您好，欢迎访问广西农业科学院 机构知识库！

Arsenic causes mitochondrial biogenesis obstacles by inhibiting the AMPK/PGC-1 alpha signaling pathway and also induces apoptosis and dysregulated mitophagy in the duck liver

文献类型： 外文期刊

作者： Zhong, Gaolong 1 ; Hu, Ting 1 ; Tang, Lixuan 1 ; Li, Tong 1 ; Wu, Shaofeng 1 ; Duan, Xuewu 2 ; Pan, Jiaqiang 1 ; Zhang, Hui 1 ; Tang, Zhaoxin 1 ; Feng, Xia 3 ; Hu, Lianmei 1 ;

作者机构： 1.South China Agr Univ, Coll Vet Med, Key Lab Anim Vaccine Dev, Minist Agr & Rural Affairs, Guangzhou 510642, Peoples R China

2.Chinese Acad Sci, Guangdong Prov Key Lab Appl Bot, South China Bot Garden, Guangzhou 510650, Peoples R China

3.Yanzhou Dist Bur Agr & Rural Dev, Jining City, Shandong, Peoples R China

4.Guangxi Acad Agr Sci, Agrofood Sci & Technol Res Inst, Nanning 530007, Peoples R China

关键词： Duck; Arsenic; Mitochondrial biogenesis; Apoptosis; Mitophagy

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：7.129； 五年影响因子：7.284 ）

ISSN： 0147-6513

年卷期： 2022 年 230 卷

页码：

收录情况： SCI

摘要： Arsenic is a dangerous metalloid-material which is known to cause liver injury in many animals and humans. However, little is known about the underlying mechanism of arsenic-induced hepatotoxicity in poultry. This study was executed to systematically investigate the potential role of mitochondrial biogenesis, mitophagy and apoptosis in duck hepatotoxicity caused by arsenic. Results showed that the body weight and liver coefficient of duck had distinct changed after arsenic-exposure, and the arsenic content in serum and liver also increased significantly in a dose-dependent manner. Meanwhile, histopathological examination and metabolomics results showed that arsenic-exposure caused severe steatosis and metabolism disorder in liver tissues. Furthermore, arsenic-exposure significantly inhibited AMPK/PGC-1 alpha-mediated mitochondrial biogenesis, determined by the ultrastructure observation and down-regulation of p-AMPK alpha/AMPK alpha, PGC-1 alpha, NRF1, NRF2, TFAM, TFB1M, TFB2M and COX-IV expression levels. Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2). Overall, our findings provided evidences that arsenic-induced duck hepatotoxicity may be caused by a combination of impaired mitochondrial biosynthesis, mitophagy, and mitochondrial-dependent apoptosis. To our knowledge, this is the first report to systematically investigate the potential mechanism of arsenic-induced hepatotoxicity in poultry.

  • 相关文献
作者其他论文 更多>>
置顶
购物车
反馈

© 京ICP备09089781号-29 主办单位：广西农业科学院

学术资源： 中国农业科学院 农业专业知识服务系统 农科联盟资源共建共享平台 中国农业科技文献与信息服务平台 中国农业期刊集成服务平台