A potential mechanism associated with lead-induced testicular toxicity in rats
A potential mechanism associated with lead-induced testicular toxicity in rats
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DOI：
10.1111/and.12750
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发表时间：
2017-11-01
期刊：
影响因子：
2.4
通讯作者：
Saleh, A. A.
中科院分区：
文献类型：
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作者：
El-Magd, M. A.;Kahilo, K. A.;Saleh, A. A.
本研究旨在探讨铅（Pb）诱导睾丸毒性的机制。我们研究了铅毒性对 17 β-雌二醇 (E2)、雌激素受体 (ER) 和芳香酶 P450 的影响，这些都是精子发生的关键因素。用醋酸铅（PbAc，饮用水中 50 mg/L）治疗大鼠可显着降低精子数量、活力、活力，并增加精子异常以及生精小管和 Leydig 细胞的退行性变化。此外，给予 PbAc 导致血清睾酮、血清和睾丸 E2 显着降低，以及睾丸睾酮水平升高。铅还会诱导睾丸氧化应激，表现为超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶抗氧化酶活性显着降低，以及睾丸中丙二醛水平升高。在分子水平上，Pb 处理下调了 P450 arom (Cyp19) 和 ERa 的 mRNA 表达。总之，Pb 至少部分通过下调 Cyp19 和 ERa 表达来诱导睾丸氧化损伤并扰乱精子发生，从而进一步降低 E2 水平。因此，这些数据可以深入了解铅引起的睾丸毒性的机制。
This study was conducted to investigate the mechanism of lead (Pb)-induced testicular toxicity. We examined the impact of Pb toxicity on 17 beta-oestradiol (E2), oestrogen receptors (ERs) and aromatase P450 which are key factors in spermatogenesis. Treatment of rats with Pb acetate (PbAc, 50 mg/L in drinking water) significantly reduced sperm count, motility, viability and increased sperm abnormalities along with degenerative changes in seminiferous tubules and Leydig cells. Additionally, administration of PbAc resulted in a significant reduction in serum testosterone, serum and testicular E2 as well as increased level of testicular testosterone. Pb also induced testicular oxidative stress as evidenced by a significant decrease in the activities of superoxide dismutase, glutathione peroxidase and catalase antioxidant enzymes, and increased malondialdehyde level in the testis. At the molecular level, Pb treatment downregulated the mRNA expression of P450 arom (Cyp19) and ERa. In conclusion, Pb induces testicular oxidative damage and disrupts spermatogenesis, at least in part, via downregulation of Cyp19 and ERa expression, which further decrease E2 level. These data, therefore, provide insight into the mechanism of lead-induced testicular toxicity.