title: Near-infrared light via light-emitting diode treatment is therapeutic against rotenone- and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity.
abstract: Parkinson's disease is a common progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta. Mitochondrial dysfunction has been strongly implicated in the pathogenesis of Parkinson's disease. Thus, therapeutic approaches that improve mitochondrial function may prove to be beneficial. Previously, we have documented that near-infrared light via light-emitting diode (LED) treatment was therapeutic to neurons functionally inactivated by tetrodotoxin, potassium cyanide (KCN), or methanol intoxication, and LED pretreatment rescued neurons from KCN-induced apoptotic cell death. The current study tested our hypothesis that LED treatment can protect neurons from both rotenone- and MPP(+)-induced neurotoxicity. Primary cultures of postnatal rat striatal and cortical neurons served as models, and the optimal frequency of LED treatment per day was also determined. Results indicated that LED treatments twice a day significantly increased cellular adenosine triphosphate content, decreased the number of neurons undergoing cell death, and significantly reduced the expressions of reactive oxygen species and reactive nitrogen species in rotenone- or MPP(+)-exposed neurons as compared with untreated ones. These results strongly suggest that LED treatment may be therapeutic to neurons damaged by neurotoxins linked to Parkinson's disease by energizing the cells and increasing their viability.
authors.affiliation: Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
authors.forename: H L
authors.initials: HL
authors.lastname: Liang
authors.forename: H T
authors.initials: HT
authors.lastname: Whelan
authors.forename: J T
authors.initials: JT
authors.lastname: Eells
authors.forename: M T T
authors.initials: MT
authors.lastname: Wong-Riley
mesh_terms: D015655:1-Methyl-4-phenylpyridinium / Q000633:toxicity*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D016923:Cell Death / Q000187:drug effects / Q000528:radiation effects; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology; D003485:Cyanates / Q000633:toxicity; D004307:Dose-Response Relationship, Radiation; D003576:Electron Transport Complex IV / Q000378:metabolism; D007259:Infrared Rays / Q000627:therapeutic use*; D054023:Lasers, Semiconductor / Q000627:therapeutic use*; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D009498:Neurotoxins / Q000633:toxicity*; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012402:Rotenone / Q000031:analogs & derivatives* / Q000633:toxicity; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism
chemical_list: D003485:Cyanates; D009498:Neurotoxins; D017382:Reactive Oxygen Species; D012402:Rotenone; C028404:rotenolone; D009569:Nitric Oxide; C002744:3-nitrotyrosine; D014443:Tyrosine; D000255:Adenosine Triphosphate; D003576:Electron Transport Complex IV; C024835:potassium cyanate; D015655:1-Methyl-4-phenylpyridinium