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Effects of ethanol on prostanoid production by liver fat‐storing cells
Author(s) -
Flisiak Robert,
Baraona Enrique,
Li Jianjun,
Lieber Charles S.
Publication year - 1993
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840180123
Subject(s) - acetaldehyde , alcohol dehydrogenase , aldehyde dehydrogenase , disulfiram , chemistry , ethanol , prostaglandin , endocrinology , medicine , alcoholic liver disease , biochemistry , ethanol metabolism , prostaglandin e , biology , enzyme , cirrhosis
Fat‐storing cells participate in the development of alcoholic liver disease. To study possible effects of ethanol on prostaglandin metabolism by fat‐storing cells, we isolated them from normal rat liver. Cultured fat‐storing cells produced substantial amounts (DNA, about 2 ng/μg every 24 hr) of prostaglandin E 2 and prostaglandin I 2 (measured as 6‐keto prostaglandin F 1α ) but no significant amounts of prostaglandin F 2α . This production was markedly enhanced by the addition of ethanol in concentrations likely to occur in the blood during alcohol consumption. We confirmed the presence of class 1 alcohol dehydrogenase activity and isoenzymes in the cytosol of cultured fat‐storing cells in their second passage. The stimulatory effect of ethanol was inhibited by 4‐methylpyrazole (an alcohol dehydrogenase inhibitor), exaggerated by disulfiram (an aldehyde dehydrogenase inhibitor) and reproduced by concentrations of acetaldehyde likely to occur in the liver. Thus, our results indicate that fat‐storing cells produce vasodilatory prostaglandins and that this production is enhanced by the acetaldehyde that results from the oxidation of ethanol catalized by alcohol dehydrogenase present in these cells. (H EPATOLOGY 1993;18:153–159).