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Short and long term influence of phenothiazines on liver peroxisomal fatty acid oxidation in rodents
Author(s) -
Van den Branden C.,
Vamecq J.,
Dacremont G.,
Premereur N.,
Roels F.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)80184-9
Subject(s) - peroxisome , clofibrate , beta oxidation , biochemistry , thioridazine , chlorpromazine , chemistry , cytoplasm , pharmacology , fatty acid , in vivo , enzyme , biology , receptor , microbiology and biotechnology
Evidence is given that phenothiazines depress hepatic peroxisomal fatty acid oxidation in vivo. After oral administration to rats thioridazine and chlorpromazine inhibit peroxisomal β‐oxidation, evaluated by H 2 O 2 production, during 2 weeks. In mice, this effect could not be demonstrated. However, in both species VLCFA are increased after short and long term drug administration. Electron microscopy reveals the presence of membranous structures in liver cytoplasm or lysosomes. The inhibition by thioridazine of peroxisomal β‐oxidation does not lead to hepatic peroxisome proliferation. The activities of enzymes related to fatty acid breakdown are not increased and liver peroxisomes are microscopically normal.