Abstract：Objective To explore the role and mechanism of mitochondrial calcium overload and mitochondrial apoptosis pathway activation in the process of neuron apoptosis induced by methylmercury (MeHg) poisoning. Methods The brains of newborn mice were anatomized within 24 hours after birth for primary culture of mouse cortical neurons. The cells were incubated with different concentration of MeHg (0 μmol/L, 0.25 μmol/L, 0.5 μmol/L and 1 μmol/L) in the culture medium for 1, 3 and 6 h respectively, and then cell viability was measured. After suitable exposure time was determined, mitochondrial calcium level, mitochondrial membrane potential, cytochrome c (Cyt c), apoptosis induce factor (AIF), cysteinyl aspartate specific proteinase 3 (caspase 3) protein expression level and apoptosis rate were detected. Results Cell viability was decreased after exposure to different concentration of MeHg. For the 0.25 μmol/L, 0.5 μmol/L and 1 μmol/L MeHg treatment groups, mitochondrial calcium levels, Cyt c, AIF and caspase 3 protein expression levels and cell early apoptosis rates were elevated, while mitochondrial membrane potential was declined, all in a dose-dependent manner. There were statistically significant differences in the above-mentioned indicators between 1 μmol/L MeHg treatment group and the control group (all P<0.01). Conclusions MeHg exposure can induce mitochondrial calcium overload, activate mitochondrial apoptosis pathway, and then lead to neuronal apoptosis.
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2018, Vol. 25 
