HISTOPATHOlOGICAL EVIDENCE OF IRREVERSIBLE TESTICULAR INJURY AND SPERMATOGENESIS DISRUPTION IN A CONTINUOUS SCROTAL HYPERTHERMIA- INDUCED AZOOSPERMIA RAT MODEL

Non-obstructive azoospermia (NOA) is a cause of male infertility characterized by impaired spermatogenesis. NOA remains a challenge for both research and treatment development. Reliable animal models are essential for better understanding its pathophysiology and evaluating therapeutic approaches. Scrotal hyperthermia induction is a cost-effective and technically feasible method for inducing NOA. However, the impact of different exposure patterns remains unsolved. In this study, a total of 30 adult male Rattus norvegicus were randomly assigned to control, discontinuous hyperthermia (every other day), and continuous hyperthermia (daily) groups. This study applied the heat exposure by immersing the scrotum in a 45°C water bath for 20 minutes over 22 days. Sperm parameters, testicular weight, and histopathological changes were assessed at baseline, during treatment, and after a recovery phase. Both hyperthermia protocols significantly reduced testicular weight and deteriorated sperm concentration, motility, and morphology compared with controls, with complete azoospermia observed by day 22. Histological examination revealed marked disruption of the seminiferous epithelium and significantly decreased Johnsen scores in both heat-treated groups. Interestingly, partial histological recovery and improved Johnsen scores were noted in the discontinuous group by day 37, whereas continuous exposure led to sustained, irreversible testicular degeneration. These findings indicate that both continuous and discontinuous scrotal hyperthermia reliably induce azoospermia in rats. The continuous exposure produces more severe and permanent impairment. On the other hand, discontinuous hyperthermia allows for partial recovery. These two induction patterns may serve as a useful model for studying disease progression and potential therapeutic interventions for NOA.