Pretreatment With Near-Infrared Light via Light-Emitting Diode Provides Added Benefit Against Rotenone- And MPP+-induced Neurotoxicity

Brain Res. 2008 Dec 3;1243:167-73. doi: 10.1016/j.brainres.2008.09.057. Epub 2008 Sep 30.


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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • 1-Methyl-4-phenylpyridinium / toxicity
  • Animals
  • Animals, Newborn
  • Apoptosis / physiology
  • Apoptosis / radiation effects
  • Cells, Cultured
  • Cytoprotection / physiology
  • Cytoprotection / radiation effects*
  • Electron Transport Complex I / metabolism
  • Electron Transport Complex I / radiation effects
  • Energy Metabolism / physiology
  • Energy Metabolism / radiation effects
  • Hazardous Substances / adverse effects
  • Herbicides / toxicity
  • Light*
  • Neurons / drug effects
  • Neurons / radiation effects*
  • Neurotoxins / toxicity
  • Parkinson Disease / metabolism*
  • Parkinson Disease / physiopathology
  • Parkinson Disease / therapy*
  • Phototherapy / methods*
  • Rats
  • Rats, Sprague-Dawley
  • Rotenone / toxicity
  • Telencephalon / cytology
  • Telencephalon / metabolism
  • Treatment Outcome
  • Uncoupling Agents / toxicity


  • Hazardous Substances
  • Herbicides
  • Neurotoxins
  • Uncoupling Agents
  • Rotenone
  • Electron Transport Complex I
  • 1-Methyl-4-phenylpyridinium