Abstract
Alcohol abuse is a serious medical and social problem. Although light to moderate alcohol consumption is beneficial to cardiovascular health, heavy drinking often results in organ damage and social problems. In addition, genetic susceptibility to the effect of alcohol on cancer and coronary heart disease differs across the population. A number of mechanisms including direct the toxicity of ethanol, its metabolites [e.g., acetaldehyde and fatty acid ethyl esters (FAEEs)] and oxidative stress may mediate alcoholic complications. Acetaldehyde, the primary metabolic product of ethanol, is an important candidate toxin in developing alcoholic diseases. Meanwhile, free radicals produced during ethanol metabolism and FAEEs are also important triggers for alcoholic damages.
Highlights
The alcohol family is comprised of three different members namely methyl alcohol, isopropyl alcohol and ethyl alcohol
Different levels of blood acetaldehyde are shown in different genotypic verifications in the alcohol dehydrogenase (ADH) or aldehyde dehydrogenase (ALDH) gene following alcohol intake [37], predisposing these individuals to alcohol damage, and the degrees of polymorphism differs depending on racial and ethnic groups [38]
Evidence has indicated that small amounts of alcohol may be removed via interaction with fatty acids to form fatty acid ethyl esters (FAEEs), the latter has been shown to contribute to damage to the heart, liver and pancreas [88,89]
Summary
The alcohol family is comprised of three different members namely methyl alcohol (methanol), isopropyl alcohol and ethyl alcohol (ethanol, EtOH or CH3CH2OH). Genetic susceptibility to alcohol-associated risk prevalence of cancer and coronary heart disease differs across the population. It is recommended that moderate drinking must be individualized to reflect the potentially confounding effects of alcohol on several chronic diseases [5]. In addition to chronic diseases, alcohol abuse may trigger a cascade of acute health problems such as traffic accident-related injuries. Acetaldehyde, the primary metabolic product of ethanol, is thought to be a candidate toxin and plays a pivotal role in priming and developing alcoholism [34]. Genetic polymorphism in alcohol dehydrogenase (ADH) [35] and aldehyde dehydrogenase (ALDH) [36,37], the two key enzymes responsible for ethanol/acetaldehyde metabolism, is involved in the susceptibility to alcoholism and alcohol-related organ damage and diseases. Different levels of blood acetaldehyde are shown in different genotypic verifications in the ADH or ALDH gene following alcohol intake [37], predisposing these individuals to alcohol damage, and the degrees of polymorphism differs depending on racial and ethnic groups [38]
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