NDLI: Therapeutic photobiomodulation for methanol-induced retinal toxicity.

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Therapeutic photobiomodulation for methanol-induced retinal toxicity.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Henry, M. M. Whelan, N. T. Wong-riley, M. T. T. Summerfelt, P. Whelan, H. T. Eells, J. T. Buchmann, E. V. Kane, M.
Description	Author Affiliation: Eells JT ( Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA. jeells@mcw.edu);
Abstract	Methanol intoxication produces toxic injury to the retina and optic nerve, resulting in blindness. The toxic metabolite in methanol intoxication is formic acid, a mitochondrial toxin known to inhibit the essential mitochondrial enzyme, cytochrome oxidase. Photobiomodulation by red to near-IR radiation has been demonstrated to enhance mitochondrial activity and promote cell survival in vitro by stimulation of cytochrome oxidase activity. The present studies were undertaken to test the hypothesis that exposure to monochromatic red radiation from light-emitting diode (LED) arrays would protect the retina against the toxic actions of methanol-derived formic acid in a rodent model of methanol toxicity. Using the electroretinogram as a sensitive indicator of retinal function, we demonstrated that three brief (2 min, 24 s) 670-nm LED treatments (4 J/cm(2)), delivered at 5, 25, and 50 h of methanol intoxication, attenuated the retinotoxic effects of methanol-derived formate. Our studies document a significant recovery of rod- and cone-mediated function in LED-treated, methanol-intoxicated rats. We further show that LED treatment protected the retina from the histopathologic changes induced by methanol-derived formate. These findings provide a link between the actions of monochromatic red to near-IR light on mitochondrial oxidative metabolism in vitro and retinoprotection in vivo. They also suggest that photobiomodulation may enhance recovery from retinal injury and other ocular diseases in which mitochondrial dysfunction is postulated to play a role.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	6
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Methanol Toxicity Phototherapy Retina Drug Effects Injuries Animals Electroretinography Formates Metabolism Infrared Rays Therapeutic Use Microscopy, Electron Mitochondria Radiation Effects Rats, Long-Evans Physiopathology Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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