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Vitamin B 12 and Folate Status in Rats after Chronic Administration of Ethanol and Acute Exposure to Nitrous Oxide
Author(s) -
Koblin Donald D.,
Everman Barbara W.
Publication year - 1991
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1991.tb00557.x
Subject(s) - ethanol , chemistry , medicine , vitamin , endocrinology , methionine synthase , liquid diet , methionine , formic acid , kidney , excretion , biochemistry , amino acid
The chronic administration of ethanol or brief exposure to nitrous oxide (N 2 O) decreases the activity of hepatic methionine synthase and disrupts normal metabolic processes that require folate and vitamin B 12 . This combination of drugs has clinical relevance since alcoholic patients often require surgery and receive N 2 O as a component of their anesthetic. To assess this clinical problem using a rodent model, rats were given a liquid ethanol diet (35% of calories as ethanol) and control rats were pair‐fed a liquid diet with carbohydrate substituting for the caloric content of ethanol. After receiving liquid diets for 6 weeks, rats were exposed to 60% N 2 O/40% 02 for 6 hr. Urinary excretions of formic acid and formiminoglutamic acid (FIGLU) were used as indirect markers of folate status. In both the ethanol‐fed and control groups, excretion of formic acid and FIGLU markedly increased the first day after N 2 O and returned towards background values by the second day after N 2 O exposure. Ethanol treatment alone decreased methionine synthase activities in liver, but not kidney or brain. Exposure to N 2 O further decreased methionine synthase activities, and recovery of methionine synthase activity after N 2 O occurred over a period of 4 days at the same rate in both the ethanol‐fed and control groups. Ethanol treatment for 6 weeks combined with acute exposure to N 2 O did not deplete the rats of vitamin B 12 in blood, liver, kidney, or brain. We conclude that in this animal model, chronic treatment with ethanol does not markedly exacerbate the disturbances in folate/vitamin B 12 metabolism caused by brief exposure to N 2 O.