Therapeutic photobiomodulation for methanol-induced retinal toxicity

被引:307
作者
Eells, JT
Henry, MM
Summerfelt, P
Wong-Riley, MTT
Buchmann, EV
Kane, M
Whelan, NT
Whelan, HT
机构
[1] Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA
[2] Med Coll Wisconsin, Dept Anat Cell Biol & Neurobiol, Milwaukee, WI 53226 USA
[3] Med Coll Wisconsin, Dept Neurol, Milwaukee, WI 53226 USA
关键词
D O I
10.1073/pnas.0534746100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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. Photo-biomodulation 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.
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收藏
页码:3439 / 3444
页数:6
相关论文
共 47 条
[1]   ENERGY-METABOLISM OF RABBIT RETINA AS RELATED TO FUNCTION - HIGH COST OF NA+ TRANSPORT [J].
AMES, A ;
LI, YY ;
HEHER, EC ;
KIMBLE, CR .
JOURNAL OF NEUROSCIENCE, 1992, 12 (03) :840-853
[3]   TEMPORAL PARAMETERS OF LOW-ENERGY LASER IRRADIATION FOR OPTIMAL DELAY OF POST-TRAUMATIC DEGENERATION OF RAT OPTIC-NERVE [J].
ASSIA, E ;
ROSNER, M ;
BELKIN, M ;
SOLOMON, A ;
SCHWARTZ, M .
BRAIN RESEARCH, 1989, 476 (02) :205-212
[4]  
Barron MJ, 2001, INVEST OPHTH VIS SCI, V42, P3016
[5]  
BEAUR G, 1994, HIST SOC RURALES, V1, P67
[6]   CORRELATION BETWEEN THE LIGHT-SCATTERING AND THE MITOCHONDRIAL CONTENT OF NORMAL-TISSUES AND TRANSPLANTABLE RODENT TUMORS [J].
BEAUVOIT, B ;
EVANS, SM ;
JENKINS, TW ;
MILLER, EE ;
CHANCE, B .
ANALYTICAL BIOCHEMISTRY, 1995, 226 (01) :167-174
[7]   Optic nerve degeneration and mitochondrial dysfunction: genetic and acquired optic neuropathies [J].
Carelli, V ;
Ross-Cisneros, FN ;
Sadun, AA .
NEUROCHEMISTRY INTERNATIONAL, 2002, 40 (06) :573-584
[8]   Biostimulation of wound healing by low-energy laser irradiation - A review [J].
Conlan, MJ ;
Rapley, JW ;
Cobb, CM .
JOURNAL OF CLINICAL PERIODONTOLOGY, 1996, 23 (05) :492-496
[9]  
COOPER CE, 1977, PHILOS T R SOC LON B, V352, P9
[10]  
Eells JT, 2000, NEUROTOXICOLOGY, V21, P321