It was observed that, at the onset of vitamin-A deficiency, the Sertoli cell-spermatid association was disrupted, resulting in a sloughing-off of the germ cells from the germinal epithelium. When the deficiency became acute, the seminiferous tubules were left with only a single layer of spermatogonia, a number of giant cells, and disorganised Sertoli cells. Even though B-type spermatogonia and preleptotene spermatocytes were present in the testes of rats maintained on retinoic acid, many of these were in a degenerated state. Peroxidase perfusion studies showed that the tracer penetrated into the lumen of the seminiferous tubules of the mildly deficient and of the retinoic-acid-maintained rats, while it was mainly concentrated at the periphery of the tubules of the normal rat testes, thereby indicating that deficiency caused disruption of the Sertoli-Sertoli cell junctional complexes and consequently the blood-testis barrier. Supplementation of the retinoate-fed rats with retinyl acetate led to several changes in the seminiferous tubules within 4 days: (1) thinning of the germinal epithelium immediately after the supplementation; (2) re-establishment of the Sertoli-Sertoli cell junctional complexes; (3) cannulation of the lumen of the tubules; (4) appearance of pachytene spermatocytes. Examination of the mitotic activity of the spermatogonial compartment revealed marked reduction in the activity in acutely deficient animals, while in the retinoate-fed rats it was slightly lower than in controls on a diet adequate in vitamin A. Supplementation of the retinoate-treated rats with retinyl acetate led to a gradual increase with time in the percentage of spermatogonia in mitosis.ADDITIONAL ABSTRACT:From 21 days old male rats were given a diet deficient in vitamin A without or with retinyl acetate 280 μg weekly. Some of the deprived rats were killed when their weight plateaued (mild deficiency). The others continued on the deficient diet until their weight had decreased considerably (acute deficiency) or were given 40 μg retinoic acid daily for 35 days when they were killed or were given 280 μg retinyl acetate by mouth and killed at intervals during the next 4 days. At the onset of deficiency the Sertoli cell-spermatid association was disrupted. At the acutely deficient stage the seminiferous tubules had only one layer of spermatogonia, disorganized Sertoli cells and some giant cells. Although B-type spermatogonia and preleptotene spermatocytes were present in rats given retinoic acid, many were degenerate. When rats given retinoic acid were given retinyl acetate, the seminiferous tubules showed thinning of the germinal epithelium, reestablishment of the Sertoli-Sertoli junctional complexes, presence of a lumen in the tubules and appearance of pachytene spermatocytes. The percentage of spermatogonia in mitosis increased when rats on retinoic acid were given retinyl acetate.