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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\u2010timepoints (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\u2010related proteins expression increased in atime\u2010 and dose\u2010dependent 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.<\/jats:p>","DOI":"10.1002\/tox.22868","type":"journal-article","created":{"date-parts":[[2019,11,4]],"date-time":"2019-11-04T08:52:26Z","timestamp":1572857546000},"page":"322-332","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats"],"prefix":"10.1002","volume":"35","author":[{"given":"Xiujing","family":"Feng","sequence":"first","affiliation":[{"name":"College of Veterinary Medicine Northeast Agricultural University  Harbin 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