The Role of Zinc in Male Fertility.
The Role of Zinc in Male Fertility.
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锌在男性生育中的作用。
DOI：
10.3390/ijms21207796
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发表时间：
2020-10-21
影响因子：
5.6
通讯作者：
Breitbart H
中科院分区：
文献类型：
--
作者：
Allouche-Fitoussi D;Breitbart H
多项研究提出了锌离子在男性生育能力中的重要性。在这里，我们描述了 Zn2+ 在精子中的特性、作用和细胞作用机制，重点关注其参与精子活力、获能和顶体胞吐作用，这三个功能对于成功受精至关重要。还描述了补充锌对辅助受精技术的影响。锌对精子活力的影响已在许多脊椎动物和无脊椎动物中进行了研究。据报道，人精浆中的 Zn2+ 会降低精子的活力，而去除 Zn2+ 会增强精子的活力。附睾运输过程中细胞内 Zn2+ 浓度的降低使得精子获能过程中的前向运动和随后的过度活跃运动得以发展。细胞外 Zn2+ 通过与 Zn2+ 传感受体 (ZnR)（也称为 GPR39）相互作用影响细胞内信号传导通路。该受体存在于精子尾部和顶体中，表明 Zn2+ 可能参与精子运动和顶体胞吐作用。我们的研究表明，Zn2+ 刺激牛精子顶体胞吐作用以及人类精子的过度活跃运动，都是由 GPR39 介导的。 Zn2+ 结合并激活 GPR39，后者激活跨膜腺苷酸环化酶 (tmAC) 以催化 cAMP 产生。 NHE（Na+/H+-交换器）被 cAMP 激活，导致 pHi 增加并激活精子特异性 Ca2+ 通道 CatSper，导致 [Ca2+]i 增加，与 HCO3− 一起激活可溶性腺苷酸环化酶 (sAC)。 [cAMP]i 的增加激活蛋白激酶 A (PKA)，随后激活 Src-表皮生长因子受体 -P 磷脂酶 C (Src-EGFR-PLC) 级联，导致肌醇三磷酸 (IP3) 的产生，从而动员顶体中的 Ca2+，导致 [Ca2+]i 进一步增加并产生过度激活的运动。 PKA 还会激活磷脂酶 D1 (PLD1)，导致获能过程中 F-肌动蛋白的形成。在顶体胞吐作用之前，PLC诱导磷脂酰肌醇-4,5-二磷酸（PIP2）水解，导致肌动蛋白切断蛋白凝溶胶蛋白释放到胞质溶胶中，该蛋白被Ca2+激活，导致F-肌动蛋白分解并发生顶体胞吐作用。
Several studies proposed the importance of zinc ion in male fertility. Here, we describe the properties, roles and cellular mechanisms of action of Zn2+ in spermatozoa, focusing on its involvement in sperm motility, capacitation and acrosomal exocytosis, three functions that are crucial for successful fertilization. The impact of zinc supplementation on assisted fertilization techniques is also described. The impact of zinc on sperm motility has been investigated in many vertebrate and invertebrate species. It has been reported that Zn2+ in human seminal plasma decreases sperm motility and that Zn2+ removal enhances motility. Reduction in the intracellular concentration of Zn2+ during epididymal transit allows the development of progressive motility and the subsequent hyper activated motility during sperm capacitation. Extracellular Zn2+ affects intracellular signaling pathways through its interaction with the Zn2+ sensing receptor (ZnR), also named GPR39. This receptor was found in the sperm tail and the acrosome, suggesting the possible involvement of Zn2+ in sperm motility and acrosomal exocytosis. Our studies showed that Zn2+ stimulates bovine sperm acrosomal exocytosis, as well as human sperm hyper-activated motility, were both mediated by GPR39. Zn2+ binds and activates GPR39, which activates the trans-membrane-adenylyl-cyclase (tmAC) to catalyze cAMP production. The NHE (Na+/H+-exchanger) is activated by cAMP, leading in increased pHi and activation of the sperm-specific Ca2+ channel CatSper, resulting in an increase in [Ca2+]i, which, together with HCO3−, activates the soluble adenylyl-cyclase (sAC). The increase in [cAMP]i activates protein kinase A (PKA), followed by activation of the Src-epidermal growth factor receptor-Pphospholipase C (Src-EGFR-PLC) cascade, resulting in inositol-triphosphate (IP3) production, which mobilizes Ca2+ from the acrosome, causing a further increase in [Ca2+]i and the development of hyper-activated motility. PKA also activates phospholipase D1 (PLD1), leading to F-actin formation during capacitation. Prior to the acrosomal exocytosis, PLC induces phosphadidylinositol-4,5-bisphosphate (PIP2) hydrolysis, leading to the release of the actin-severing protein gelsolin to the cytosol, which is activated by Ca2+, resulting in F-actin breakdown and the occurrence of acrosomal exocytosis.
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影响因子：
3.6
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Bajpai, M;Fiedler, SE;Carr, DW
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