Oxidative stress-mediated mitochondrial damage and apoptosis induced by typical iodoalkanes from shale gas wastewater

页岩气废水中典型碘代烷烃诱导的氧化应激介导的线粒体损伤和细胞凋亡

阅读:1

Abstract

Iodide organic compounds, the conversion reaction by-products in shale gas wastewater, have potential risks to ecological environment and human health. However, information about their negative effects and molecular mechanism remains limited. In this study, three typical iodoalkanes (C(2)H(5)I, C(2)H(4)I(2), and C(3)H(6)I(2)) identified in shale gas wastewater from Chongqing of China were utilized to investigate their cytotoxicity and potential mechanisms in Hela cells. Results showed that three iodoalkanes reduced cell proliferation in a dose-dependent manner, and cytotoxicity of di-iodoalkanes (C(2)H(4)I(2) and C(3)H(6)I(2)) was stronger than that of mono-iodoalkanes (C(2)H(5)I). Furthermore, C(2)H(4)I(2) and C(3)H(6)I(2) significantly decreased colony formation of HeLa cells, accompanying by disorder of cell cycle checkpoint genes (CyclinA2, CyclinD1, CyclinE1, CDK2 and p21). Three iodoalkanes stimulated production of intracellular ROS, caused GSH/GSSG ratio decrease, MMP loss, and promoted expression of NRF2, HO-1 and NQO-1. Additionally, C(2)H(4)I(2) and C(3)H(6)I(2) induced cell membrane damage, cell apoptosis and enhanced expression of apoptosis markers (Caspase-3, Caspase-8, Cyt-c, and p53). Combined use of antioxidant NAC obviously alleviated the toxic effects of iodoalkanes, including cell proliferation inhibition, oxidative stress and apoptosis induction. Generally, iodoalkanes might suppress cell proliferation via inhibiting cycle progression from G(1) to S phase, inducing mitochondrial apoptosis, which was closely related to oxidative stress-mediated mitochondrial damage.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。