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Treatment of male Fischer 344 rats with various hypolipidemic drugs of different peroxisome proliferating potency (1-benzylimidazole, acetylsalicylic acid, clofibrate, tiadenol) led to an induction of liver lauric acid hydroxylase, whereas probucol, which is not a peroxisome proliferator, did not induce this enzyme. Activity of bilirubin UDP-glucuronosyltransferase was increased by all the compounds tested. The highest increase was observed after treatment with acetylsalicylic acid (2.3-fold). High correlation (r = 0.953) was observed between the activities of lauric acid hydroxylase and the corresponding activities of cytosolic epoxide hydrolase reported previously. The amount of microsomal epoxide hydrolase was not changed by any of the compounds. Whereas clofibrate and tiadenol decreased glutathione S-transferase activity with 1-chloro-2,4-dinitrobenzene as substrate, 1-benzylimidazole and probucol increased this activity. With 4-hydroxynonenal as a substrate qualitatively the same results were obtained with the exception that probucol did not affect the enzyme activity. When glutathione S-transferase activity was measured with cis-stilbene oxide as substrate only the more than five-fold increase after treatment with 1-benzylimidazole was significantly different from control values. Activity of dihydrodiol dehydrogenase was increased after treatment of rats with 1-benzylimidazole (1.5-fold), whereas application of tiadenol led to a decrease of enzyme activity. Feeding of male guinea pigs with clofibrate did not change the activity of peroxisomal beta-oxidation, cytosolic epoxide hydrolase or lauric acid hydroxylase. However, treatment with tiadenol caused an increase of these activities.
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
November 2011,
Chemical communications (Cambridge, England),
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
March 1987,
Biochemical pharmacology,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
November 1986,
Biochimica et biophysica acta,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
December 1982,
Lipids,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
April 1972,
Biochemical and biophysical research communications,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
May 1988,
Drug and alcohol dependence,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
December 1979,
Biochemical pharmacology,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
April 2009,
Biological chemistry,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
January 1973,
Biochemical and biophysical research communications,
H Thomas, and
L Schladt, and
M Knehr, and
K Post, and
F Oesch, and
A F Boiteux-Antoine, and
S Fournel-Gigleux, and
J Magdalou, and
G Siest
January 1982,
Drug metabolism and disposition: the biological fate of chemicals,
