Effects of Melatonin on FSH/LH/Testosterone and StAR/P450scc/17β-HSD3 Pathways in Acrylamide-Induced Testicular Toxication in Rats

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Abstract
Acrylamide (ACR) is a toxic compound formed during high-temperature food processing that is known to induce oxidative stress and reproductive toxicity. This study investigated the protective effects of melatonin (MEL) on ACR-induced testicular toxicity, with a focus on hormonal regulation and steroidogenic pathways. Forty adults male Wistar rats were divided into five groups: control, ACR (50 mg/kg), ACR+MEL10 (ACR + 10 mg/kg MEL), ACR+MEL20 (ACR + 20 mg/kg MEL), and MEL20 (20 mg/kg MEL alone). Treatments were administered via intragastric gavage for 14 days. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured via ELISA, alongside testicular steroidogenic enzyme levels (StAR, P450scc, 17β-HSD3). Histopathological analysis was used to assess spermatogenic integrity via Johnsen scoring. ACR exposure significantly reduced the serum FSH, LH, and testosterone levels (p< .001), with a concurrent decrease in StAR, P450scc, and 17β-HSD3 expression. Histological evaluation revealed severe spermatocyte degeneration, necrosis, and disrupted spermatogenesis. MEL administration ameliorated these effects in a dose-dependent manner. ACR+MEL10 resulted in partial restoration of hormonal and enzymatic levels (p< .05), whereas ACR+MEL20 restored these parameters to near-control levels (p> .05). MEL also mitigated histopathological damage, preserving seminiferous tubule integrity and spermatogenic function. These findings suggest that MEL exerts protective effects against ACR-induced testicular toxicity through its antioxidant and antiapoptotic effects, restoring steroidogenic enzyme activity and the hormonal balance. MEL supplementation may be a potential therapeutic strategy against environmental toxicants affecting male reproductive health. Further mechanistic studies are warranted to elucidate its full protective scope.

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