EXCRETION OF MALONDIALDEHYDE, FORMALDEHYDE, ACETALDEHYDE AND ACETONE IN THE URINE OF RATS FOLLOWING ACUTE AND CHRONIC ADMINISTRATION OF ETHANOL

Recent studies have shown that xenobiotics which induce oxidative stre ss result in an increased production and excretion of acetaldehyde (AC T), formaldehyde (FA), acetone (ACON) and malondialdehyde (MDA) in the urine of rats. We have therefore examined the effect of acute and chr onic ethanol administration on the excretion of these four lipid metab olites in female Sprague-Dawley rats. Urine samples were collected ove r dry ice for 6 hr time periods. Aliquots of urine were derivatized wi th 2,4-dinitrophenylhydrazine HCl, and extracted with n-pentane. High pressure liquid chromatography (HPLC) was used to quantitate and the h ydrazones of the four lipid metabolite products. Following a single, o ral, acute dose of 5 g ethanol/kg, urinary excretion of ACT increased approximately 5.8-fold from 6 to 12 hr post-treatment, and decreased t hereafter. FA excretion decreased by approximately 50% from 0 to 12 hr , returned to control values in the 18-24 hr urine samples, and was 1. 3-fold greater than control values at 42-48 hr. ACON increased 3.1-fo ld over control values from 0 to 30 hr and remained elevated throughou t the remaining 18 hr of the study. The excretion of MDA increased app roximately 1. 5-fold from 18 to 36 hr, then remained constant through, the 48 hr time point. In a separate series of experiments, a chronic oral dose of 0.5 g ethanol/kg was administered to rats for 10 consecut ive days and the urinary excretion of the lipid metabolites MDA, FA, A CT and ACON was examined for 11 days, beginning with the first day of ethanol administration. During the chronic administration of ethanol, a significant increase in the urinary excretion of ACT began on day 4. An increase in ACON excretion was first observed on day 6, and increa ses in MDA and FA excretion were first observed on days 8 and 10, resp ectively. The results clearly demonstrate that both acute and chronic alcohol consumption markedly alter lipid metabolism and the excretion of lipid metabolites.