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Blood actaldehyde and ethanol levels were measured in 11 subjects, six with chronic alcholoism and five nonalcholic controls, after alcohol had been given intravenously. Despite a progressive fall in blood ethanol over a range of 54 to 33 mM/acetaldehyde did not decrease in any of the 11 subjects. The mean acetaldehyde plateau level was significantly (p less than 0.001) higher in alcoholic (42.7 plus or minus 1.2 mum) than in nonalcoholic (26.5 plus or minus 1.5 mum) subjects. When the mean blood ethanol concentration reached 24 mM,the acetaldehyde plateau ended abruptly in each subject. The ethanol concentration at which this fall of blood acetaldehyde occurred suggests desaturation of an ethanol oxidizing system other than alcohol dehydrogenase and indicates that at high ethanol blood levels, such a system contributes to ethanol oxidation. The highet acetaldehyde levels in alcholism may result from both greater activity of this system and mitochondrial damage, and could contribut to the neurologic, hepatic and cardiac complications of alcoholism.
Korsten et al. (1975) studied this question.