ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Systemic mitochondrial injection protects against methanol-induced optic neuropathy through restoration of mitochondrial function and attenuation of oxidative stress.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Methanol poisoning can cause severe and irreversible optic neuropathy, for which effective neuroprotective strategies remain limited. Mitochondrial dysfunction is important contributors to methanol-induced neuronal injury. Therefore, this study evaluated whether systemic mitochondrial injection could attenuate methanol-induced optic nerve injury. Adult rats were randomly assigned to control, methanol, methanol + single mitochondrial injection, and methanol + double mitochondrial injection groups. Following methanol intoxication, freshly isolated functional mitochondria (250 µg/kg) were administered intravenously. Motor and visual functions were evaluated using the beam walking and visual cliff tests. Mitochondrial dysfunction was assessed by flow cytometric analysis of mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) production. Oxidative stress was assessed by measuring reduced glutathione (GSH) and malondialdehyde (MDA), and optic nerve histopathology was also examined. Methanol exposure impaired motor coordination and visual performance (P < 0.05) and was associated with increased ROS formation (P < 0.001), lipid peroxidation (P < 0.01), MMP collapse (P < 0.001), and GSH depletion (P < 0.05), accompanied by histopathological alterations in the optic nerve. Mitochondrial injection attenuated these changes (P < 0.05) and improved functional and histopathological outcomes. Overall, the double mitochondrial injection was associated with a relatively greater improvement than the single administration in some of the evaluated parameters. Systemic mitochondrial injection attenuated methanol-associated mitochondrial and oxidative disturbances and was accompanied by improved behavioral and histopathological outcomes in this experimental model. Obtained finding in the current study support further investigations of mitochondrial-based approaches as potential strategies for methanol-induced optic neuropathy, while additional works are required to establish their underlying mechanisms, durability, and translational potential.
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