Hydrogen sulfide-induced oxidative stress mediated apoptosis via mitochondria pathway in embryo-larval stages of zebrafish

作者：Yinai Liu, Qianqian Chen, Yaoqi Li, Liuliu Bi, Sue Lin, Hao Ji, Da Sun, Libo Jin, Renyi Peng · 发表于：Ecotoxicology and Environmental Safety · 年份：2022 · DOI：10.1016/j.ecoenv.2022.113666 · 被引用次数：34 · 研究领域：Sulfur Compounds in Biology、Neuroscience of respiration and sleep、Heme Oxygenase-1 and Carbon Monoxide

Hydrogen sulfide (H2S), a highly toxic gas, has become a polluting gas that cannot be ignored, while H2S exposure results in acute or chronic poisoning or even death in humans or animals and plants, but the relevant mechanisms remain poorly understood. In this study, 9-day-old zebrafish larvae were exposed continuously to culture medium containing 30 μM survival rate was counted on H2S, and our results indicated that H2S exposure increased intracellular ROS, Ca2+, NO and MDA contents and decreased SOD activity, meaning that H2S caused oxidative stress in embryo-larval stages of zebrafish. Furthermore, we found that transgenic zebrafish (cms Tg/+ AB) displayed a lower fluorescence intensity, and cytochrome c oxidase (COX) activity and JC-1 monomer fluorescence ratio increased under H2S treatment conditions. These findings indicated that H2S caused mitochondrial dysfunction. Moreover, in this experiment, after H2S treatment, the increase of apoptotic cells, activity of caspase 3 and transcription of typical apoptosis-associated genes including BCL2 associated agonist of cell death (Bad), and BCL2 associated X apoptosis (Baxa) and so on were found, which suggested that H2S caused apoptosis in zebrafish larvae. Therefore, our data meant that H2S-traggered oxidative stress mediate mitochondrial dysfunction, thus triggering apoptosis. In conclusion, oxidative stress triggered H2S-induced apoptosis via mitochondria pathway in embryo-larval stages of zebrafish.