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.

中文翻译：

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解释H 2 O 2在甲基汞诱导的非洲爪蟾神经毒性中的可能作用

背景资料

甲基汞（MeHg）被认为是一种发育性神经毒剂，但其详细机理尚不完全清楚。

方法

将非洲爪蟾胚胎暴露于甲基汞氯化物，并通过qRT-PCR或Western印迹检测神经发育和氧化应激基因的表达。将PC12细胞暴露于不同水平的H ₂ O _2中，然后检测细胞周期，神经突长度，神经发育相关基因，细胞凋亡的蛋白表达和自噬。

结果

甲基汞氯化物破坏了神经发育和氧化应激的基因，有趣地增加了X. laevis胚胎中的H ₂ O ₂。然后，将PC12细胞暴露于H ₂ O ₂，结果显示细胞周期，神经突长度和神经发育相关基因，蛋白质凋亡和自噬发生了变化。

结论

这些结果支持了这样的想法，即神经发育相关基因的表达受到氧化应激的调节，而凋亡和自噬途径被H ₂ O ₂激活并参与甲基汞的神经毒性。