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Sirtuin3 deficiency exacerbates carbon tetrachloride−induced hepatic injury in mice
Author(s) -
Li Xinshuai,
Song Shu,
Xu Mengting,
Hua Yuyun,
Ding Yun,
Shan Xiaoyu,
Meng Guoliang,
Wang Yuqin
Publication year - 2019
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22249
Subject(s) - sirt3 , oxidative stress , carbon tetrachloride , ccl4 , knockout mouse , liver injury , endocrinology , chemistry , medicine , biochemistry , sirtuin , gene , acetylation , organic chemistry , receptor
Sirtuin3 (SIRT3) plays an important role in maintaining normal mitochondrial function and alleviating oxidative stress. After carbon tetrachloride (CCl 4 ) administration, the expression of SIRT3 decreased in the liver of mice, which indicated that the SIRT3 might play a crucial role during chemical‐induced acute hepatic injury. To verify the hypothesis, CCl 4 was given to induce acute hepatic injury in SIRT3 knockout (KO) mice and wild‐type (WT) mice. CCl 4 ‐induced liver injury was more severe in SIRT3 KO mice compared with the WT mice. In addition, the oxidative stress induced by CCl 4 was enhanced in the SIRT3 KO mice. Furthermore, the increased expression of dynamin‐related protein 1 was also aggravated in SIRT3 KO mice after CCl 4 administration. In conclusion, our study demonstrated that SIRT3 deficiency exacerbated CCl 4 ‐induced impairment of the liver in mice, and the mechanism might be related to enhanced oxidative stress.