PFOA evokes extracellular Ca2 influx and compromises progesterone-induced response in human sperm

PFOA evokes extracellular Ca2 influx and compromises progesterone-induced response in human sperm
复制标题

PFOA 会引起细胞外 Ca2 内流并损害人类精子中黄体酮诱导的反应

DOI:
10.1016/j.chemosphere.2019.125074
复制
发表时间:
2020
期刊:
影响因子:
8.8
通讯作者:
Dalei Zhang
Dalei Zhang
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Yangyang Yuan;Xinbao Ding;Yimin Cheng;Hang Kang;Tao Luo;Xiaoning Zhang;Haibin Kuang;Ying Chen;Xuhui Zeng;Dalei Zhang

文献摘要

被引文献

相似文献

全氟辛烷酸(PFOA)是一种持久性有机污染物,在环境中无处不在,可能对男性生殖健康产生不利影响。本研究将成熟的人类精子体外暴露于不同浓度的PFOA(0.25、2.5或25 μg/ml)单独或与孕酮(P4)联合,以评估其毒性和可能的作用机制。单独暴露于高剂量PFOA(25 μg/ml) 4 小时,导致人类精子穿透合成黏液的能力下降,活性氧(ROS)的产生增加。此外,PFOA处理(2.5和25 μg/ml)通过激活精子特异性的CatSper通道,引起细胞内钙浓度[Ca2+]的短暂升高。然而,PFOA(2.5-25 μg/ml)预孵育4 小时可显著抑制p4刺激的人精子细胞外Ca2+内流。此外,所有浓度的PFOA预处理都显著降低了p4诱导的顶体反应和精子对粘性介质的渗透。综上所述,这些结果表明PFOA暴露可能通过诱导氧化应激和干扰p4诱导的Ca2+信号传导而损害人类精子功能。
Perfluorooctane acid (PFOA), a persistent organic pollutant, is ubiquitously present in the environment and may detrimentally affect male reproductive health. In this study, mature human sperm werein vitroexposed to different concentrations of PFOA (0.25, 2.5 or 25 μg/ml) alone or in combination with progesterone (P4) to evaluate the toxicity and the potential mechanism of action. Exposure to high-dose PFOA (25 μg/ml) alone for 4 h caused a decline in capacity of human spermatozoa to penetrate synthetic mucus, with an increased production of reactive oxygen species (ROS). Furthermore, PFOA treatment (2.5 and 25 μg/ml) evoked a transient rise in intracellular calcium concentration [Ca2+]iby activating the sperm-specific CatSper channel. However, preincubation with PFOA (2.5–25 μg/ml) for 4 h significantly suppressed P4-stimulated extracellular Ca2+influx in human spermatozoa. Moreover, PFOA pretreatment at all concentrations evaluated markedly compromised P4-induced acrosome reaction and sperm penetration into viscous medium. Taken together, these results suggest that PFOA exposure may impair human sperm function through inducing oxidative stress and disturbing P4-induced Ca2+signaling.