Suppr超能文献

全氟己烷磺酸对猪卵母细胞成熟、缝隙连接细胞间通讯、线粒体膜电位和卵丘细胞 DNA 损伤的体外影响。

Effect of perfluorohexane sulfonate on pig oocyte maturation, gap-junctional intercellular communication, mitochondrial membrane potential and DNA damage in cumulus cells in vitro.

机构信息

Departament of Health Sciences, Universidad Autónoma Metropolitana, Iztapalapa, México City 09340, Mexico; Biological and Health Sciences PhD Program, Universidad Autónoma Metropolitana, Iztapalapa, México City 09340, Mexico.

Departament of Health Sciences, Universidad Autónoma Metropolitana, Iztapalapa, México City 09340, Mexico.

出版信息

Toxicol In Vitro. 2021 Feb;70:105011. doi: 10.1016/j.tiv.2020.105011. Epub 2020 Oct 7.

Abstract

Perfluorohexane sulfonate (PFHxS) is one of the most abundant perfluorinated compounds in the environment. Exposure to this compound has been correlated to a decrease in human fertility, although the molecular and cellular mechanisms underlying this correlation have not been described. The adverse reproductive effects of PFHxS could be based on alterations in oocyte maturation, the process rendering oocytes competent for fertilization. The aim of this study was to evaluate the effect of PFHxS on porcine oocyte viability and maturation in vitro, as well as on gap-junctional intercellular communication (GJIC) in cumulus-oocyte complexes (COCs), oocyte mitochondrial membrane potential (mΔΨ) and DNA damage in cumulus cells, as possible mechanisms of action. PFHxS caused cytotoxicity (medium lethal concentration, LC = 329.1 μM) and inhibition of oocyte maturation (medium inhibitory concentration, MIC = 91.68 μM). GJIC was not affected in exposed COCs. However, the mitochondrial membrane potential was significantly decreased in PFHxS-exposed oocytes at the germinal vesicle breakdown (GVBD) stage. In addition, exposure to PFHxS induced DNA damage in cumulus cells. Thus, inhibition of oocyte maturation by PFHxS could be attributed to a decreased oocyte mΔΨ at the GVBD and to DNA damage of the cumulus cells that support the oocyte.

摘要

全氟己烷磺酸(PFHxS)是环境中最丰富的全氟化合物之一。接触这种化合物与人类生育力下降有关,尽管尚未描述这种相关性的分子和细胞机制。PFHxS 的不良生殖效应可能基于卵母细胞成熟的改变,即使卵母细胞具有受精能力的过程。本研究旨在评估 PFHxS 对体外猪卵母细胞活力和成熟的影响,以及对卵丘-卵母细胞复合物(COCs)中的缝隙连接细胞间通讯(GJIC)、卵母细胞线粒体膜电位(mΔΨ)和卵丘细胞中的 DNA 损伤的影响,作为可能的作用机制。PFHxS 引起细胞毒性(中等致死浓度,LC = 329.1 μM)和卵母细胞成熟抑制(中等抑制浓度,MIC = 91.68 μM)。暴露的 COCs 中的 GJIC 不受影响。然而,在GVBD 阶段,暴露于 PFHxS 的卵母细胞中的线粒体膜电位显著降低。此外,PFHxS 暴露诱导卵丘细胞中的 DNA 损伤。因此,PFHxS 对卵母细胞成熟的抑制作用可能归因于 GVBD 时卵母细胞 mΔΨ 的降低,以及支持卵母细胞的卵丘细胞的 DNA 损伤。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验