Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

• DOI: 10.1002/tox.22868
• Publication Date: 2019-11-04T08:52:26Z
• Authors: Xiujing Feng; Haiyang Zhang; Mingxian Shi; Yongping Chen; Tianyuan Yang; Honggang Fan
• Keywords: Electron Transport Complex IV; Male; 0303 health sciences; 03 medical and health sciences; Liver; Animals; Apoptosis; Mitochondria, Liver; Hydrogen Sulfide; Sulfides; Reactive Oxygen Species; Rats

AbstractIn recent years, the protective effect of hydrogensulfide donor sodium hydrosulfide(NaHS) on multiple organs has been widely reported. The study aimed to explorethe effect of commonly used concentration of NaHS on theliver and its potential damage mechanism. Rats divided into 4 groups: control, NaHS I (1 mg/kg), II (3 mg/kg) and III(5 mg/kg) groups, and each group is divided into four‐timepoints (2, 6, 12, and 24 hours). Results showed that H2S concentration increased, mitochondrial complex IV activity inhibited, the COX I and IV subunits and mitochondrial apoptosis pathway‐related proteins expression increased in atime‐ and dose‐dependent manner. We confirmed that 1 mg/kg NaHS had no injuryeffect on the liver, 3 and 5 mg/kg NaHS inhibitsthe activity of mitochondrial complex IV by promoting COX I and IV subunits expression, leading to the increase in ROS and ultimately inducing apoptosis and liver injury.