Metabolic interactions

• Carbon tetrachloride

Concurrent exposure to methanol vapours enhances the hepatotoxicity of carbon tetrachloride (Cornish and Adefuin, 1967; Allis et al., 1996). Animal studies show that there is increased metabolism of carbon tetrachloride in the microsomes of methanol treated animals (Allis et al., 1996). Methanol is an inducer of the CYP2E1 enzyme, which plays a large role in the metabolism of carbon tetrachloride.

As ethanol is the preferred substrate of alcohol dehydrogenase (ADH), it blocks the metabolism of methanol, and the production of toxic formic acid. As a result of this interaction, ethanol is used as an antidote in methanol poisoning. It is only useful in the immediate phase after exposure, as administration of ethanol is of very little benefit once the methanol has been metabolised. The drug, fomepizole, has a similar action to ethanol, and could be used as a substitute for ethanol in methanol intoxication (Brent et al., 2001).

MEK may have inhibited methanol metabolism following ingestion of approximately 240 ml of an ink cleaning solution thought to contain MEK 47% and methanol 45%. There was minimal metabolism of methanol to formate despite a high methanol concentration (2,020 mg/l; 63 mmol/l) and the anion gap remained normal. The MEK probably acted by inhibiting alcohol dehydrogenase (Price et al., 1994).

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