Hu Nan, Zhang Yingmei, Nair Sreejayan, Culver Bruce W, Ren Jun
Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA.
Recent Pat Endocr Metab Immune Drug Discov. 2014;8(3):180-5. doi: 10.2174/1872214808666141020162000.
Chronic alcohol intake is considered as an independent lifestyle factor that may influence the risk of a number of cardiovascular anomalies including hypertension. In healthy adults, binge drinking and chronic alcohol ingestion lead to the onset and development of hypertension although the precise mechanism(s) remains obscure. Although oxidative stress and endothelial injury have been postulated to play a major contributing role to alcoholism-induced hypertension, recent evidence depicted a rather unique role for the genotype of the acetaldehyde-metabolizing enzyme mitochondrial aldehyde dehydrogenase (ALDH2), which is mainly responsible for detoxifying ethanol consumed, in alcoholism-induced elevation of blood pressure. Genetic polymorphism of ALDH2 in human results in altered ethanol pharmacokinetic properties and ethanol metabolism, leading to accumulation of the ethanol metabolite acetaldehyde following alcohol intake. The unfavorable consequence of the ALDH2 variants is believed to be governed by the accumulation of the ethanol metabolite acetaldehyde. Presence of the mutant or inactive ALDH2*2 gene often results in an increased risk of hypertension in human. Such association between blood pressure and ALDH2 enzymatic activity may be affected by the interplay between gene and environment, such as life style and ethnicity. The aim of this mini-review is to summarize the possible contribution of ALDH2 genetic polymorphism in the onset and development of alcoholism-related development of hypertension. Furthermore, the double-edged sword of ALDH2 gene and genetic polymorphism in alcoholism and alcoholic tissue damage and relevant patents will be discussed.
长期饮酒被认为是一种独立的生活方式因素，可能会影响包括高血压在内的多种心血管异常的风险。在健康成年人中，暴饮和长期饮酒会导致高血压的发生和发展，尽管确切机制仍不清楚。虽然氧化应激和内皮损伤被认为在酒精性高血压中起主要作用，但最近的证据表明，乙醛代谢酶线粒体醛脱氢酶（ALDH2）的基因型在酒精性高血压中起着相当独特的作用，该酶主要负责将摄入的乙醇解毒。人类ALDH2的基因多态性导致乙醇药代动力学特性和乙醇代谢改变，导致饮酒后乙醇代谢产物乙醛的积累。据信，ALDH2变体的不良后果是由乙醇代谢产物乙醛的积累所控制的。突变或无活性的ALDH2*2基因的存在通常会增加人类患高血压的风险。血压与ALDH2酶活性之间的这种关联可能会受到基因与环境之间相互作用的影响，如生活方式和种族。本综述的目的是总结ALDH2基因多态性在酒精性高血压发病和发展中的可能作用。此外，还将讨论ALDH2基因和基因多态性在酒精中毒、酒精性组织损伤中的双刃剑作用以及相关专利。
