Intracellular magnesium level determines cell viability in the MPP(+) model of Parkinson's disease.

摘要: Parkinson's disease (PD) is a neurodegenerative disorder resulting from mitochondrial dysfunction in dopaminergic neurons. Mitochondria are believed to be responsible for cellular Mg²⁺ homeostasis. indispensable maintaining ordinal functions, hence perturbation of the homeostasis may disorders physiological functions and diseases including PD. However, changes intracellular concentration ([Mg²⁺]i) role PD have still been obscure. In this study, we investigated [Mg²⁺]i its effect on neurodegeneration 1-methyl-4-phenylpyridinium (MPP⁺) model differentiated PC12 cells. Application MPP⁺ induced an increase immediately via two different pathways: release mitochondria influx across cell membrane, increased sustained more than 16 h after application. Suppression decreased viability cells exposed MPP⁺. The correlated highly with [Mg²⁺]i. suppressed influx, ATP amount reactive oxygen species (ROS) 8h exposure Our results indicate that inhibited ROS generation maintained production, which resulted protection toxicity.