Nicotine exposure of male mice protects offspring against carbon tetrachloride‐induced acute liver injury

• Published in: Journal of biochemical and molecular toxicology Vol. 36; no. 7; pp. e23069 - n/a
• Main Authors: Zhang, Dong, Dai, Jingbo, Cao, Yong, Wang, Zhaoxia, Qiao, Zhiguang, Qiao, Zhongdong
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.07.2022
• Subjects: acute liver injury; Alanine; Alanine transaminase; Aspartate aminotransferase; Bioinformatics; Carbon; Carbon tetrachloride; Cell proliferation; cellular regeneration; CYP2E1; Exposure; Injuries; Liver; Males; Nicotine; Offspring; Repair; Transaminases; Wnt pathway; Wnt protein; nicotine; CYP2E1; Wnt pathway; cellular regeneration; acute liver injury
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.23069

Paternal nicotine exposure can cause a phenotypic change in offspring. To study whether paternal nicotine exposure influences acute liver injury and repair of the offspring, we established a paternal nicotine exposure model in mice and treated the offspring mice with carbon tetrachloride (CCl4) to induce acute liver injury. After the treatment of CCl4, the levels of alanine aminotransferase and aspartate aminotransferase in offspring serum of paternal nicotine exposed mice are about 37.44%, and 30.21% lower than the control mice, respectively. Transcription profiling screen and bioinformatics analysis of differently expressed genes in F1 mice liver revealed that the Wnt pathway was altered. The results demonstrate that nicotine exposure in male mice could enhance the activation of the Wnt pathway in F1 mice liver. The Wnt pathway facilitates cell proliferation and tissue repair. In conclusion, our findings showed that nicotine exposure of male mice protects hepatic against CCl4‐induced acute injury in offspring by activating the Wnt pathway in the F1 liver.