EFFECTS OF VITAMIN-A-DEFICIENCY ON THE INTERSERTOLI CELL TIGHT JUNCTIONS AND ON THE GERM-CELL POPULATION

When 20-day-old rats are placed on a vitamin A deficient diet (VAD) for a period of 10 weeks, the seminiferous tubules are found to contain only Sertoli cells, a few residual A0, A1 spermatogonia, and preleptotene spermatocytes (PL). The type A1 spermatogonia and PL spermatocytes are arrested in their G2 phase. In VAD rats type A2-A4, intermediate (In) and B spermatogonia and all types of spermatocytes (except PL spermatocytes) and spermatids are eliminated from the seminiferous tubules. Two questions were raised in this investigation: 1) Is there, in VAD rats, any correlation between a breakdown of the blood-testis barrier (e.g., Sertoli cell tight junctions) and germ cell loss? 2) Is the disappearance of most germinal cells due to their degeneration during spermatogenesis or to a maturation depletion process resulting from an arrest of spermatogenesis at the spermatogonial stage? To investigate these questions four groups of male Sprague-Dawley rats (20-days old) were fed a VAD diet for 7 to 12 weeks. The testes were fixed by perfusion with 2.5% glutaraldehyde in 0.1 M sodium cacodylate containing 2% lanthanum nitrate, an electron opaque tracer used to test the patency of Sertoli cell tight junctions. The lanthanum permeated the intercellular space of the basal compartment but was arrested by normal inter-Sertoli cell tight junctions. The seminiferous epithelium showed numerous degenerating germ cells, some being internalized by Sertoli cells as membrane-bound phagosomes. Thus, these results indicate firstly that inter-Sertoli cell tight junctions remain intact during vitamin A deficiency, and secondly that in a first phase nonviable germinal cells degenerate during spermatogenesis and their residues are actively phagocytosed by Sertoli cells followed by a second phase where the regressed state of the seminiferous epithelium is maintained by a maturation depletion condition resulting from an arrest of spermatogonial proliferation and differentiation.