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Marina T. Seme, Phyllis Summerfelt, Jay Neitz, Janis T. Eells, Michele M. Henry; Differential Recovery of Retinal Function after Mitochondrial Inhibition by Methanol Intoxication. Invest. Ophthalmol. Vis. Sci. 2001;42(3):834-841. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. The authors’ laboratory has previously documented formate-induced retinal toxicity
in a rodent model of methanol intoxication. These studies determined
functional, bioenergetic, and structural recovery of the retina after
methods. Rats were intoxicated with methanol, and retinal function was assessed
by electroretinography 72 hours after the initial dose of methanol and
after a 72-hour recovery period. Retinal energy metabolites,
glutathione (GSH) concentrations, and histology were determined at the
same time points.
results. Both rod-dominated and UV-cone–mediated electroretinogram responses
were profoundly attenuated in methanol-intoxicated rats. In rats
allowed to recover from methanol intoxication, there was significant,
although incomplete, recovery of rod-dominated retinal function.
However, there was no demonstrable improvement in UV-cone–mediated
responses. Retinal adenosine triphosphate (ATP), adenosine diphosphate
(ADP), and GSH concentrations were significantly reduced after
intoxication. Although retinal energy metabolites returned to control
values after the recovery period, retinal GSH remained significantly
depleted. Histopathologic changes were apparent in the photoreceptors
after methanol intoxication, with evidence of inner segment swelling
and mitochondrial disruption. In animals allowed to recover from
methanol intoxication, there was no evidence of histopathology at the
light microscopic level; however, ultrastructural studies revealed
subtle photoreceptor mitochondrial alterations.
conclusions. These findings support the hypothesis that formate inhibits retinal
mitochondrial function and increases oxidative stress. They also
provide evidence for a differential sensitivity of photoreceptors to
the cytotoxic actions of formic acid, with a partial recovery of
rod-dominated responses and no recovery of UV-cone–mediated
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