Von Wartburg J P, Bühler R, Maring J A, Pestalozzi D
Pharmacol Biochem Behav. 1983;18 Suppl 1:123-5. doi: 10.1016/0091-3057(83)90158-2.
Evidence is growing that acetaldehyde is responsible for some toxic effects after ethanol intake. Large individual and racial differences in blood and breath acetaldehyde concentrations are observed after alcohol consumption. In many Orientals but few Caucasians extremely high blood acetaldehyde levels occur leading to an acute aldehyde syndrome also observed after treatment with aldehyde dehydrogenase inhibitors. Individuals suffering from the aversive symptoms of that syndrome will be protected from excessive drinking and the related problems. In chronic aldehydism slightly elevated aldehyde concentrations are observed possibly leading to organic injury due to the cytotoxic action of acetaldehyde. Sites exhibiting high alcohol dehydrogenase activity may specifically be affected in alcoholics.
越来越多的证据表明，乙醛是乙醇摄入后产生某些毒性作用的原因。饮酒后，血液和呼出气体中的乙醛浓度存在很大的个体差异和种族差异。在许多东方人中，但在少数白种人中，饮酒后会出现极高的血液乙醛水平，导致急性醛综合征，在用醛脱氢酶抑制剂治疗后也会观察到这种情况。患有该综合征厌恶症状的个体将免受过度饮酒及相关问题的影响。在慢性醛中毒中，观察到醛浓度略有升高，这可能由于乙醛的细胞毒性作用导致器官损伤。酒精脱氢酶活性高的部位可能在酗酒者中受到特异性影响。
