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Effects of Bezafibrate on Ethanol Oxidation in Rats
Author(s) -
Tsukamoto Shojiro,
Kanegae Takashi,
Isobe Eiji,
Hirose Makoto,
Shimamura Masao,
Nagoya Tadaaki
Publication year - 1996
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.1530-0277.1996.tb01704.x
Subject(s) - bezafibrate , clofibrate , chemistry , clofibric acid , ethanol , endocrinology , peroxisome , medicine , aldehyde dehydrogenase , biochemistry , pharmacology , enzyme , receptor
Bezafibrate is used to lower serum lipid levels in humans. Fibrate derivatives induce an enzyme participating in the β‐oxidation by peroxisomes. We gave ethanol (2 g/kg) orally to bezafibrate‐treated (300 mg/kg) male rats of the Wistar strain. Blood ethanol levels were remarkably lower and ethanol elimination stood at 432.6 mg/kg/hr (control, 336.6 mg/kg/hr) in the bezafibrate group ( p < 0.01). Blood acetate levels were conversely higher in the bezafibrate group. The fatly acid β‐oxidation activity of liver peroxisome in bezafibratetreated, clofibrate‐treated, or γ‐linolenic acid‐treated rats for 4 days was assayed. The activity was 5.8‐fold higher in rats given bezafibrate, 5.4‐fold in the clofibrate ( p < 0.01), and 2.0‐fold in the γ‐linolenic acid ( p < 0.05). Alcohol dehydrogenase and aldehyde dehydro‐genase activity of cytosol in the liver was not induced by the hypolipidemic drugs, but aldehyde dehydrogenase activity in the liver homogenate was induced. From foregoing results, bezafibrate induced in the organism p‐oxidation by peroxisomes and increased H 2 O 2 production, which led to augmented ethanol metabolism by catalase.