Figure 7.

Schematic diagram of the proposed model for stress-induced spermatogenesis impairment. A proposed molecular mechanism for the stress-induced decrease of sperm concentration in the rat epididymis involves two parts: (i) stress activates GR signaling due to increased levels of glucocorticoids, which then induces spermatids apoptosis via upregulating BAX, p53, and cleaved CASPASE 3 and (ii) stress inhibits cell cycle progression of spermatogonia at the G₀/G₁ phase by downregulation of CDK4, CYCLIN D1, and p-RB. Both of these two aspects may explain the decreased number of spermatids, leading to reduced epididymal sperm concentration.