Spermatogenesis and blood–testis barrier in rats after long-term Vitamin A deprivation

Retinoids and spermatogenesis: Lessons from mutant mice lacking the plasma retinol binding protein

“…3I). The large variety of abnormal tubule sections found within a given VADD8 or VADD10 Rbp4-null testis has also been described in vitamin A-deficient rats (Morales and Cavicchia, 2002) and most probably reflects differences in the local stores of ROL and RE along the seminiferous epithelium. VADD8 Rbp4-null males displayed both normal and abnormal tubules, and 82 Ϯ 8% (mean Ϯ SD; n ϭ 3) of the abnormal ones belonged to the first type (T1, Fig.…”

“…In the extensively studied vitamin A-deficient rat model, meiotic and post-meiotic germ cells vanish within 1 to 2 weeks following the disappearance of circulating ROL, yielding tubules containing Sertoli cells, preleptotene spermatocytes, and type A spermatogonia Sobhon et al, 1979;Huang et al, 1988;van Pelt and de Rooij, 1990b;de Rooij et al, 1994;Morales and Cavicchia, 2002; and references therein). The rapidity of the seminiferous epithelium regression and the fact that, due to the disorganization of the seminiferous epithelium, tubule sections cannot be staged (Huang and Hembree, 1979;de Rooij et al, 1994;Morales and Cavicchia, 2002) represent serious drawbacks for investigating the kinetic of VAD-induced testis degeneration.…”

“…In the extensively studied vitamin A-deficient rat model, meiotic and post-meiotic germ cells vanish within 1 to 2 weeks following the disappearance of circulating ROL, yielding tubules containing Sertoli cells, preleptotene spermatocytes, and type A spermatogonia Sobhon et al, 1979;Huang et al, 1988;van Pelt and de Rooij, 1990b;de Rooij et al, 1994;Morales and Cavicchia, 2002; and references therein). The rapidity of the seminiferous epithelium regression and the fact that, due to the disorganization of the seminiferous epithelium, tubule sections cannot be staged (Huang and Hembree, 1979;de Rooij et al, 1994;Morales and Cavicchia, 2002) represent serious drawbacks for investigating the kinetic of VAD-induced testis degeneration. Actually, the vast majority of the studies published so far have focused on the re-initiation of spermatogenesis by retinoid feeding after vitamin A depletion and, thus, on the function of RA in the regeneration, but not in the degeneration of the seminiferous epithelium (Huang and Hembree, 1979;Morales and Griswold, 1987;Ismail et al, 1990;Meistrich, 1991, 1992;Wang and Kim, 1993;van Pelt et al, 1995;and references therein).…”

Retinoic Acid Metabolism and Signaling Pathways in the Adult and Developing Mouse Testis

“…In the testis, it enhances testosterone production (3,4), permits the maintenance of Sertoli cell tight junctions that contribute to the blood-testis barrier (Ref. 5 and references therein), and plays indispensable roles in spermatogenesis by promoting spermatogonia differentiation, adhesion of germ cells to Sertoli cells, and release of mature spermatids into the lumen of seminiferous tubules (Refs. 6 and 7 and references therein).…”

Role of retinoid signaling in the regulation of spermatogenesis

“…This suggests that the degeneration of germ cells occurring in VAD rats was not due to a breakdown of the inter-Sertoli cell tight junctions, but instead, was an immediate consequence of the absence of vitamin A. Recent studies support the effect of VAD on Sertoli cell tight junctions, noting that lanthanum nitrate penetrated deeply into the seminiferous cords in VAD rat testis (3-9 weeks after the onset of growth retardation) (Morales and Cavicchia, 2002). The Sertoli cell barrier could be restored by vitamin A replenishment following prolonged VAD (7-9 weeks after the onset of growth retardation).…”