Dietary vitamin E intake and mammary carcinogenesis in rats.

Abstract

Using the dimethylbenz[a]anthracene-induced mammary tumor model, the present study demonstrated that a low vitamin E intake (7.5 mg/kg of diet) had minimal effect on carcinoma development in rats fed a 5% stripped corn oil diet, but resulted in a marked enhancement in tumor incidence and yield in those rats fed a 25% stripped corn oil ration. Control animals in this experiment received an adequate supply of vitamin E (30 mg/kg as DL-alpha-tocopheryl acetate). Thus, the effect of vitamin E deficiency on mammary carcinogenesis was accentuated in rats maintained on a high polyunsaturated fat diet, an observation similar to that of selenium deficiency which was reported by the author in a previous publication. In view of the biochemical interaction between vitamin E and selenium as endogenous antioxidants, another experiment was conducted to determine whether supranutritional supplementation of vitamin E (1000 mg/kg) was able to block the enhancement in mammary tumorigenesis due to selenium deprivation. Results of this experiment indicated that vitamin E excess failed to overcome the augmented tumor yield in selenium-deficient rats, nor did it provide any protection in rats that received an adequate supply of selenium. In summary, vitamin E deficiency may increase the risk of neoplastic development, especially when coupled with a high polyunsaturated fat intake; however, a high vitamin E supplementation does not seem to have any prophylactic effect on tumorigenesis by itself.