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Abstract
Metabolism of methanol, methyl ethers, esters and amides give rise to formic acid.
This acid is an inhibitor of the mitochondrial cytochrome oxidase causing histotoxic
hypoxia. Formic acid is a weaker inhibitor than cyanide and hydrosulphide anions.
The body burden of formate in methanol poisoning is high enough to cause acidosis,
and other clinical symptoms. Part of the protons can be attributed to formic acid
whereas the most significant acid load results from the hypoxic metabolism. The acidosis
causes e.g. dilatation of cerebral vessels, facilitation of the entry of calcium ions
into cells, loss of lysosomal latency and deranged production of ATP. The latter effect
seems to impede parathormone-dependent calcium reabsorption in the kidney tubules.
Besides, urinary acidification is affected by formic acid. Its excretion causes continuous
recycling of the acid by the tubular cell Cl-/formate exchanger. This sequence of
events may partially explain an accumulation of formate in urine. Occupational exposure
to vapours of methanol and formic acid can be quantitatively monitored by urinary
formic acid determinations. Formic acid toxicity may prove a suitable model for agents
causing histotoxic hypoxia.