Deciphering the possible role of H 2 O 2 in methylmercury-induced neurotoxicity in Xenopus laevis

Molecular & Cellular Toxicology

article

Fu, Xufeng¹  Yang, Xiuyu¹  Du, Xing¹  Cui, Qinghua¹ 

[1] School of Life Sciences, Yunnan University;Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Department of Biochemistry and Molecular Biology, Ningxia Medical University;Lincang Health School;Key Lab of Molecular Cancer Biology, Yunnan Education Department;Key Laboratory for Biochemistry and Molecular Biology of High Education in Yunnan Province, Yunnan University

关键词: Methylmercury;    Neurotoxicity;    H 2 O 2;    Oxidative stress;    Apoptosis;    Autophagy;   

DOI  :  10.1007/s13273-020-00082-w

来源: Korean Society of Toxicogenomics and Toxicoproteomics

【 摘 要 】

Backgrounds Methylmercury (MeHg) is regarded as a developmental neurotoxicant but the detailed mechanism remains not completely clear. Methods The Xenopus laevis embryos were exposed to methylmercury chloride and the expression of neurodevelopment and oxidative stress genes was detected by qRT-PCR or Western blotting. PC12 cells were exposed to various levels of H2O2, and then cell cycle, neurite length, neurodevelopment-related genes, protein expression of apoptosis and autophagy were detected. Results The genes of neurodevelopment and oxidative stress were disrupted by methylmercury chloride and H2O2 were increased interestingly in X. laevis embryos. Then, PC12 cells were exposed to H2O2 and the results showed the cell cycle, neurite length, and neurodevelopment-related genes, the proteins apoptosis and autophagy were changed. Conclusion These results supported the idea that neurodevelopment-related gene expression was regulated by oxidative stress and that apoptosis and autophagy pathways were activated by H2O2 and involved in methylmercury neurotoxicity.

【 授权许可】

Unknown