Pretreatment with near-infrared light via light-emitting diode provides added benefit against rotenone- and MPP+-induced neurotoxicity.
Parkinson's disease (PD) is a movement disorder caused by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to nigrostriatal degeneration. The inhibition of mitochondrial respiratory chain complex I and oxidative stress-induced damage have been implicated in the pathogenesis of PD. The present study used these specific mitochondrial complex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP(+)) on striatal and cortical neurons in culture. The goal was to test our hypothesis that pretreatment with near-infrared light (NIR) via light-emitting diode (LED) had a greater beneficial effect on primary neurons grown in media with rotenone or MPP(+) than those with or without LED treatment during exposure to poisons. Striatal and visual cortical neurons from newborn rats were cultured in a media with or without 200 nM of rotenone or 250 microM of MPP(+) for 48 h. They were treated with NIR-LED twice a day before, during, and both before and during the exposure to the poison. Results indicate that pretreatment with NIR-LED significantly suppressed rotenone- or MPP(+)-induced apoptosis in both striatal and cortical neurons (P<0.001), and that pretreatment plus LED treatment during neurotoxin exposure was significantly better than LED treatment alone during exposure to neurotoxins. In addition, MPP(+) induced a decrease in neuronal ATP levels (to 48% of control level) that was reversed significantly to 70% of control by NIR-LED pretreatment. These data suggest that LED pretreatment is an effective adjunct preventative therapy in rescuing neurons from neurotoxins linked to PD.
Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Rong
R
Ying
Huan Ling
HL
Liang
Harry T
HT
Whelan
Janis T
JT
Eells
Margaret T T
MT
Wong-Riley
D015655:1-Methyl-4-phenylpyridinium / Q000633:toxicity; D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000502:physiology / Q000528:radiation effects; D002478:Cells, Cultured; D019610:Cytoprotection / Q000502:physiology / Q000528:radiation effects*; D042967:Electron Transport Complex I / Q000378:metabolism / Q000528:radiation effects; D004734:Energy Metabolism / Q000502:physiology / Q000528:radiation effects; D015386:Hazardous Substances / Q000009:adverse effects; D006540:Herbicides / Q000633:toxicity; D008027:Light; D009474:Neurons / Q000187:drug effects / Q000528:radiation effects*; D009498:Neurotoxins / Q000633:toxicity; D010300:Parkinson Disease / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D010789:Phototherapy / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012402:Rotenone / Q000633:toxicity; D013687:Telencephalon / Q000166:cytology / Q000378:metabolism; D016896:Treatment Outcome; D014475:Uncoupling Agents / Q000633:toxicity
D015386:Hazardous Substances; D006540:Herbicides; D009498:Neurotoxins; D014475:Uncoupling Agents; D012402:Rotenone; D042967:Electron Transport Complex I; D015655:1-Methyl-4-phenylpyridinium