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.
Ying
Rong
R
Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.
Liang
Huan Ling
HL
Whelan
Harry T
HT
Eells
Janis T
JT
Wong-Riley
Margaret T T
MT
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