Mechanism of neuronal death induced by oxidative stress in Parkinson's disease

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Parkinson's disease(PD) is the second most common, chronic age-related neurodegenerative disease. The mechanisms of cell death of dopaminergic neurons in PD have not yet been fully elucidated, but increased oxidative stress is perhaps the most important initiators or mediators of neuronal damage. In this study, to identify target proteins of reactive oxygen species(ROS) oxidation, we investigated oxidative damage of proteins in substantia nigra(SN) isolated from Japanese monkeys after transient cerebral ischemia-reperfusion. The carbonyl levels of molecular chaperones(heat shock 70k Da protein 1, T-complex protein 1 subunit alpha, etc), energy metabolism-related enzymes(mitochondrial aconitase, glutamate dehydrogenase 1, etc) and structural proteins(dihydropyrimidinase-related protein 2, etc) were increased. Therefore, oxidative damage to these proteins in SN may lead to loss of the neuroprotective function, which contributes to neuronal death. Furthermore, carbonylation of these proteins may be used as a biomarker for assessing the neuronal cell death induced by oxidative stress.