Pentachlorophenol (PCP), a highly toxic contaminant of chlorophenols, is common in a variety of environments and presents serious risks to animal and human health. However, the reproductive toxicity and potential actions of PCP have not been investigated thoroughly, especially in humans. Here, human spermatozoa were used to evaluate the effect of PCP on cell function and to explore the underlying mechanisms. PCP had no substantive effects on sperm viability or motility, nor on the ability to penetrate viscous medium, sperm hyperactivation or spontaneous acrosome reactions. However, PCP significantly inhibited these properties induced by progesterone (P4). Consistent with the functional observations, although PCP itself did not affect the basal intracellular Ca²⁺ concentrations and CatSper current, PCP dose-dependently inhibited increases of intracellular Ca²⁺ concentrations caused by P4. In addition, the activation of CatSper induced by P4 was largely suppressed by PCP. This is the first report showing that PCP may serves as an antagonist of the P4 membrane receptor to interfere with Ca²⁺ signaling by compromising the action of P4 on regulating sperm function. These findings suggest that the reproductive toxicity of PCP should also be a matter of concern as a mammalian health risk.

五氯苯酚（PCP）是一种高度毒性的氯苯酚污染物，在多种环境中都很常见，对动物和人类健康构成严重威胁。但是，PCP的生殖毒性和潜在作用尚未得到彻底研究，尤其是在人类中。在这里，人类的精子被用来评估五氯苯酚对细胞功能的影响并探讨其潜在机制。五氯苯酚对精子的活力或活力没有实质性影响，对渗透粘性介质，精子过度活化或自发顶体反应也没有任何实质性影响。但是，PCP显着抑制了孕酮（P4）诱导的这些特性。与功能观察结果一致，尽管PCP本身并不影响基础细胞内Ca ²⁺浓度和CatSper电流，PCP剂量依赖性地抑制了P4引起的细胞内Ca ²⁺浓度增加。此外，PCP大大抑制了P4诱导的CatSper活化。这是第一个报道，表明PCP可能通过破坏P4调节精子功能的作用而充当P4膜受体的拮抗剂来干扰Ca ²⁺信号传导。这些发现表明，作为哺乳动物健康风险，五氯苯酚的生殖毒性也应引起关注。