Acceleration of ethanol metabolism by past thiamine deficiency.
Six months after severe thiamine deficiency, when their body and liver weights had normalized, male Sprague-Dawley rats were exposed to constant ethanol vapor concentrations for 6 days in an inhalation chamber and blood ethanol concentrations (BECs) were determined. Previously induced thiamine deficiency was associated with about a 50% reduction of BECs and a significant increase in liver alcohol dehydrogenase (ADH) activity suggesting a persistent acceleration of ethanol metabolism. No significant changes were found in liver aldehyde dehydrogenase activity, plasma levels of thyroxine, testosterone, or estradiol, or brain or liver histology. Plasma growth hormone concentrations were about 60% lower in the experimental group than in controls, but this effect of previous thiamine deprivation did not correlate with changes in ADH activity. Therefore, it remains to be elucidated how thiamine deficiency-induced central nervous system alterations may contribute to the development of metabolic tolerance to ethanol.
Martin
P R
PR
Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.
Impeduglia
G
G
Giri
P R
PR
Karanian
J
J
D000426:Alcohol Dehydrogenase / Q000097:blood; D000437:Alcoholism / Q000201:enzymology*; D000444:Aldehyde Dehydrogenase / Q000097:blood; D000818:Animals; D000431:Ethanol / Q000493:pharmacokinetics*; D008099:Liver / Q000201:enzymology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013832:Thiamine Deficiency / Q000201:enzymology*
D000431:Ethanol; D000426:Alcohol Dehydrogenase; D000444:Aldehyde Dehydrogenase