Effect of Acute Ethanol on Membrane Transport of Folate

Abstract

Chronic ethanol ingestion is a primary cause of vitamin deficiency, particularly folic acid deficiency (5). Although poor diet plays a role in the etiology of folic acid deficiency, ethanol ingestion produces effects on folate metabolism in such tissues as the bone marrow (19). Serum folate levels can be markedly depleted by acute ethanol ingestion by humans (3) as well as by rats (10). Ethanol ingestion could alter normal folate homeostasis at numerous sites. Dietary folates are mostly pteroylpolyglutamates and must be hydrolyzed by pteroylpolyglutamate hydrolase (21), prior to jejunal absorption by a carrier–mediated process (15). Folate is then distributed to various tissues as 5-methyl-tetrahydrofolate (5-CH₃-H₄PteGlu), the primary form in the plasma (5). Intracellular folates are primarily in the form of polyglutamates, either for storage (8) or for increased catalytic efficiency (2). The liver contains the largest stores of folates in the body, and may release its stores by biliary secretion to support folate levels in other tissues (18). Folates are freely filtered from the plasma at the glomerulus and can be reabsorbed or secreted (4) by the renal tubules for eventual excretion in the urine.