Modification of Sertoli cell functions in vitamin A-deficient rats.

FSH binding and cAMP responses to FSH in Sertoli cell-enriched testes were not affected by the vitamin A (retinol) status of the animals. These results indicate that changes in Sertoli cell functions during vitamin A deficiency are independent of FSH-Sertoli cell interactions. Concentrations of serum androgen binding protein (ABP) in vitamin A-deficient rats were consistently higher than those of control animals throughout the study period. The accumulation of testicular fluid after efferent duct ligation, an indication of Sertoli cell secretory function, was normal in vitamin A-deficient rats at least until 70 days of age, but declined thereafter. ABP concentrations in seminiferous tubular fluid of vitamin A-deficient rats increased transitorily during the 70-80-day age period but returned to normal by 90 days. The increment of ABP in seminiferous tubular fluid after efferent duct ligation, and ABP concentrations in interstitial fluid were consistently lower in vitamin A-deficient rats. The higher serum ABP in vitamin A-deficient rats therefore cannot be explained by an increase in the permeability of Sertoli-cell tight junctions or basement membrane.

Dissociation of qualitative and quantitative effects of the suppression of testicular testosterone upon spermatogenesis.

The present study examined the quantitative and qualitative effects of suppressed testicular testosterone concentration upon spermatogenesis. Adult male rats were given sc implants of 0.5- to 5-cm long testosterone filled silastic capsules (TC) for 10 weeks. Testicular testosterone concentrations were suppressed to below 5% of the control level in rats receiving 1.5- to 5-cm TC implants. Spermatogenesis was arrested at early spermatids in rats given 1.5-cm TC implants, but was maintained in those given 3- or 5-cm TC implants. The number of A1 spermatogonia was 10-15% higher in rats bearing 0.75- to 1.5-cm TC implants, while a 5-15% reduction in preleptotene spermatocytes was noted in rats receiving 1.5-cm or longer TC implants. Linear regression analysis revealed a significant negative correlation between the number of A1 spermatogonia and the percent yield of preleptotene spermatocytes. This result illustrates the presence of a negative feedback mechanism in the regulation of A1 spermatogonia. The lack of a correlation between the quantitative changes in germ cell number and the hormonal states suggests that factors or local mechanisms independent of the concentration of hormones are involved in the regulation of germ cell differentiation.

Disruption of sustentacular (Sertoli) cell tight junctions and regression of spermatogenesis in vitamin-A-deficient rats.

The relationship between the intactness of sustentacular (Sertoli) cell tight junctions and the status of spermatogenesis was examined in rats fed a vitamin-A-deficient diet after weaning (VAD rats). Both serum and testicular retinol concentrations of the VAD rats declined to a nadir by 80 days of age. At this time, it was observed that Sertoli cell tight junctions of the VAD animals were intact and complete spermatogenesis was maintained. Leakage in Sertoli cell tight junctions, as demonstrated by the presence of lanthanum in the adluminal compartment of the seminiferous epithelium, was first observed in 90-day-old VAD rats. Severe regression of spermatogenic cells was noted in 100-day or older VAD animals. These results suggest that severe germ cell loss observed during chronic vitamin A deficiency may result from abnormal intratubular environment due to the disruption of the blood-testis barrier.