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Peroxisome-proliferating effects of fenoprofen in mice

(1998) LIPIDS. 33(5). p.539-543
Author
Organization
Abstract
We report on hepatic effects obtained in vivo by treating mice with different doses of fenoprofen, an arylpropionic acid previously shown to inhibit in vitro peroxisomal very long chain fatty acid oxidation. A strong and dose-related induction of peroxisomal palmitoyl-CoA oxidase, and of carnitine acyltransferase and acyl-CoA hydrolase activities was recorded in liver homogenates of mice fed diets supplemented with different contents [0.01, 0.05, 0.1, or 1% (w/w)] of fenoprofen for 6 d. Peroxisomal glycolate oxidase and mitochondrial butyryl-CoA, octanoyl-CoA, and palmitoyl-CoA dehydrogenases were unaffected or increased. Hepatic catalase activity was significantly increased in mice fed the diet with 0.05 and 0.1% fenoprofen but, surprisingly, was not stimulated in mice fed the 1% fenoprofen-containing diet. A time-related but unequal induction of acyl-CoA oxidases and catalase was observed with the 0.1% fenoprofen diet: at 21 d of treatment, the induction of lignoceroyl-CoA and palmitoyl-CoA oxidase activities were fivefold stronger than that of catalase activity. In mice treated with 1% fenoprofen for up to 6 d, only acyl-CoA oxidase activities were found to be significantly increased. Morphometric analysis of the liver peroxisomes in mice treated with 0.1% fenoprofen evidenced an increase in size, volume density, and surface density along with a reduced ratio between perimeter and area of the peroxisomal profiles. No morphological marker for very long chain fatty acid deposition could be detected in livers from fenoprofen-treated animals. Our findings clearly demonstrate that fenoprofen acts as a peroxisome proliferator in the liver of mice and do not support the occurrence of in vivo reduction of very long chain fatty acid oxidation in liver from treated animals.
Keywords
CHONDRODYSPLASIA PUNCTATA, RAT-LIVER, BETA-OXIDATION, ADRENOLEUKODYSTROPHY, INCLUSIONS, DISORDERS, INDUCTION, CHAIN, FORM

Citation

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MLA
De Craemer, Dirk et al. “Peroxisome-proliferating Effects of Fenoprofen in Mice.” LIPIDS 33.5 (1998): 539–543. Print.
APA
De Craemer, D., Van den Branden, C., Pauwels, M., & Vamecq, J. (1998). Peroxisome-proliferating effects of fenoprofen in mice. LIPIDS, 33(5), 539–543.
Chicago author-date
De Craemer, Dirk, Christiane Van den Branden, Marina Pauwels, and J Vamecq. 1998. “Peroxisome-proliferating Effects of Fenoprofen in Mice.” Lipids 33 (5): 539–543.
Chicago author-date (all authors)
De Craemer, Dirk, Christiane Van den Branden, Marina Pauwels, and J Vamecq. 1998. “Peroxisome-proliferating Effects of Fenoprofen in Mice.” Lipids 33 (5): 539–543.
Vancouver
1.
De Craemer D, Van den Branden C, Pauwels M, Vamecq J. Peroxisome-proliferating effects of fenoprofen in mice. LIPIDS. 1998;33(5):539–43.
IEEE
[1]
D. De Craemer, C. Van den Branden, M. Pauwels, and J. Vamecq, “Peroxisome-proliferating effects of fenoprofen in mice,” LIPIDS, vol. 33, no. 5, pp. 539–543, 1998.
@article{887127,
  abstract     = {We report on hepatic effects obtained in vivo by treating mice with different doses of fenoprofen, an arylpropionic acid previously shown to inhibit in vitro peroxisomal very long chain fatty acid oxidation. A strong and dose-related induction of peroxisomal palmitoyl-CoA oxidase, and of carnitine acyltransferase and acyl-CoA hydrolase activities was recorded in liver homogenates of mice fed diets supplemented with different contents [0.01, 0.05, 0.1, or 1% (w/w)] of fenoprofen for 6 d. Peroxisomal glycolate oxidase and mitochondrial butyryl-CoA, octanoyl-CoA, and palmitoyl-CoA dehydrogenases were unaffected or increased. Hepatic catalase activity was significantly increased in mice fed the diet with 0.05 and 0.1% fenoprofen but, surprisingly, was not stimulated in mice fed the 1% fenoprofen-containing diet. A time-related but unequal induction of acyl-CoA oxidases and catalase was observed with the 0.1% fenoprofen diet: at 21 d of treatment, the induction of lignoceroyl-CoA and palmitoyl-CoA oxidase activities were fivefold stronger than that of catalase activity. In mice treated with 1% fenoprofen for up to 6 d, only acyl-CoA oxidase activities were found to be significantly increased. Morphometric analysis of the liver peroxisomes in mice treated with 0.1% fenoprofen evidenced an increase in size, volume density, and surface density along with a reduced ratio between perimeter and area of the peroxisomal profiles. No morphological marker for very long chain fatty acid deposition could be detected in livers from fenoprofen-treated animals. Our findings clearly demonstrate that fenoprofen acts as a peroxisome proliferator in the liver of mice and do not support the occurrence of in vivo reduction of very long chain fatty acid oxidation in liver from treated animals.},
  author       = {De Craemer, Dirk and Van den Branden, Christiane and Pauwels, Marina and Vamecq, J},
  issn         = {0024-4201},
  journal      = {LIPIDS},
  keywords     = {CHONDRODYSPLASIA PUNCTATA,RAT-LIVER,BETA-OXIDATION,ADRENOLEUKODYSTROPHY,INCLUSIONS,DISORDERS,INDUCTION,CHAIN,FORM},
  language     = {eng},
  number       = {5},
  pages        = {539--543},
  title        = {Peroxisome-proliferating effects of fenoprofen in mice},
  volume       = {33},
  year         = {1998},
}

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