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Methanol-induced visual toxicity in the rat.

J T Eells1

  • 1Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee.

The Journal of Pharmacology and Experimental Therapeutics
|April 1, 1991
PubMed
Summary
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Rats exposed to methanol developed formic acidemia, metabolic acidosis, and visual toxicity, mimicking human methanol poisoning. This study establishes a nonprimate model for methanol

Area of Science:

  • Toxicology
  • Neuroscience
  • Ophthalmology

Background:

  • Human methanol poisoning causes formic acidemia, metabolic acidosis, and visual impairment.
  • Nonprimate species typically resist formate accumulation and methanol's toxic effects.
  • Developing a nonprimate model is crucial for studying methanol toxicity.

Purpose of the Study:

  • To establish a nonprimate model of methanol-induced visual toxicity.
  • To investigate the mechanisms of visual impairment in methanol poisoning.
  • To correlate formate levels with visual dysfunction.

Main Methods:

  • Rats were treated with subanesthetic nitrous oxide to inhibit formic acid oxidation.
  • Methanol was administered to induce intoxication.

Related Experiment Videos

  • Visual function was assessed using flash-evoked cortical potentials and electroretinograms.
  • Blood formate levels were measured.
  • Main Results:

    • Methanol-intoxicated rats exhibited formic acidemia, metabolic acidosis, and visual toxicity within 36 hours.
    • Reductions in electroretinogram and flash-evoked cortical potentials indicated visual dysfunction.
    • Visual changes correlated with blood formate accumulation.
    • Electroretinogram alterations occurred at lower formate concentrations, suggesting direct retinal toxicity.

    Conclusions:

    • A rat model successfully mimics human methanol poisoning, including visual toxicity.
    • Nitrous oxide effectively inhibits formic acid oxidation, enabling toxicity studies in rats.
    • The electroretinogram is a sensitive indicator of direct retinal toxicity in methanol poisoning.