镉通过诱导特定蛋白质亚组中的酪氨酸磷酸化来抑制小鼠精子活力。
Cadmium inhibits mouse sperm motility through inducing tyrosine phosphorylation in a specific subset of proteins.
作者信息
Wang Lirui, Li Yuhua, Fu Jieli, Zhen Linqing, Zhao Na, Yang Qiangzhen, Li Sisi, Li Xinhong
机构信息
Shanghai Key Lab of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China.
Shanghai Key Lab of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai Jiaotong University, Shanghai 200240, China.
出版信息
Reprod Toxicol. 2016 Aug;63:96-106. doi: 10.1016/j.reprotox.2016.05.018. Epub 2016 May 24.
Cadmium (Cd) has been reported to impair male fertility, primarily by disrupting sperm motility, but the underlying molecular mechanism remains unclear. Here we investigated the effects of Cd on sperm motility, tyrosine phosphorylation, AMP-activated protein kinase (AMPK) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity, and ATP levels in vitro. Our results demonstrated that Cd inhibited sperm motility, GAPDH activity, AMPK activity and ATP production, and induced tyrosine phosphorylation of 55-57KDa proteins. Importantly, all the parameters affected by Cd were restored to normal levels when incubated with 10μM Cd in the presence of 30μM ethylene diamine tetraacetic acid (EDTA). Interestingly, changes of tyrosine phosphorylation levels of 55-57KDa proteins are completely contrary to that of other parameters. These results suggest that Cd-induced tyrosine phosphorylation of 55-57KDa proteins might act as an engine to block intracellular energy metabolism and thus decrease sperm motility.
据报道，镉（Cd）会损害男性生育能力，主要是通过破坏精子活力，但潜在的分子机制仍不清楚。在此，我们在体外研究了镉对精子活力、酪氨酸磷酸化、AMP活化蛋白激酶（AMPK）和甘油醛-3-磷酸脱氢酶（GAPDH）活性以及ATP水平的影响。我们的结果表明，镉抑制精子活力、GAPDH活性、AMPK活性和ATP生成，并诱导55 - 57 kDa蛋白的酪氨酸磷酸化。重要的是，当在30μM乙二胺四乙酸（EDTA）存在的情况下与10μM镉一起孵育时，所有受镉影响的参数都恢复到了正常水平。有趣的是，55 - 57 kDa蛋白酪氨酸磷酸化水平的变化与其他参数的变化完全相反。这些结果表明，镉诱导的55 - 57 kDa蛋白酪氨酸磷酸化可能作为一种机制来阻断细胞内能量代谢，从而降低精子活力。
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