Reactive oxygen/nitrogen species and their functional correlations in neurodegenerative diseases.
The continuous production and efflux of reactive oxygen/nitrogen species from endogenous and exogenous sources can damage biological molecules and initiate a cascade of events. Mitochondria are pivotal in controlling cell survival and death. Cumulative oxidative stress, disrupted mitochondrial respiration, and mitochondrial damage are related with various neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and others. Biochemical cascades of apoptosis are mediated in signaling molecules, including protein kinases and transcription factors. The expressions in the pro-apoptotic signal transduction networks may indeed promote cell death and degeneration in brain cells. The regulation of that protein phosphorylation by kinases and phosphatases is emerging as a prerequisite mechanism in the control of the apoptotic cell death program. In this review, we attempt to put forth the evidence for possible mechanistic explanations for involvement of free radicals in the pathogenesis of neurodegenerative diseases.
Department of Pharmacology and Toxicology, Metabolic Diseases Research Laboratory, School of Dentistry, Kyung Hee University, #1 Hoegi-dong, Dongdaemun-gu, Seoul, Republic of Korea.
Mahesh
M
Ramalingam
Sung-Jin
SJ
Kim
D000818:Animals; D001921:Brain / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D009410:Nerve Degeneration / Q000378:metabolism* / Q000503:physiopathology; D019636:Neurodegenerative Diseases / Q000378:metabolism* / Q000503:physiopathology; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
D005609:Free Radicals; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species