Alteration of peroxisomal enzyme activities in the liver of guinea pigs caused by coplanar PCB

M. Iwasaki, H. Kato, N. Ariyoshi, K. Oguri

Research output: Contribution to journalArticle

Abstract

The hyperlipidemia is a well-known typical symptom in Yusho patients and experimental animals treated with PCBs. We have found a significant induction of CYP4A1, which catalyzes omega-hydroxylation of fatty acids, in guinea pigs by the treatment with a coplanar PCB, 3, 4, 5, 3',4-pentachlorobiphenyl (PenCB), though the P450 is reduced in the treated rats. Peroxisome has beta-oxidation enzymes distinct from mitochondrial enzymes, and also play an important role in lipid metabolism. Peroxisome proliferators have been shown to regulate the expression of CYP4A1 and peroxisomal enzymes by the same mechanism in the rat. In the present study, we examine the effect of PenCB treatment on peroxisomal enzymes in the liver of guinea pigs. As a result, the enzyme activities of hepatic peroxisome, e.g. fatty acid oxidizing system, catalase and urate oxidase, had a rising tendency by the treatment with PenCB in the animal. The results suggest that the regulation of peroxisomal enzymes and CYP4A1 is also associated in guinea pigs, and PenCB provides a similar effect of peroxisomal proliferators to the animal. The possible toxicity through the peroxisomal alteration was discussed.

Original languageEnglish
Pages (from-to)144-152
Number of pages9
JournalFukuoka Acta Medica
Volume86
Issue number5
Publication statusPublished - May 1995
Externally publishedYes

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Polychlorinated Biphenyls
Guinea Pigs
Liver
Enzymes
Peroxisomes
Fatty Acids
Urate Oxidase
Peroxisome Proliferators
Hydroxylation
Hyperlipidemias
Lipid Metabolism
Catalase
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

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Alteration of peroxisomal enzyme activities in the liver of guinea pigs caused by coplanar PCB. / Iwasaki, M.; Kato, H.; Ariyoshi, N.; Oguri, K.

In: Fukuoka Acta Medica, Vol. 86, No. 5, 05.1995, p. 144-152.

Research output: Contribution to journalArticle

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