Neuropsychological stress impairs reproductive success via glucocorticoid-mediated endocrine disruption and testosterone-dependent spermatogenic failure

Abstract

Neuropsychological stress has been implicated in male reproductive dysfunction; however, the mechanistic pathways linking stress exposure to fertility impairment remain insufficiently defined. Activation of the hypothalamic–pituitary–adrenal (HPA) axis during stress elevates glucocorticoids, which may suppress androgen signalling and compromise spermatogenesis. This study investigated whether neuropsychological stress impairs male fertility through glucocorticoid-mediated endocrine disruption and testosterone-dependent spermatogenic failure in male rats. Sixty Wistar rats were randomized into control and stress-exposed groups subjected to swinging stress for 3, 7, 14, or 21 days. Stressed males were paired with non-stressed female rats to assess reproductive outcomes. Serum corticosterone and testosterone concentrations, semen quality indices (sperm count, motility, morphology), testicular weight and volume, litter characteristics, and testicular histology were evaluated. Neuropsychological stress produced a graded, duration-dependent increase in serum corticosterone accompanied by a significant reduction in testosterone levels. These endocrine alterations were associated with declines in sperm count, progressive motility, and normal morphology, together with reductions in testicular weight and volume. Reproductive success decreased progressively with increasing stress duration, and mating failure occurred following 21-day exposure, whereas pup weight and litter size were not significantly altered in matings that resulted in pregnancy. Qualitative H & E evaluation did not reveal overt structural disruption of seminiferous tubules or leydig cell distribution; however, quantitative morphometric analysis was not performed. These findings are consistent with glucocorticoid-associated suppression of androgen signalling and testosterone-dependent spermatogenic failure, rather than overt testicular structural damage. Although LH, FSH, and GnRH were not directly measured, the observed endocrine pattern suggests possible HPA–HPG axis interaction linking stress exposure to male infertility. • Stress raises corticosterone and lowers testosterone in male rats. • Longer stress reduces sperm count, motility, and morphology. • Reproductive success declines with stress; mating fails at 21 days. • Testicular weight and volume fall despite intact histology. • HPA–gonadal endocrine disruption mediates stress-linked infertility.