Lindros K O
Alcohol Clin Exp Res. 1983 Winter;7(1):70-5. doi: 10.1111/j.1530-0277.1983.tb05414.x.
New reliable methods for the determination of acetaldehyde in human blood, either from separated plasma or from acid-precipitated whole blood, demonstrate that the blood of healthy Caucasians contains at most only extremely small amounts of acetaldehyde (less than 1 microM) after moderate alcohol intoxication. On the other hand, among about 50% of the Japanese population ethanol ingestion results in elevated blood acetaldehyde levels (10-50 microM) with consequent unpleasant cardiovascular responses such as facial flushing and tachycardia, apparently because of a lack of one of the acetaldehyde-oxidizing aldehyde dehydrogenase isozymes. Elevated acetaldehyde levels may eventually occur also among intoxicated Caucasian alcoholics, primarily as a consequence of abuse-induced loss of hepatic aldehyde dehydrogenase activity, but accentuated by an accelerated ethanol oxidation rate. The elevation is probably reversible, since no acetaldehyde is seen in alcoholics after abstinence and hospital treatment. There is thus little evidence that an elevation of acetaldehyde could serve as a marker for predisposition for alcoholism.
用于测定人体血液中乙醛的新可靠方法，无论是来自分离的血浆还是酸沉淀的全血，都表明健康的白种人在中度酒精中毒后，其血液中最多仅含有极少量的乙醛（低于1微摩尔）。另一方面，在约50%的日本人群中，乙醇摄入会导致血液中乙醛水平升高（10 - 50微摩尔），随之产生不愉快的心血管反应，如面部潮红和心动过速，这显然是由于缺乏一种乙醛氧化醛脱氢酶同工酶。在醉酒的白种人酗酒者中最终也可能出现乙醛水平升高的情况，这主要是滥用导致肝脏醛脱氢酶活性丧失的结果，但乙醇氧化速率加快会加剧这种情况。这种升高可能是可逆的，因为在戒酒和住院治疗后，酗酒者体内未见乙醛。因此，几乎没有证据表明乙醛升高可作为酗酒易感性的标志物。
