Wall T L, Ehlers C L
Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037, USA.
Alcohol Clin Exp Res. 1995 Jun;19(3):617-22. doi: 10.1111/j.1530-0277.1995.tb01557.x.
Asian men were genotyped for alleles of aldehyde dehydrogenase (ALDH2) and tested on two separate occasions following oral administration of placebo and 0.75 ml/kg alcohol. Sixty minutes after beverage ingestion, event-related potentials were elicited using an auditory oddball paradigm. Repeated measures ANOVA revealed that alcohol produced significant increases in P300 latency and significant decreases in P300 amplitude compared with placebo. Subjects with ALDH21/22 genotype (n = 14) demonstrated some significantly greater P300 effects after alcohol than subjects with ALDH21/21 genotype (n = 15), despite equivalent blood alcohol concentrations. These data suggest that neurocognitive functioning may be more impaired following alcohol in subjects with an ALDH2*2 allele. These findings further suggest that a genetically controlled factor (deficiency in ALDH enzyme activity) might contribute to a decreased likelihood of alcohol intake and protection from alcoholism, because of an enhanced sensitivity to alcohol.
对亚洲男性的乙醛脱氢酶(ALDH2)等位基因进行基因分型,并在口服安慰剂和0.75毫升/千克酒精后的两个不同时间点进行测试。饮用饮料60分钟后,使用听觉oddball范式诱发事件相关电位。重复测量方差分析显示,与安慰剂相比,酒精使P300潜伏期显著延长,P300波幅显著降低。尽管血液酒精浓度相当,但携带ALDH21/22基因型的受试者(n = 14)在饮酒后表现出比携带ALDH21/21基因型的受试者(n = 15)更大的P300效应。这些数据表明,携带ALDH2*2等位基因的受试者在饮酒后神经认知功能可能受损更严重。这些发现进一步表明,一个受基因控制的因素(ALDH酶活性缺乏)可能导致饮酒可能性降低并预防酒精中毒,因为对酒精的敏感性增强。