary tocopherols and tocotrienols on the lipid stability of pre-cooked chicken breast and thigh. The birds were supplemented with one of two doses of a commercial mixture of tocopherols and tocotrienols (Oryza1, Oryza2) or one of two doses of all-rac α-tocopherol acetate (Toc1, Toc2). Diets were formulated so that Oryza1 and Toc1 and Oryza2 and Toc2 contained similar tocopherol concentrations. No quantifiable amounts of tocotrienols were found in either breast or thigh muscles. Tocotrienols present in the diet reduced muscle α-tocopherol concentration. The effect of Oryza1 on the tocopherol content in muscle and on its lipid stability was not significant. The Oryza2, Toc1 and Toc2 diets increased the α- and γ-tocopherol in breast and thigh muscles and enhanced their lipid stability. This improvement was only due to the antioxidant action of the tocopherols. Lipid stability of pre-cooked chicken was not enhanced by adding tocotrienols to a tocopherol supplement.

Influence of age and vitamin E on post-ischemic acute renal failure

The aging process causes progressive deterioration in kidney structure and function. Aberrant generation of reactive oxygen species has been implicated in both age-related and ischemia-related tissue injury. Vitamin E (VE), one of the most powerful and effective exogenous antioxidants, prevents lipid peroxidation and protects against the effects of oxidative stress. The objective of this study was to determine the influence of age and VE on post-ischemic acute renal failure (ARF). Young adult, middle-aged and aged male Wistar rats were maintained on three different 30-day diets: Normal, VE absent and VE supplemented. On day 30, urinary protein and serum cholesterol and VE were measured. On day 31, rats were subjected to 60′ clamping of the left renal artery plus right nephrectomy. Inulin clearance (InCl) was performed 48 h after renal ischemia. Malondialdehyde (MDA) was measured in the cortex of normal and 48-h post-ischemic kidneys. Urinary protein and serum cholesterol were higher in aged rats than in other rats. With aging, InCl decreased progressively. Vitamin E deficiency aggravated ARF. In middle-aged and aged rats, VE supplementation protected against ARF. In the absence of VE, MDA increased with age. In conclusion, our data suggest that ARF becomes more severe with age and that ischemia/reperfusion injury is exacerbated when antioxidant-scavenging ability of the kidney is impaired by VE deficiency. Supplementation with VE is essential for protecting aging kidneys against ischemic ARF.