title: Beneficial effect of low ethanol intake on the cardiovascular system: possible biochemical mechanisms.
abstract: Low ethanol intake is known to have a beneficial effect on cardiovascular disease. In cardiovascular disease, insulin resistance leads to altered glucose and lipid metabolism resulting in an increased production of aldehydes, including methylglyoxal. Aldehydes react non-enzymatically with sulfhydryl and amino groups of proteins forming advanced glycation end products (AGEs), altering protein structure and function. These alterations cause endothelial dysfunction with increased cytosolic free calcium, peripheral vascular resistance, and blood pressure. AGEs produce atherogenic effects including oxidative stress, platelet adhesion, inflammation, smooth muscle cell proliferation and modification of lipoproteins. Low ethanol intake attenuates hypertension and atherosclerosis but the mechanism of this effect is not clear. Ethanol at low concentrations is metabolized by low Km alcohol dehydrogenase and aldehyde dehydrogenase, both reactions resulting in the production of reduced nicotinamide adenine dinucleotide (NADH). This creates a reductive environment, decreasing oxidative stress and secondary production of aldehydes through lipid peroxidation. NADH may also increase the tissue levels of the antioxidants cysteine and glutathione, which bind aldehydes and stimulate methylglyoxal catabolism. Low ethanol improves insulin resistance, increases high-density lipoprotein and stimulates activity of the antioxidant enzyme, paraoxonase. In conclusion, we suggest that chronic low ethanol intake confers its beneficial effect mainly through its ability to increase antioxidant capacity and lower AGEs.
authors.affiliation: Discipline of Medicine, Faculty of Medicine, Memorial University of Newfoundland, Health Sciences Centre, St.John's, Newfoundland, Canada. svasdev@mun.ca
authors.forename: Sudesh
authors.initials: S
authors.lastname: Vasdev
authors.forename: Vicki
authors.initials: V
authors.lastname: Gill
authors.forename: Pawan K
authors.initials: PK
authors.lastname: Singal
mesh_terms: D050197:Atherosclerosis / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D002319:Cardiovascular System / Q000187:drug effects*; D050171:Dyslipidemias / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000502:physiology; D000431:Ethanol / Q000494:pharmacology*; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007333:Insulin Resistance; D009243:NAD / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology
chemical_list: D017127:Glycation End Products, Advanced; D009243:NAD; D000431:Ethanol