BPS has detrimental effects on human reproductive health and emerged as an environmental contaminant for global health concern. This study deals with the adverse impact of BPS exposure on testicular oxidative stress, inflammation and apoptosis in adult male golden hamster, Mesocricetus auratus and its amelioration by melatonin. BPS (75 mg/kg BW/day) exposure caused testicular impairment as evident by histological degenerative changes, declined sperm quality (viability and motility), serum levels of testosterone and melatonin with a concomitant decrease in testicular androgen receptor (AR) and melatonin receptor (MT1) expression. The BPS exposure caused marked increase in testicular oxidative load, inflammation (NF-kB/COX-2) and apoptosis (caspase-3). Melatonin (10 mg/kg BW/alternate day) pretreatment to BPS exposed hamsters resumed normal testicular histoarchitecture, sperm quality and decreased testicular oxidative load as evident by enhanced antioxidant enzymes (SOD and catalase) activities and decreased lipid peroxidation (LPO) level. Further, melatonin also stimulated the testicular antioxidant proteins Nrf-2/HO-1, SIRT-1/FOXO-1 and reduced inflammatory proteins NF-kB/COX-2 expression to counteract BPS induced testicular damages. Melatonin administration to the BPS treated hamsters resulted in increased testicular cell proliferation (PCNA), survival (Bcl-2), gap junction (connexin-43) and decreased apoptosis (caspase-3). In conclusion, our study documented the detrimental effects of BPS on testes that compromises male fertility. Further, melatonin was found as a potent molecule that rescued the BPS induced testicular damages in male golden hamster Mesocricetus auratus.

中文翻译：

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褪黑激素通过调节 Nrf-2/HO-1 和 SIRT-1/FOXO-1 表达改善双酚 S 诱导的睾丸损伤

BPS 对人类生殖健康有不利影响，并已成为引起全球健康关注的环境污染物。本研究涉及 BPS 暴露对成年雄性金仓鼠 Mesocricetus auratus 睾丸氧化应激、炎症和细胞凋亡的不利影响及其通过褪黑激素的改善。BPS（75 毫克/千克体重/天）暴露导致睾丸损伤，表现为组织学退行性变化、精子质量下降（活力和活力）、血清睾酮和褪黑激素水平以及睾丸雄激素受体 (AR) 和褪黑激素受体的降低(MT1) 表达。BPS 暴露导致睾丸氧化负荷、炎症 (NF-kB/COX-2) 和细胞凋亡 (caspase-3) 显着增加。褪黑激素（10 毫克/千克体重/隔天）对暴露于 BPS 的仓鼠进行预处理恢复了正常的睾丸组织结构、精子质量和降低的睾丸氧化负荷，这可以通过增强的抗氧化酶（SOD 和过氧化氢酶）活性和降低的脂质过氧化（LPO）水平来证明。此外，褪黑激素还刺激睾丸抗氧化蛋白 Nrf-2/HO-1、SIRT-1/FOXO-1 并降低炎症蛋白 NF-kB/COX-2 的表达，以抵消 BPS 诱导的睾丸损伤。向 BPS 处理的仓鼠施用褪黑激素导致睾丸细胞增殖 (PCNA)、存活 (Bcl-2)、间隙连接 (connexin-43) 和细胞凋亡 (caspase-3) 增加。总之，我们的研究记录了 BPS 对影响男性生育能力的睾丸的不利影响。更多，