High dietary vitamin A interferes with tissue α-tocopherol concentrations in fattening pigs: a study that examines administration and withdrawal times

This study aimed to assess the interaction between different dietary vitamin A (dVitA) levels and the same concentration of vitamin E (100 IU all-rac-α-tocopheryl acetate/kg feed) in growing-finishing pigs. In the first experiment, two fat sources × two dVitA levels (0 v. 100 000 IU) were used. The supplementation of 100 000 IU dVitA induced a range of 5.13 to 30.03 μg retinol/g liver, 62.78 to 426.88 μg retinol palmitate/g liver, and 0.60 to 1.96 μg retinol/g fat. Dietary fat did not affect retinol or retinyl palmitate deposition in pigs. The high concentration of dVitA produced lower fat and liver α-tocopherol concentrations, and increased susceptibility of muscle tissue to oxidation. A second experiment was carried out to study the retinol and α-tocopherol retention at different withdrawal times prior to slaughter (two dVitA levels; 0 v. 100 000 IU). A high dose of 100 000 IU vitamin A during a short 2-week period was enough to induce α-tocopherol depletion in liver and fat to a similar extent as when 100 000 IU were administered during the whole fattening. Muscle, fat and liver α-tocopherol concentrations were not affected by dVitA in the 1300-13 000 IU/kg range, but liver α-tocopherol concentration was higher when vitamin A was removed from the vitamin mix 5 weeks prior to slaughter (experiment 3).     

Influence of vitamin E supplementation and basal diet on the vitamin E status, performance and tissue fatty acid concentration in lambs

In order to determine the effect of dietary vitamin E level and basal diet on vitamin E status, performance and tissue fatty acid content, five groups of eight Suffolk × Charollais wether lambs with an initial live weight of 28.4 (s.d. 1.6) kg were allocated to one of five concentrate-based diets supplemented with all-rac-α-tocopheryl acetate to contain 30 mg (C-30), 60 mg (C-60), 120 mg (C-120), 250 mg (C-250) or 500 mg (C-500) α-tocopheryl acetate/kg dry matter (DM), for 63 days. Two additional groups of eight lambs entered the study at 31.2 (s.d. 3.3) kg and were fed grass silage and 400 g/day concentrate for 56 days, with the whole diet providing the equivalent of 60 mg (S-60) or 500 mg (S-500) α-tocopheryl acetate/kg DM. Lambs were weighed and blood samples obtained by venipuncture weekly. Dietary vitamin E level did not affect performance (P > 0.05), but lambs fed grass silage grew more slowly (P < 0.001) and had a higher (P < 0.001) feed conversion ratio (kg feed/kg gain) than those fed concentrates. At day 0 plasma α-tocopherol concentrations were 0.8 μg/ml and did not differ between treatments (P > 0.05). Plasma α-tocopherol concentrations then decreased in all lambs except for those fed S-500, which increased, and at slaughter were (μg/ml) 0.07, 0.23, 0.39, 0.76 and 1.57 in C-30, C-60, C-120, C-250 and C-500 and 1.18 and 1.93 in S-60 and S-500, respectively. At slaughter, muscle and liver α-tocopherol concentrations were in the deficiency range for lambs fed C-30, C-60 or C-120, whereas plasma creatine kinase and tissue polyunsaturated fatty acids were unaffected by dietary vitamin E level, but creatine kinase levels were higher (P < 0.05) and glutathione peroxidise levels lower (P < 0.001) in lambs fed grass silage than concentrates alone. Muscle and liver α-tocopherol concentrations were 1.8- and 4.1-fold higher in lambs fed S-60 than C-60, but there was less of a difference between lambs fed S-500 or C-500 with muscle and liver differences of 0.4- and 0.7-fold, respectively. Tissue n-3 polyunsaturated fatty acid concentrations were higher (P < 0.05) and n-6 fatty acids lower in lambs receiving the grass silage compared to concentrate-based diets, but were not affected by dietary vitamin E level. It is concluded that lower plasma and tissue levels of α-tocopherol are present in lambs supplemented with all-rac-α-tocopheryl acetate on a concentrate compared to a mixed diet of silage and concentrates, and that normal growth can be achieved at tissue levels previously considered to represent deficiency.     

Vitamin E attenuates acute lung injury in sheep with burn and smoke inhalation injury

Abstract

Introduction: A decrease in α-tocopherol (vitamin E) plasma levels in burn patients is typically associated with increased mortality. We hypothesized that vitamin E supplementation (α-tocopherol) would attenuate acute lung injury induced by burn and smoke inhalation injury.

Materials and Methods: Under deep anesthesia, sheep (33 ± 5 kg) were subjected to a flame burn (40% total body surface area, third degree) and inhalation injury (48 breaths of cotton smoke, < 40°C). Half of the injured group received α-tocopherol (1000 IU vitamin E) orally, 24 h prior to injury. The sham group was neither injured nor given vitamin E. All three groups (n = 5 per group) were resuscitated with Ringer's lactate solution (4 ml/kg/%burn/24 h), and placed on a ventilator (PEEP = 5 cmH₂O; tidal volume = 15 ml/kg) for 48 h.

Results: Plasma α-tocopherol per lipids doubled in the vitamin E treated sheep. Vitamin E treatment prior to injury largely prevented the increase in pulmonary permeability index and moderated the increase in lung lymph flow (52.6 ± 6.2 ml/min, compared with 27.3 ± 6.0 ml/min, respectively), increased the PaO₂/FiO₂ ratio, ameliorated both peak and pause airway pressure increases, and decreased plasma conjugated dienes and nitrotyrosine.

Conclusions: Pretreatment with vitamin E ameliorated the acute lung injury caused by burn and smoke inhalation exposure.     

Effects of supplementation with vitamin E on the performance and the tissue peroxidation of broiler chicks and the stability of thigh meat against oxidative deterioration

Two experiments were conducted: Expt 1 determined the optimal allowance of vitamin E in the diet for broiler chicks aged 0–3 weeks; Expt 2 investigated the effects of different dietary levels of vitamin E (α-tocopherol) on the performance and the oxidative stability of thigh meat of broiler chicks during storage. In Expt 1, 1-day-old 900 broiler chicks were allocated to five treatments, each with six replicates (cages) of 22 as-hatched chicks for performance evaluation, and another cage of 45 male chicks for determining plasma and hepatic α-tocopherol and thiobarbituric acid reactive substances (TBARS) concentration in blood and liver. The basal dietary α-tocopherol concentration was 13 mg/kg, and the five α-tocopherol acetate supplementation levels were 0, 5, 10, 50 and 100 mg/kg. For 0–3-week-old broiler chicks fed with maize–soya bean meal–soya oil type diet, supplementation of vitamin E did not influence the feed intake, but tended to improve growth and feed utilization, however there was no significant correlation between performance and vitamin E supplementation level. Significant positive correlations existed between dietary supplemental vitamin E level and plasma or hepatic α-tocopherol concentrations (P<0.05), and a negative correlation with hepatic TBARS levels no matter at what age (11, 16 and 21 days). In Expt 2, 2200 broiler chicks were randomly allocated to five treatments with four replicates (pens) in each. Chicks were fed ad libitum five pellet diets supplemented with vitamin E at 5, 10, 20, 50 and 100 mg/kg of diet, respectively. The basal dietary α-tocopherol level of grower and finisher diets were 7 and 6 mg/kg, respectively. Supplementation of vitamin E tended to improve growth and feed utilization of birds during 0–3 weeks of age, but the performance from 0 to 6 weeks of age were not influenced. The hepatic α-tocopherol concentrations of 6-week-old chicks linearly increased with the dietary vitamin E levels (R²=0.98, P<0.001). The content of TBARS in the thigh meat over 4 days of storage under 4°C was significantly decreased by increasing dietary vitamin E level (P<0.05). There was a significant inverse relationship between TBARS value in the thigh meat and the dietary vitamin E level (R²=0.93, P<0.01). Supplementation of vitamin E significantly improved the meat quality stability substantially against oxidative deterioration. Comparing the hepatic α-tocopherol levels of chicks in Expts 1 and 2, total allowance of dietary α-tocopherol of 20–30 mg/kg could sustain relatively constant hepatic α-tocopherol level at round about 2–2.5 μg/kg.     

Estimation of α-tocopherol concentration necessary to optimise lamb meat quality stability during storage in high-oxygen modified atmosphere using broken-line regression analysis

The research was carried out to evaluate the effect of different α-tocopherol concentrations in lamb meat on oxidative stability during storage in high-oxygen atmosphere. Thirty-six lambs were randomly distributed to four groups and given diets containing four levels of vitamin E (20, 270, 520 and 1020 mg vitamin E/kg feed) from an initial weight of 13.2 ± 0.5 kg to a slaughter weight of 26.2 ± 0.3 kg. Supplementation of the diet with vitamin E increased (P < 0.001) the concentration of α-tocopherol in the meat and concentrations were obtained in the 0.46 to 4.14 mg/kg meat range. Broken-line analysis of data indicated a target dietary vitamin E supplementation of 287 mg/kg feed, which corresponded with a concentration of 2.26 mg α-tocopherol/kg meat. α-Tocopherol in meat was highly correlated with the oxidation of lipids and pigments. Broken-line analysis of data indicated the target α-tocopherol concentration in lamb for improved protection against lipid and pigment oxidation during 14, 21 and 28 days of storage in high-oxygen atmosphere was in the range 1.87 to 2.37 mg/kg meat. These concentrations of α-tocopherol in the meat made it possible to maintain the indicator values of lipid and pigment oxidation below the values considered in the bibliography as unacceptable to the consumer.     

The effect of late pregnancy supplementation of ewes with vitamin E on lamb vigour

The experiment measured lamb responses to supplementation of the pregnant ewe diet with vitamin E above requirement. Crossbred ewes were mated with either Suffolk or Texel rams. Twin-bearing ewes were randomly allocated (approximately 21 months of age at allocation) to one of four treatment groups (20 ewes per group, 10 mated with Suffolk and 10 with Texel rams). Treatments imposed were 50, 100, 150 or 250 IU supplementary vitamin E per ewe per day to give a four treatment by two sire-type factorial experimental design. Ewes were fed concentrates to meet energy requirements for stage of pregnancy and hay ad libitum. Diets were introduced approximately 6 weeks before lambing. Blood samples were obtained prior to introduction of diets, 17 days after introduction of diets and within 24 h of lambing from a subset of eight ewes per treatment (32 total). Colostrum samples were obtained from 10 ewes per treatment, 12 h after birth of the first lamb. All births were observed and a lamb vigour score was assigned to each lamb 5 min after birth. At 1 and 12 h after birth, rectal temperature, and at 12 h after birth, sex, crown-rump length and BW of each lamb were recorded. Mean ewe plasma α-tocopherol concentration prior to introduction of the diets was 1.5 μg/ml (s.e.m. 0.09) and did not differ between groups. There were positive linear (P < 0.001) effects of dietary vitamin E on plasma (17 days after introduction of diets) and colostrum (12 h after birth) α-tocopherol concentrations. Lamb vigour scores were superior (P < 0.001) for lambs sired by Texel rather than Suffolk rams but there were no differences as a result of vitamin E supplementation. Lamb mortality was low and unrelated to either sire or supplementary vitamin E. Lamb birth and weaning weights were also unaffected by vitamin E supplementation. Supplementing the ewe with vitamin E therefore had no effect on any lamb measurements.     

Response to different sources of vitamin E orally injected and to various doses of vitamin E in calf starter on the plasma vitamin E level in calves around weaning

Calves often face a lower plasma vitamin E level than the recommended level (3 µg/ml for adult cows) after weaning, a level which has been related to a good immune response. Two experiments were performed to determine the most effective source and level of vitamin E to be included in a calf starter to maintain the plasma vitamin E level above the recommended level after weaning. Experiment 1 (Exp 1) and experiment 2 (Exp 2) included a total of 32 and 40 calves, respectively, from 2 weeks before weaning until 2 weeks after weaning. In Exp 1, calves were orally injected a daily dose of different vitamin E sources including, no α-tocopherol (0 dose; Control), 200 mg/d of RRR-α-tocopherol (ALC), 200 mg/d of RRR-α-tocopheryl acetate (ACT), or 200 mg/d of all-rac-α-tocopheryl acetate (SYN). In Exp 2, a dose response study was carried out with 0, 60, 120, and 200 mg/kg of ALC in a pelleted calf starter. Final BW (100 ± 16 and 86 ± 11 kg) and average daily gain (956 ± 303 and 839 ± 176 g/d in Exp 1 and 2, respectively; mean ± SD) were unaffected by either source or level of α-tocopherol. In Exp 1, the plasma RRR-α-tocopherol level was affected by α-tocopherol source (P < 0.001), week (P < 0.001), and interaction between them (P < 0.001). At weaning time, the plasma RRR-α-tocopherol was 2.7, 2.1, 1.1, and 0.8 μg/ml in ALC, ACT, SYN, and Control, respectively. In Exp 2, the plasma α-tocopherol level was affected by ALC dose (P = 0.04), week (P < 0.001), and a tendency for an interaction between them was observed (P = 0.06). At weaning, a 36, 31, and 28% reduction in plasma α-tocopherol level was observed compared to the beginning of the experiment with 0, 60, and 120 mg/kg of ALC, respectively; however, with 200 mg/kg of ALC, a 9% increase in the plasma α-tocopherol level was observed. In addition, 200 mg/kg of ALC was able to maintain plasma α-tocopherol after weaning higher than the recommended level. The results showed that the ALC was the most efficient source of α-tocopherol supplementation to be used in a calf starter. In addition, the 200 mg/kg of ALC in the calf starter was the only effective dose to maintain the postweaning plasma vitamin E concentration at the recommended level after weaning and α-tocopherol similar to that observed before weaning.     

EFFECT OF VITAMIN E SUPPLEMENTATION AND PARTIAL SUBSTITUTION OF POLY- WITH MONO-UNSATURATED FATTY ACIDS IN PIG DIETS ON MUSCLE,AND MICROSOME EXTRACT a-TOCOPHEROL CONCENTRATION AND LIPID OXIDATION

The experiment was organized in a 3×2 factorial arrangement with three dietary fat blends and a basal (20 mg kg^?1 diet) or supplemented (220 mg kg^?1) level of α-tocopheryl acetate. Dietary vitamin E and monounsaturated to polyunsaturated fatty acid ratio (dietary MUFA/PUFA) affected muscle α-tocopherol concentration (α-tocopherol [log μg g^?1]=0.18 (±0.105)+0.0034 (±0.0003)·dietary α-tocopherol [mg kg^?1 diet] (P<0.0001)+0.39 (±0.122)·dietary MUFA/PUFA (P<0.0036)). An interaction between dietary α-tocopherol and dietary MUFA/PUFA exists for microsome α-tocopherol concentration (α-tocopherol [log μg g^?1]=1.14 (±0.169) (P<0.0001)+0.0056 (±0.00099)·dietary α-tocopherol [mg kg^?1 diet] (P<0.0001)+0.54 (±0.206)·dietary MUFA/PUFA (P<0.0131)?0.0033 (±0.0011)·dietary α-tocopherol [mg kg^?1)]×dietary MUFA/PUFA (P<0.0067)), and hexanal concentration in meat (hexanal [ng·g^?1]=14807.9 (±1489.8)?28.8 (±10.6) dietary α-tocopherol [mg·kg^?1] (P<0.01)?8436.6 (±1701.6)·dietary MUFA/PUFA (P<0.001)+24.0 (±11.22)·dietary α-tocopherol·dietary MUFA/PUFA (P<0.0416)). It is concluded that partial substitution of dietary PUFA with MUFA lead to an increase in the concentration of α-tocopherol in muscle and microsome extracts. An interaction between dietary α-tocopherol and fatty acids exists, in which at low level of dietary vitamin E inclusion, a low MUFA/PUFA ratio leads to a reduction in the concentration of α-tocopherol in microsome extracts and a concentration of hexanal in meat above the expected values.     

α-Tocopherol supplementation does not affect monocyte endothelial adhesion or C-reactive protein levels but reduces soluble vascular adhesion molecule-1 in the plasma of healthy subjects

Abstract

Vascular monocyte retention in the subintima is pivotal to the development of cardiovascular disease and is facilitated by up-regulation of adhesion molecules on monocytes/endothelial cells during oxidative stress. Epidemiological studies have shown that cardiovascular disease risk is inversely proportional to plasma levels of the dietary micronutrients, vitamin C and vitamin E (α-tocopherol). We have tested the hypothesis that α-tocopherol supplementation may alter endothelial/monocyte function and interaction in subjects with normal ascorbate levels (> 50 μM), as ascorbate has been shown to regenerate tocopherol from its oxidised tocopheroxyl radical form in vitro. Healthy male subjects received α-tocopherol supplements (400 IU RRR-α-tocopherol/day for 6 weeks) in a placebo-controlled, double-blind intervention study. There were no significant differences in monocyte CD11b expression, monocyte adhesion to endothelial cells, plasma C-reactive protein or sICAM-1 concentrations post-supplementation. There was no evidence for nuclear translocation of NF-κB in isolated resting monocytes, nor any effect of α-tocopherol supplementation. However, post-supplementation, sVCAM-1 levels were decreased in all subjects and sE-selectin levels were increased in the vitamin C-replete group only; a weak positive correlation was observed between sE-selectin and α-tocopherol concentration. In conclusion, α-tocopherol supplementation had little effect on cardiovascular disease risk factors in healthy subjects and the effects of tocopherol were not consistently affected by plasma vitamin C concentration.     

Nutrition of Captive Cheetahs: Food Composition and Blood Parameters

Diet and nutrition of cheetahs was evaluated through survey, in conjunction with chemical analysis of feed and plasma samples, as part of a multidisciplinary effort to investigate underlying causes of low reproductive success in North American captive cheetah populations. Cheetahs consumed an average of 1.32 ± 0.4 kg of food daily, containing approximately 1,800 kcal, and maintained an average body mass of 36.7 ± 1.0 kg (n = 34). A commercially prepared horsemeat-based mixture comprised the dietary staple in 10 of 13 zoos responding to the survey, with additional whole or carcass portions offered 1--2 days per week to maintain variety and provide periodontal stimulation. Seven of 13 respondents fasted animals 1 day/week; five maintained no fast days. The primary meat product (n = 14 samples) contained: 58% crude protein, 28% crude fat, 7% total ash, 52 Iu/kg vitamin E, 9.7 Iu/g vitamin A, and 2,200 mg/kg taurine (dry basis). Mineral content of the same food item was: 1.9% Ca, 10.0 mg/kg Cu, 645.2 mg/kg Fe, 0.08% Mg, 22.6 mg/kg Mn, 1.3% P, 0.4% Na, and 127.8 mg/kg Zn. Nutrient levels, except vitamin E (and possibly Mg), met or exceeded recommendations established for domestic felids. Plasma α-tocopherol, retinol, and taurine (18.1, 1.82, 128.4 μmol/L, respectively) concentrations were similar to normals for domestic felids, as were mean plasma mineral levels (n = 81; in mEq/L: 5.64 (Ca), 0.03 (Cu), 0.03 (Fe), 2.0 (Mg), 166.0 (Na), 12.3 (P), and 0.026 (Zn)). No gross physiological or dietary nutrient imbalances were evident from this survey. © 1993 Wiley-Liss, Inc.     

Absorption,Transport and Metabolism of Vitamin E

Vitamin E includes eight naturally occurring fat-soluble nutrients called tocopherols and dietary intake of vitamin E activity is essential in many species. α-Tocopherol has the highest biological activity and the highest molar concentration of lipid soluble antioxidant in man. Deficiency of vitamin E may cause neurological dysfunction, myopathies and diminished erythrocyte life span. α-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma α-tocopherol is found in all lipoprotein fractions, but mostly associated with apo B-containing lipoproteins in man. In rats approximately 50% of α-tocopherol is bound to high density lipoproteins (HDL). After intestinal absorption and transport with chylomicrons α-tocopherol is mostly transferred to parenchymal cells of the liver were most of the fat-soluble vitamin is stored. Little vitamin E is stored in the non-parenchymal cells (endothelial, stellate and Kupffer cells). α-Tocopherol is secreted in association with very low density lipoprotein (VLDL) from the liver. In the rat about 90% of total body mass of α-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most α-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. Clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of α-tocopherol, causing reduced tissue concentrations of α-tocopherol. Increased demand for vitamin E has also been observed in premature babies and patients with malabsorption, but there is little evidence that the well balanced diet of the healthy population would be improved by supplementation with vitamin E.     

High dietary level of synthetic vitamin E on lipid peroxidation,membrane fatty acid composition and cytotoxicity in breast cancer xenograft and in mouse host tissue

Background  

d-α-tocopherol is a naturally occurring form of vitamin E not previously known to have antitumor activity. Synthetic vitamin E (sE) is a commonly used dietary supplement consisting of a mixture of d-α-tocopherol and 7 equimolar stereoisomers. To test for antilipid peroxidation and for antitumor activity of sE supplementation, two groups of nude mice bearing a MDA-MB 231 human breast cancer tumor were fed an AIN-76 diet, one with and one without an additional 2000 IU/kg dry food (equivalent to 900 mg of all-rac-α-tocopherol or sE). This provided an intake of about 200 mg/kg body weight per day. The mice were killed at either 2 or 6 weeks after the start of dietary intervention. During necropsy, tumor and host tissues were excised for histology and for biochemical analyses.     

Relative resistance of the hamster to aortic atherosclerosis in spite of prolonged vitamin E deficiency and dietary hypercholesterolemia. Putative effect of increased HDL?

Male golden hamsters were rendered hypercholesterolemic by feeding diets enriched with cholesterol and fat. In the first series of experiments, 5% butter and 1% cholesterol were added to a chow diet and plasma cholesterol levels were maintained at 350–390 mg/dl over the entire experimental period. Groups of hamsters and their age controls consuming the chow diet, were killed after 7, 15 and 20 months when the aorta was examined for atherosclerosis by determination of cholesterol mass. In the controls, aortic total cholesterol (TC) increased with age by 28% and esterified cholesterol increased to 11% of TC. In the hypercholesterolemic animals aortic TC was only 28% higher than in the controls and cholesteryl ester was also 11.5% of TC. In the second series, one group of hamsters were fed a semi-purified diet deficient in vitamin E, containing 1% cholesterol and 10% lard; a second group received the same diet, but supplemented with vitamin E. Controls consumed local chow. After 7 months on the vitamin E deficient diet plasma α-tocopherol was 0.05 mg/l, in those supplemented with vitamin E it was 20 mg/l, while in the controls it was 3.3 mg/l. Plasma thiobarbituric acid reactive substances (TBARS) were higher in the vitamin E deficient group and there was a greater propensity of lipoproteins (d < 1.063 g/ml to peroxidation in vitro than in the vitamin E supplemented group. Plasma cholesterol was 366 mg/dl in the vitamin E deficient, 336 mg/dl in the vitamin E supplemented group, and 64 mg/dl in controls. Aortic cholesterol was 79.1 in vitamin E supplemented and 84.4 μg/ 10 mg dry weight in vitamin E deficient hamsters. In both series of experiments, HDL amounted to 36–41% of plasma TC in the hypercholesterolemic animals and 59–62% in the controls. In conclusion: the hamster appears to be quite resistant to atherosclerosis in face of sustained hypercholesterolemia, even in the presence of increased peroxidative stress caused by vitamin E deficiency. This relative resistance could be related to commensurate increase in plasma HDL which was observed in both series of experiments. Since vitamin E deficiency did not enhance aortic cholesteryl ester deposition, the protective effect of HDL seems to be related to its role in reverse cholesterol transport, rather than in prevention of peroxidation.     

Effect of dietary vitamin E level on growth, tissue lipid peroxidation, and erythrocyte fragility of transgenic coho salmon, Oncorhynchus kisutch

This study was conducted to investigate the effect of dietary vitamin E concentration on growth performance, iron-catalyzed lipid peroxidation in liver and muscle tissue, and erythrocyte fragility of transgenic growth hormone coho salmon (Oncorhynchus kisutch). Fish were fed one of four isoenergetic and isonitrogenous experimental diets that contained either 11, 29, 50, or 105 IU of vitamin E/kg. Following the 10-week feeding trial, no significant (P>0.05) diet-related differences were detected in growth, whole body proximate composition or erythrocyte fragility. The vitamin E contents of liver and muscle, however, were affected by the dietary treatment. Fish fed diets containing > or =50 IU of vitamin E/kg had significantly increased vitamin E concentrations in their tissues. Iron-catalyzed lipid peroxidation of liver and muscle tissue of fish fed elevated dietary vitamin E (> or =50 IU vitamin E/kg diet) was significantly lower (P<0.05) than that noted for fish fed the diet containing no supplemental vitamin E. The results indicated that changes in tissue lipid peroxidation measurements precede clinical signs of sub-optimal vitamin E intake.     

Oral a-tocopherol Supplementation Inhibits Lipid Oxidation in Established Human Atherosclerotic Lesions

Background: Much experimental evidence suggests that lipid oxidation is important in atherogenesis and in epidemiological studies dietary antioxidants appear protective against cardiovascular events. However, most large clinical trials failed to demonstrate benefit of oral antioxidant vitamin supplementation in high-risk subjects. This paradox questions whether ingestion of antioxidant vitamins significantly affects lipid oxidation within established atherosclerotic lesions. Methods and results: This placebo-controlled, double blind study of 104 carotid endarterectomy patients determined the effects of short-term α-tocopherol supplementation (500 IU/day) on lipid oxidation in plasma and advanced atherosclerotic lesions. In the 53 patients who received α-tocopherol there was a significant increase in plasma α-tocopherol concentrations (from 32.66±13.11 at baseline to 38.31±13.87 (mean±SD) μmol/l, p&lt;0.01), a 40% increase (compared with placebo patients) in circulating LDL-associated α-tocopherol (p&lt;0.0001), and their LDL was less susceptible to ex vivo oxidation than that of the placebo group (lag phase 115.3±28.2 and 104.4±15.7 min respectively, p&lt;0.02). Although the mean cholesterol-standardised α-tocopherol concentration within lesions did not increase, α-tocopherol concentrations in lesions correlated significantly with those in plasma, suggesting that plasma α-tocopherol levels can influence lesion levels. There was a significant inverse correlation in lesions between cholesterol-standardised levels of α-tocopherol and 7β-hydroxycholesterol, a free radical oxidation product of cholesterol. Conclusions: These results suggest that within plasma and lesions α-tocopherol can act as an antioxidant. They may also explain why studies using &lt;500 IU α-tocopherol/day failed to demonstrate benefit of antioxidant therapy. Better understanding of the pharmacodynamics of oral antioxidants is required to guide future clinical trials.     

Dietary zinc deficiency decreases plasma concentrations of vitamin E

Experiments were conducted to examine the effects of dietary zinc (Zn) upon plasma vitamin E (E) concentrations to test the hypothesis that there may be a significant dietary interaction between these two nutrients. Weanling female Sprague-Dawley rats were fed diets that were (i) Zn-deficient (less than 0.9 micrograms Zn/g diet) ad libitum; (ii) Zn-adequate (50.9 micrograms Zn/g diet), pair-fed to the Zn-deficient group; and (iii) Zn-adequate (50.9 micrograms Zn/g diet) ad libitum. Plasma E in Zn-deficient animals (4.02 +/- 1.20 micrograms/ml) was significantly reduced (P less than or equal to 0.05) compared with results in both Zn-adequate pair-fed (9.21 +/- 0.70 micrograms/ml) and Zn-adequate ad libitum-fed (9.47 +/- 0.90 micrograms/ml) animals. Zn deficiency in this model system also resulted in significant (P less than or equal to 0.05) reductions in femur and plasma Zn concentrations as well as in plasma retinol, plasma triglyceride, and plasma cholesterol concentrations. Plasma albumin and total plasma protein concentrations were normal in Zn-deficient animals. With dietary Zn deficiency, the decrease in plasma E appeared to be out of proportion to associated decreases in plasma triglyceride and plasma cholesterol concentrations. Since E is associated with plasma lipoproteins, these data suggest that lipid and/or E malabsorption may be a consequence of Zn deficiency. In response to increased dietary intake of E, increments of plasma E were lower in Zn-depleted than in Zn-adequate, pair-fed animals. These findings suggest that dietary Zn deficiency possibly may increase the nutritional requirement for E necessary to maintain adequate plasma concentrations.     

Asian elephant (Elephas maximus) milk composition during the first 280 days of lactation

Milk samples (n = 10) taken during the first 280 days of lactation from one Asian elephant were examined for nutrient composition including total solids, protein, fat, ash, α-tocopherol, and retinol levels. Total solids averaged 19.7 ± 2.7% SD (range 15.0–23.3). Percent protein remained fairly stable throughout this portion of lactation and averaged 3.4 ± 0.3% (range 3.0–.4.0). Ash content averaged 0.54 ± 0.03%. Milk fat and fat soluble vitamin levels varied considerably with a suggestion of a cyclic pattern. Fat content of milk averaged 7.6 ± 2.6% (range 3.9–.12.1); α-tocopheral levels averaged 0.33 ± 0.12 μg/ml; and retinol levels averaged 0.46 ± 0.1 μg/ml. © 1994 Wiley-Liss, Inc.     

Effects of vitamin E and C supplementation either alone or in combination on exercise-induced lipid peroxidation in trained cyclists

Seven trained male cyclists (ate 22.3 +/- 2 years) participated in 4 separate supplementation phases. They ingested 2 capsules per day containing the following treatments: placebo (placebo plus placebo); vitamin C (1 g per day vitamin C plus placebo); vitamin C and E (1 g per day vitamin C plus 200 IU per kg vitamin E); and vitamin E (400 IU per kg vitamin E plus placebo). The treatment order (placebo, vitamin C, vitamin C and E, and vitamin E) was the same for all subjects. Performance trials consisting of a 60-minute steady state ride (SSR) and a 30-minute performance ride (PR) on Cybex 100 Metabolic cycles were performed after each trial. Workloads of 70% of the VO2max were set for the SSR and PR rides, with pedal rate maintained at 90 rpm (SSR) or self determined (PR). Blood samples (5 ml) were drawn pre- and postexercise and analyzed for malonaldehyde (MDA) and lactic acid. The results indicate that vitamin E treatment was more effective than vitamin C alone or vitamin C and E. Pre-exercise plasma levels of MDA in the vitamin E trial was 39% below the pre-exercise MDA levels of the placebo: 2.94 +/- 0.54 and 4.81 +/- 0.65 micromol per ml, respectively. Plasma MDA following exercise in the vitamin E group was also lower than teh placebo: 4.32 +/- 0.37 vs 7.89 +/- 1.0 micromol per ml, respectively. Vitamin C supplementation, on the other hand, elevated both the resting and exercise plasma levels of MDA. None of th supplemental phases had any significant effect on performance. In conclusion, the results indicate that 400 IU/day of vitamin E reduces membrane damage more effectively than vitamin C but does not enhance performance. Athletes are encouraged to include antioxidants, such as vitamin E and C, in their diet to counteract these detrimental effects of exercise. The data presented here suggests that 400 IU/day of vitamin E will provide adequate protection but supplementing the diet with 1 g per day of vitamin C may promote cellular damage. However neither of these vitamins, either alone or in combination, will enhance exercise performance.     

Dietary Vitamin E Deficiency Increases Anxiety-Like Behavior in Juvenile and Adult Rats

Vitamin E deficiency from birth or infancy has recently been found to increase anxiety-like behavior in rodents. The present study was undertaken to elucidate the effect of dietary vitamin E deficiency on anxiety in adult rats in comparison with juvenile rats. Male Wistar rats, 3 or 10 weeks old, were divided into two groups and fed a control or vitamin E-deficient diet for 4 weeks. The results of behavioral analysis revealed that vitamin E-deficiency increased anxiety in both juvenile and adult rats. Plasma, liver, and brain α-tocopherol concentrations decreased significantly due to vitamin E deficiency in both age groups. Plasma corticosterone concentrations were higher in the vitamin E-deficient rats in response to the stress of a behavioral test. Based on these results, we conclude that dietary vitamin-E deficiency induces anxiety in adult rats as well as juvenile rats. This might be due to an elevated plasma corticosterone concentration.