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Effect of vitamin E deficiency on serum concentrations of follicle-stimulating hormone and testosterone during testicular maturation and degeneration.

Although vitamin E has been recognized as a requirement for normal testicular function for more than 50 yr, the functional role of this fat soluble vitamin in the maintenance of spermatogenesis has not been clarified. Vitamin E deficiency has a deleterious effect on germ cell proliferation and differentiation in the rat and a variety of other animal species. The potential effect of vitamin E on the sensitivity of the hypothalmo-hypophyseal-gonadal feedback system has not been previously evaluated. Therefore, serum testosterone concentrations, androgen function in maintaining seminal vesicle weight, and citrate synthesis, as well as the circulating amounts of FSH, were determined in rats fed semipurified diets with vitamin E, control, and without vitamin E, vitamin E-deficient. To assess dietary effects before, during, and after testicular degeneration, analyses were carried out on animals fed the diets starting at 3 weeks of age and continuing for 1 yr. The defect produced by vitamin E deficiency does not reflect impaired gonadotropin function. There are no effects of vitamin E deprivation on either serum levels of testosterone or on seminal vesicle weight and citrate content suggesting that the LH-testosterone feedback loop is not impaired. The feedback loop of FSH and inhibin also appears to be normal. Serum FSH concentrations are not elevated, although the testis is germ cell depleted. Comparison of the vitamin E-deficient model to other models of testicular degeneration suggests that the effect of vitamin E occurs directly or indirectly on the regulation of intratesticular factors which regulate specific steps of germ cell development.