Like ethylene glycol, methanol is relatively non-toxic; however, it is metabolized to highly toxic compounds that are responsible for the acidosis and blindness characteristic of methanol poisoning.
As in ethylene glycol poisonings, the initial step in the metabolism of methanol involves the enzyme alcohol dehydrogenase (ADH) (see Figure 2). First, methanol is slowly oxidized by ADH to yield formaldehyde. Next,formaldehyde is oxidized by formaldehyde dehydrogenase to yield formic acid (or formate, depending on the pH). This oxidation occurs rapidly so that little formaldehyde accumulates in the serum. FInally, formic acid is metabolized to carbon dioxide and water, which are excreted by the kidneys and lungs.
The accumulation of formic acid is responsible for the presence of metabolic acidosis. Formic acid also inhibits cellular respiration leading to lactic acidosis. The ocular injury caused by methanol may be due to retinal injury, which results from intra-retinal metabolism of methanol and the accumulation of formic acid. Alternatively, it may be caused be the inhibition of normal metabolism in optic nerve calls (Jacobsen 1997).