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%A TIAN Xiao-fei, LI Jian-feng, PANG Hao %T Paraquat-induced Neuronal Apoptosis Associated with Parkinson's Disease %0 Journal Article %D 2011 %J ACTA NEUROPHARMACOLOGICA %R %P 27-33 %V 1 %N 5 %U {http://actanp.hebeinu.edu.cn/CN/abstract/article_48.shtml} %8 2011-10-26 %X Parkinson’s disease (PD) is a neurodegenerative disorder characterized by selective loss of dopaminergic neurons in the substantia nigra (SN); however, the causes of PD remain unknown. Over the years the etiologic involvement of genetic inheritance versus environmental exposures has been under debate. In this sense, a lack of evidence for heritability of the idiopathic PD has pointed to environmental risk factors as potential contributors to the disease etiology. It is reported that, Paraquat (PQ) (1,1-dimethyl-4,4′-bipyridinium dichloride), a widely used herbicide, was suggested as a potential etiologic factor for the development of PD. Paraquat is structurally similar to the neurotoxin MPP+ (1-methyl-4-phenylpyridinium), the latter being an active metabolite derived from MPTP (1- methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and being capable of inducing the apoptosis of neural cells. In this paper, we used the model of PQ induced toxicity on SH-SY5Y to study the mechanism underlying its effect in causing dopaminergic cells degeneration and necrosis. To this end, we determined whether PQ activated apoptotic pathways leading to the pathogenesis of PD as MPP+ does, or caused intracellular oxidative stress， mitochondrial dysfunction or proteasome abnormality to induce PD. Intensive study of the molecular mechanisms for PQ induction of PD will be of great value for the prevention and treatment of PD.