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

Abstract

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.

Keywords: Apoptosis; Hydrogen sulfide; Mitochondrial dysfunction; ROS; Zebrafish.