Dietary vitamin E and beta-carotene sources influence vitamin A and E storage in young rats fed marginal and adequate vitamin E

The effects of two vitamin E levels (30 and 75 IU/kg diet) and the interrelation of two vitamin E sources [dl-alpha-tocopheryl acetate (dl-alpha-TA) and d-alpha-tocopheryl acid succinate (d-alpha-TAS)] and three vitamin A sources [retinyl palmitate (RP), all-trans synthetic beta-carotene (SBC), and natural beta-carotene (NBC)] were studied. Dietary vitamin A sources provided 4,000 IU/kg. Twelve groups of Fischer 344 rats (10/group) were fed designated diets for eight weeks. For RP, SBC, and NBC, the increase in each vitamin E source from a marginal to an adequate dietary level caused a significant increase in liver and heart alpha-tocopherol. Among rats fed diets with an adequate level of vitamin E, d-alpha-TAS was not as effective as dl-alpha-TA in increasing liver alpha-tocopherol levels. Plasma retinol was lower in rats fed d-alpha-TAS than in those fed dl-alpha-TA. Among rats fed diets with an adequate level of dl-alpha-TA, those fed SBC had significantly higher liver and heart alpha-tocopherol concentrations than did all other groups (p < 0.05). Liver retinol equivalents for rats fed NBC were approximately 66% lower than those in rats fed SBC or RP (p < 0.05). The roles of the two vitamin E sources in alpha-tocopherol metabolism are not equivalent. These data indicate that vitamin A source influences the magnitude of the tissue vitamin A and E changes in response to the two vitamin E sources.     

The promotion of vitamin E

Investigations that have influenced the promotion of vitamin E supplementation are reviewed. The various forms of vitamin E found in foods and the composition of synthetic vitamin E in common use are described with note of a frequent error of identification made in reports of studies on vitamin E. Recent communications on the use of antioxidants to delay carcinogenesis in animals and in humans are discussed. The publicity given the reports of cancer prevention by antioxidants will probably increase self-supplementations. It is therefore necessary to understand the pharmacological limits of such supplementation with vitamin E. Daily supplementation of adults with about 200 mg of d-alpha-tocopherol equivalents per day has not been proven to be harmful, but the effects of ingestion of more than 800 mg a day have not been studied sufficiently. Special precautions should be taken in administering emulsified vitamin E preparations intravenously to premature infants.     

Adipose tissues and vitamin E

1. Vitamin E content in the adipose tissue was examined in rats with and without vitamin E deficiency. With the progression of vitamin E depletion, the more rapid decrease in tocopherol concentration was observed in brown adipose tissue (BAT) than in white adipose tissue (WAT), and the rate of decrease of tocopherol was approximately three times faster in BAT than in WAT. After the intramuscular administration of 10 mg/kg of all-rac-tocopheryl acetate twice a week for two weeks to vitamin E-deficient rats, a similar pattern of increase was observed in the tocopherol concentrations of BAT and WAT, although the rate of increase was slower in WAT than in BAT. 2. Changes of tocopherol concentration in BAT and WAT were investigated in normo-nourished rats with hyperlipemia produced by the intramuscular injection of Triton WR-1339 for 7 days. A marked increase in tocopherol concentration was observed in both BAT and WAT in the late period of hyperlipemia, with the increase being greater in WAT. 3. The fatty acid composition of adipose tissue was compared between rats with and without vitamin E deficiency. No significant differences were observed in BAT and WAT between the two groups. 4. The glucose uptake of WAT was not altered in vitamin E-deficient rats when compared with control rats.     

Comparison of a vitamin E-rich diet and supplemental vitamin E on measures of vitamin E status and lipoprotein profile

OBJECTIVE: To determine whether dietary modification rather than use of supplements can raise indices of vitamin E status to potentially cardioprotective levels. DESIGN: Eight week randomised controlled trial with parallel treatments to compare increased use of vitamin E-rich foods, supplementation with 200 IU of vitamin E, and a placebo. SETTING: Dunedin, New Zealand. SUBJECTS: Ninety subjects were recruited, of whom 82 non-smoking, free-living individuals aged 22-72 y with plasma cholesterol <7.5 mmol/l completed the trial. MAIN OUTCOME MEASURES: Dietary intakes, plasma alpha tocopherol, plasma alpha tocopherol/cholesterol ratio and lipoprotein cholesterol. RESULTS: Consumption of an additional 12 mg of vitamin E (alpha tocopherol equivalents) from dietary sources was primarily achieved through the replacement of saturated fat-rich foods with unsaturated fats rich in vitamin E, nuts and vegetables. This resulted in a 3.4 micromol/l increase in plasma alpha tocopherol at week 6 (95% CI 1.6-5.3), and 0.9 micromol/mmol in plasma alpha tocopherol/cholesterol at weeks 4 and 6 (95% CI 0.3-1.4 and 0.4-1.4, respectively) when compared with the placebo group. In the supplement group, plasma alpha tocopherol and plasma alpha tocopherol/cholesterol were significantly increased within 2 weeks and remained so throughout the 8 week intervention. CONCLUSION: Increasing dietary vitamin E intake can increase plasma alpha tocopherol levels, although factors other than dietary intake are also important determinants. The extent of dietary modification required to achieve potentially cardioprotective levels of plasma alpha tocopherol is difficult in practice. SPONSORSHIP: The study was supported through the Otago Medical Research Foundation Laurenson Award.     

Relationships between vitamin A and vitamin E in the chick

Plasma levels of vitamins A and E were analysed during the dietary administration of two levels of vitamin A (10 000 or 50 000 IU/kg) in combination with four levels of supplemental vitamin E (0, 50, 100, or 150 mg/kg) and with or without a supplement of oil to the diet. Tocopherol levels in plasma were markedly decreased by the higher vitamin A supplementation. In contrast, the various vitamin E intakes had no influence on plasma retinol levels. The addition of oil to the diet did not affect this interaction. The absorption, distribution and elimination of labeled 3H-dl-alpha-tocopheryl acetate after an oral or intravenous administration, in combination with a high oral dose of vitamin A (100 000 IU/chick), were studied. The high oral single dose of vitamin A reduced the levels of radioactivity in all the analysed tissues and organs, when both vitamins were administered orally. However, vitamin A did not affect distribution and elimination of radioactivity, when an interaction in the gastro-intestinal tract was avoided by different routes of administration.     

Serum vitamin E levels in very low-birth weight infants receiving vitamin E in parenteral nutrition solutions

Serum vitamin E levels were measured in 17 very low-birth weight infants in the first 2 wk of life, before and after the institution of intravenous vitamin E supplementation in a dosage of 4.5 mg/day, as a component of MVI Pediatric multivitamin preparation. Serum vitamin E levels were 0.22 +/- 0.16 (SD) mg/dl before supplementation, and rose to 2.55 +/- 0.65 (SD) mg/dl in nine infants more than 899 g birth weight, and rose to 3.68 +/- 0.70 (SD) mg/dl in six infants less than 900 g at birth. These postsupplementation serum vitamin E levels are in the range in which a reduction of incidence or severity of retinopathy of prematurity and intraventricular cerebral hemorrhage has been reported by others. No toxic effects of the preparation or of the increased vitamin E levels were found.