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Methanol-induced optic neuropathy: a still-present problem.
Sławomir Liberski1, Bartlomiej J Kaluzny2, Jarosław Kocięcki3
1Department of Ophthalmology, Poznan University of Medical Sciences, ul. Augustyna Szamarzewskiego 84, 61-848, Poznań, Poland. liberski.slawomir@gmail.com.
Archives of Toxicology
|January 6, 2022
Summary
Methanol-induced optic neuropathy (Me-ION) causes vision loss by damaging the optic nerve and retina. Formic acid from methanol inhibits cellular energy production, leading to irreversible visual impairment in survivors.
Area of Science:
- Ophthalmology
- Toxicology
- Neuroscience
Background:
- Methanol-induced optic neuropathy (Me-ION) is a severe condition leading to vision loss or blindness.
- It disproportionately affects impoverished populations globally, often occurring in mass poisoning incidents.
- Damage to the optic nerve and retina underlies the visual impairment.
Purpose of the Study:
- To elucidate the molecular mechanisms and pathological changes in Me-ION.
- To highlight the public health significance of Me-ION, particularly in developing countries.
- To review the persistent visual sequelae despite therapeutic interventions.
Main Methods:
- Review of the molecular mechanisms of Me-ION pathogenesis.
- Description of histopathological changes in ocular tissues.
- Analysis of clinical outcomes and persistent visual deficits.
Main Results:
- Methanol's toxic metabolite, formic acid, inhibits mitochondrial oxidative phosphorylation via cytochrome c oxidase.
- Oxidative stress, inflammation, and altered protein expression also contribute to Me-ION.
- Histopathology reveals optic nerve axon and glial cell degeneration, with retinal damage.
Conclusions:
- Me-ION poses a significant global health challenge due to its potential for irreversible vision loss.
- Understanding the multifaceted pathogenesis is crucial for developing effective treatments.
- Persistent visual sequelae in 30-40% of survivors underscore the need for continued research and prevention strategies.

