Background

Bisphenol A (BPA), a widely used plastic monomer and plasticizer, is detectable in blood, urine and semen of a healthy people, with concentrations ranging from 0.1 nM to 10 nM. It has been shown that in vitro exposure of BPA as low as 0.001 nM could significantly inhibited mouse sperm motility and acrosome reaction. However, it is still unclear whether BPA at those physiologically detectable concentration affects human sperm.

Methods

The effects of different concentrations of BPA (0, 10⁻³, 10⁻², 10⁻¹, 10, 10³ nM) on sperm functions were examined, including human sperm viability, kinematic parameters, hyperactivation and capacitation.

Results

BPA caused a remarkable decline in human sperm viability, motility and progressive motility, hyperactivation, capacitation and progesterone-induced acrosome reaction. Mechanism studies showed that BPA could suppress the protein tyrosine phosphorylation level of human sperm, but had no effect on sperm calcium signaling.

Conclusions

Physiologically detectable concentrations of BPA may impair human sperm functions via suppressing protein tyrosine phosphorylation of human sperm, implying that environmental pollution of BPA might be a factor contributing to male infertility.

中文翻译：

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生理学上可检测的双酚 A 通过减少蛋白质-酪氨酸磷酸化来损害人类精子功能

背景

双酚 A (BPA) 是一种广泛使用的塑料单体和增塑剂，可在健康人的血液、尿液和精液中检测到，浓度范围为 0.1 nM 至 10 nM。已经表明，低至 0.001 nM 的 BPA 的体外暴露可以显着抑制小鼠精子活力和顶体反应。然而，目前尚不清楚这些生理可检测浓度的 BPA 是否会影响人类精子。

方法

检查了不同浓度的 BPA (0, 10 ^-3 , 10 ^-2 , 10 ^-1 , 10, 10 ³ nM) 对精子功能的影响，包括人类精子活力、运动学参数、过度活化和获能。

结果

BPA 导致人类精子活力、运动性和进行性运动、过度活化、获能和孕酮诱导的顶体反应显着下降。机制研究表明，BPA 可以抑制人类精子的蛋白质酪氨酸磷酸化水平，但对精子钙信号没有影响。

结论

生理上可检测的 BPA 浓度可能通过抑制人类精子的蛋白质酪氨酸磷酸化来损害人类精子的功能，这意味着 BPA 的环境污染可能是导致男性不育的一个因素。