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

Hydrogen sulfide (HS), a highly toxic gas, has become a polluting gas that cannot be ignored, while HS 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 HS, and our results indicated that HS exposure increased intracellular ROS, Ca, NO and MDA contents and decreased SOD activity, meaning that HS 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 HS treatment conditions. These findings indicated that HS caused mitochondrial dysfunction. Moreover, in this experiment, after HS 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 HS caused apoptosis in zebrafish larvae. Therefore, our data meant that HS-traggered oxidative stress mediate mitochondrial dysfunction, thus triggering apoptosis. In conclusion, oxidative stress triggered HS-induced apoptosis via mitochondria pathway in embryo-larval stages of zebrafish.