Mode of action

Metabolism of methanol ultimately leads to the formation of formic acid. This acid inhibits mitochondrial cytochrome oxidase activity leading to hypoxia. Tissues with a high oxygen demand are affected: optic nerve, brain, heart and kidneys. Formic acid inhibits cytochrome oxidase activity by binding at the sixth coordination position of the ferric haem iron (Liesivuori and Savolainen, 1997).

The inhibition of cytochrome oxidase by formic acid increases with decreasing pH, suggesting that the active inhibitor is the undissociated acid. Thus acidosis may potentiate the inhibition of cellular respiration and hasten the onset of cellular injury. The progressive acidosis will induce circulatory failure, leading to tissue hypoxia and lactic acid production, which further increases the acid load, and in turn increases the concentration of undissociated formic acid (Garner et al., 1995; Liesivuori and Savolainen, 1997).

The ocular toxicity from methanol poisoning is thought to be due to inhibition of retinal and optic cytochrome oxidase by the accumulated formic acid (Garner et al., 1995). Correction of metabolic acidosis is associated with vision improvement (Herken and Rietbrock, 1968).

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