Short and long term influence of phenothiazines on liver peroxisomal fatty acid oxidation in rodents

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 2O 2 production, during 2 weeks. In mice, this effect could not be demonstrated. However,...

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Bibliographic Details
Published in:FEBS letters 1987-09, Vol.222 (1), p.21-26
Main Authors: Van den Branden, C., Vamecq, J., Dacremont, G., Premereur, N., Roels, F.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Chlorpromazine
Chlorpromazine - pharmacology
CPZ, chlorpromazine
Fatty Acids - metabolism
LCFA, long chain fatty acid
Liver - drug effects
Liver - metabolism
Male
Medical sciences
Microbodies - drug effects
Microbodies - metabolism
Microbodies - ultrastructure
Microscopy, Electron
Neuropharmacology
Peroxisome
Pharmacology. Drug treatments
Psycholeptics: tranquillizer, neuroleptic
Psychology. Psychoanalysis. Psychiatry
Psychopharmacology
Rats
Rats, Inbred Strains
RCA, residual catalase activity
T, thioridazine
Thioridazine
Thioridazine - pharmacology
VLCFA
VLCFA, very long chain fatty acid
β-Oxidation
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Summary: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 2O 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.
ISSN:0014-5793
1873-3468
DOI:10.1016/0014-5793(87)80184-9