Liu Jing, Wang Ermeng, Xi Zhipeng, Dong Jingwei, Chen Chienmin, Xu Peng, Wang Lan
School of Life Science, Shanxi University, Taiyuan 030006, Shanxi, China.
Department of Environmental Resource Management, Chia Nan University of Pharmacy and Science, Tainan City 000700, Taiwan.
Comp Biochem Physiol C Toxicol Pharmacol. 2024 May;279:109860. doi: 10.1016/j.cbpc.2024.109860. Epub 2024 Feb 20.
Cadmium (Cd) is a highly toxic heavy metal element that might adversely affect sperm function such as the acrosome reaction (AR). Although it is widely recognized that zinc (Zn) plays a crucial role in sperm quality, the complete elucidation of how Zn ameliorates Cd-induced sperm dysfunction is still unclear. In this study, we aimed to explore the protective effects of Zn against the sperm dysfunction induced by Cd in the freshwater crab Sinopotamon henanense. The results demonstrated that Cd exposure not only impaired the sperm ultrastructure, but also caused sperm dysfunction by decreasing the AR induction rate, acrosome enzyme activity, and Ca content in sperm while elevating the activity and transcription expression of key Ca signaling pathway-related proteins Calmodulin (CAM) and Ca-ATPase. However, the administration of Zn was found to alleviate Cd-induced sperm morphological and functional disorders by increasing the activity and transcription levels of CaM and Ca-ATPase, thereby regulating intracellular Ca homeostasis and reversing the decrease in Ca contents caused by Cd. Furthermore, this study was the first to investigate the distribution of metallothionein (MT) in the AR of S. henanense, and it was found that Zn can reduce the elevated levels of MT in crabs caused by Cd, demonstrating the significance of Zn in inducing MT to participate in the AR process and in metal detoxification in S. henanense. These findings offer novel perspectives and substantiation regarding the utilization of Zn as a protective agent against Cd-induced toxicity and hold significant practical implications for mitigating Cd-induced sperm dysfunction.
镉(Cd)是一种剧毒重金属元素,可能会对精子功能产生不利影响,如顶体反应(AR)。尽管人们普遍认识到锌(Zn)在精子质量中起着关键作用,但锌如何改善镉诱导的精子功能障碍仍未完全阐明。在本研究中,我们旨在探讨锌对河南华溪蟹镉诱导的精子功能障碍的保护作用。结果表明,镉暴露不仅损害精子超微结构,还通过降低顶体反应诱导率、顶体酶活性和精子中的钙含量,同时提高关键钙信号通路相关蛋白钙调蛋白(CAM)和钙-ATP酶的活性及转录表达,导致精子功能障碍。然而,发现锌的施用通过增加钙调蛋白和钙-ATP酶的活性及转录水平来减轻镉诱导的精子形态和功能障碍,从而调节细胞内钙稳态并逆转镉引起的钙含量下降。此外,本研究首次研究了金属硫蛋白(MT)在河南华溪蟹顶体反应中的分布,发现锌可以降低镉引起的蟹体内金属硫蛋白水平升高,证明锌在诱导金属硫蛋白参与河南华溪蟹顶体反应过程和金属解毒中的重要性。这些发现为锌作为镉诱导毒性的保护剂的利用提供了新的视角和依据,对减轻镉诱导的精子功能障碍具有重要的实际意义。