[Pathobiochemistry of alcoholism].
Liver alcohol dehydrogenase (ADH) represents the main enzyme of normal alcohol metabolism. Total activity of this enzyme varies largely due to the occurrence of isoenzymes and of genetic polymorphisms. One genetic variant, called "atypical", is characterized by a higher specific activity. In carriers of this variant enzyme an initially faster rate of ethanol metabolism leads to higher blood acetaldehyde levels. Acetaldehyde, as a toxic intermediary metabolite, causes tachycardia, nausea and flushing of the face. A high frequency for "atypical" ADH is observed in mongolid races and consequently a hypersensitivity to alcohol is often observed in Orientals. Hence, certain genetically determined enzyme patterns may represent an aversive factor with regard to alcohol consumption. In Caucasians the phenotypes with "atypical" ADH are less frequent. However, in individuals with the "atypical" variant regular intake of alcohol may lead to an increased organotoxicity due to acetaldehyde.
D000079:Acetaldehyde / Q000097:blood; D000429:Alcohol Oxidoreductases / Q000235:genetics / Q000378:metabolism*; D000437:Alcoholism / Q000378:metabolism*; D014644:Genetic Variation; D006801:Humans; D008099:Liver / Q000378:metabolism*; D010641:Phenotype; D011110:Polymorphism, Genetic; D044469:Racial Groups
D000429:Alcohol Oxidoreductases; D000079:Acetaldehyde
Pathobiochemie des Alkoholismus.