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Methanol PoisoningA Rodent Model With Structural and Functional Evidence for Retinal Involvement
Timothy G. Murray, MD;
Thomas C. Burton, MD;
Cynthia Rajani, MS;
Michael F. Lewandowski, RDMS;
Janice M. Burke, PhD;
Janis T. Eells, PhD
Arch Ophthalmol. 1991;109(7):1012-1016.
Abstract
Methanol ingestion can lead to visual impairment, central nervous system dysfunction, or death. The extent of ocular involvement has been difficult to determine because the toxicity is restricted to humans and nonhuman primates due to species differences in methanol metabolism. A rodent model of methanol toxicity recently developed by us was used to evaluate retinal dysfunction in methanol poisoning. Formic acidemia and visual toxic reactions developed in methanol-intoxicated rats. Electroretinographic analysis indicated a significant early deficit in b-wave amplitude followed by a temporally delayed, lesser reduction in a-wave amplitude. Histologic evaluation of the eyes 60 hours after methanol administration revealed generalized retinal edema and vacuolation in the photoreceptors and retinal pigment epithelium. Ultrastructural examination showed swelling and disruption of the mitochondria in photoreceptor inner segments, optic nerve, and the retinal pigment epithelium. These studies document direct retinal involvement in this nonprimate model of methanol toxicity.
Author Affiliations
From the Departments of Ophthalmology (Drs Murray, Burton, and Burke, and Mr Lewandowski), and Pharmacology and Toxicology (Dr Eells and Ms Rajani), Medical College of Wisconsin, Milwaukee.
Footnotes
Accepted for publication February 15, 1991.
Reprint requests to Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226 (Dr Eells).
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