Effect of Heavy Metals on Tyrosine Kinases Signaling during Sperm Capacitation

Bhawna Kushwaha, R. Beniwal, Aradhana Mohanty, Ajay K. Singh, R. Yadav, S. K. Garg
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引用次数: 1

Abstract

Sperm capacitation is the key event prior to fertilization. Success rate of currently used assisted reproductive technology like in-vitro fertilization is 50% dependent on sperm maturation or capacitation. In-vivo capacitation occur almost in female reproductive tract in response to various signaling or enzymatic molecules. Interestingly, both early and late events of capacitation are centrally regulated by protein kinase A (PKA). Influx of Ca2+ and HCO3-transmembrane drive leads to change in pH and intracellular cAMP which ultimately activate PKA regulated capacitation. PKA phosphorylates several target proteins that are presumed to initiate different signaling pathways. Some divalent heavy metals like lead, mercury, arsenic and cadmium mimic Ca++ entry and its functions and ultimately affect capacitation by inhibiting or inducing tyrosine phosphorylation. In this chapter we review the mechanism of heavy metals by which they affect the tyrosine phosphorylation during sperm capacitation.
重金属对精子获能过程中酪氨酸激酶信号传导的影响
精子获能是受精前的关键事件。目前使用的辅助生殖技术如体外受精的成功率为50%,取决于精子的成熟或获能。体内能化几乎发生在女性生殖道,是对各种信号或酶分子的反应。有趣的是,早期和晚期的获能事件都是由蛋白激酶A (PKA)集中调节的。Ca2+和hco3跨膜驱动的内流导致pH和细胞内cAMP的变化,最终激活PKA调节的容能。PKA磷酸化几种被认为启动不同信号通路的靶蛋白。一些二价重金属如铅、汞、砷和镉模拟ca2 +的进入及其功能,并最终通过抑制或诱导酪氨酸磷酸化来影响能化。本章综述了重金属对精子获能过程中酪氨酸磷酸化的影响机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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