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.
Keywords: Acetaldehyde, alcohol, cardiovascular complications, hypertension, metabolism, mitochondrial aldehyde dehydrogenase.
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