Methylmercury-induced testis damage is associated with activation of oxidative stress and germ cell autophagy.,Journal of Inorganic Biochemistry

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Methylmercury-induced testis damage is associated with activation of oxidative stress and germ cell autophagy.
Journal of Inorganic Biochemistry ( IF 3.8 ) Pub Date : 2018-10-18 , DOI: 10.1016/j.jinorgbio.2018.10.007
Na Chen ₁ , Meng Lin ₁ , Na Liu ₁ , Shanshan Wang ₂ , Xianjin Xiao ₁

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Methylmercury (MeHg) is a widespread environmental pollutant and causes a serious hazard to testicular development and spermatogenesis. However, molecular mechanisms underlying male reproductive toxicity induced by MeHg remain elusive. The objective of this study was to explore the effects of MeHg on autophagy induction in germ cells (GCs). In this study, we showed that orally administered MeHg 10 mg/kg per day for five consecutive days resulted in reduced sperm count and impaired sperm motility. Noteworthy, MeHg impaired the seminiferous tubule of rats and increased the apoptotic index of GCs of rats. Furthermore, the levels of the autophagy markers light chain 3-II (LC3-II) and beclin-1 were significantly increased following MeHg treatment, possibly via inhibiting the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (m-TOR) signaling pathway. In addition, these effects are concomitant with the overgeneration of reactive oxygen species (ROS) and the decreased expression of the antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Interestingly, supplementation with MeHg induced oxidative DNA damage in testes of rats. Taken together, our data indicated that MeHg stimulates GC apoptosis through oxidative stress and autophagy, which may be the mechanism responsible for the regulation of testis function and differentiation following MeHg exposure.

中文翻译：

甲基汞诱导的睾丸损伤与氧化应激的激活和生殖细胞自噬有关。

甲基汞（MeHg）是一种广泛的环境污染物，对睾丸发育和精子发生造成严重危害。但是，由甲基汞诱导的男性生殖毒性的分子机制仍然难以捉摸。这项研究的目的是探讨MeHg对生殖细胞（GCs）自噬诱导的影响。在这项研究中，我们显示连续5天每天口服MeHg 10 mg / kg导致精子数量减少和精子活动力受损。值得注意的是，MeHg损害了大鼠的生精小管并增加了大鼠GC的凋亡指数。此外，MeHg处理后自噬标记轻链3-II（LC3-II）和beclin-1的水平显着增加，可能是通过抑制雷帕霉素的磷酸肌醇3-激酶（PI3K）/蛋白激酶B（Akt）/哺乳动物靶标（m-TOR）信号传导途径来实现的。此外，这些影响还伴随着活性氧（ROS）的过度生成以及抗氧化酶超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）的表达降低。有趣的是，补充MeHg会引起大鼠睾丸的DNA氧化损伤。两者合计，我们的数据表明MeHg通过氧化应激和自噬刺激GC凋亡，这可能是MeHg暴露后调节睾丸功能和分化的机制。这些影响与活性氧（ROS）的过度生成以及抗氧化酶超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）的表达降低有关。有趣的是，补充MeHg会引起大鼠睾丸的DNA氧化损伤。两者合计，我们的数据表明MeHg通过氧化应激和自噬刺激GC凋亡，这可能是MeHg暴露后调节睾丸功能和分化的机制。这些影响与活性氧（ROS）的过度生成以及抗氧化酶超氧化物歧化酶（SOD），谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）的表达降低有关。有趣的是，补充MeHg会引起大鼠睾丸的DNA氧化损伤。两者合计，我们的数据表明MeHg通过氧化应激和自噬刺激GC凋亡，这可能是MeHg暴露后调节睾丸功能和分化的机制。

更新日期：2018-10-18

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