The effect of acetaldehyde on mitochondrial respiration

Abstract

The inhibiting effect of acetaldehyde on the pyruvate oxidation in mitochondria from various tissues has been investigated. The following sequence was found as to the degree of aldehyde inhibition: liver < kidney < cerebrum < muscle < cerebellum. At least partly this depends on the fact that liver, kidney and, although less pronounced, cerebral mitochondria rapidly recover from the inhibition, while mitochondria from muscle and cerebellum do not. Liver and kidney mitochondria oxidize acetaldehyde rapidly compared with muscle and brain mitochondria. The possibility that this oxidation capacity might be a contributory cause to the abolition of the acetaldehyde inhibition is briefly discussed. When reduced diphosphopyridine nucleotide is substituted for pyruvate, addition of acetaldehyde only slightly inhibits the oxidation rate in brain mitochondria. This localizes the site of action of aldehyde to somewhere between the pyruvate and the reduced diphosphopyridine nucleotide dehydrogenase. The acetaldehyde inhibition of pyruvate oxidation is abolished by thiamine diphosphate and diphosphopyridine nucleotide. The latter, however, only exerts its action after the mitochondrial structure has been disorganized.