Fig. 1.

Schematic illustration of ethanol (EtOH) destination in human body after ingestion of alcoholic beverages. (a) EtOH is oxidized to acetaldehyde in hepatocytes through alcohol dehydrogenases (ADH1A, ADH1B^*1, ADH1C^*1 and ADH4) and cytochrome P450 2E1 (CYP2E1). Reactive oxygen species (ROS) are generated due to the interference of EtOH with electron transport complexes in mitochondrial membrane. Acetaldehyde is converted to acetate by aldehyde dehydrogenases (ALDH1/2). (b) Acetate is metabolized to acetyl CoA, which is considered as an important metabolic intermediate of the tricarboxylic acid (TCA) cycle and β-oxidation of fatty acids. (c) Citrate could be converted to acetyl CoA by ATP citrate lyase (ACL). The generated acetyl CoA may result in DNA acetylation or be involved in fatty acyl CoA production. (d) Fatty acyl CoA is associated with lipogenesis reactions, which results in triglycerides, very low density lipoproteins (VLDL) and, finally, alcoholic fatty liver in chronic alcoholic patients. The excess amount of EtOH in chronic alcoholic patients may result in elevated acetate in blood, lactic acidemia and hyperlipidemia.