Peroxisome proliferator-induced hepatocarcinogenesis: Histochemical analysis of ciprofibrate-induced preneoplastic and neoplastic lesions for γ-glutamyl transpeptidase activity

M. Sambasiva Rao, V. Subbarao, J. K. Reddy

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Previous studies revealed that putative preneoplastic and neoplastic lesions induced in the liver by Wy-14,643, a peroxisome proliferator, were γ-glutamyl transpeptidase (GGT) negative. For ascertainment as to whether phenotypes of foci and carcinomas induced by all peroxisome proliferators are similary GGT negative, altered areas (AAs), neoplastic nodules (NNs), and hepatocellular carcinomas (HCCs) induced in the livers of male F344 rats by chronic dietary administration of ciprofibrate (0.025% wt/wt in chow; CAS:52214-84-3) were analyzed histochemically for GGT activity. Eighty-nine percent of AAs, 91% of NNs, and 91% of HCCs were GGT negative. The GGT-negative property of these various hepatic preneoplastic and neoplastic lesions persisted at 8 weeks after the withdrawal of ciprofibrate treatment. The results of this study indicate that the absence of GGT activity is a common feature in hepatic lesions induced by structurally unrelated peroxisome proliferators and is not related to the drug toxicity. The proposal was made that peroxisome proliferators do not derepress the activity of the GGT gene during hepatocarcinogenesis in the rat.

Original languageEnglish (US)
Pages (from-to)951-956
Number of pages6
JournalJournal of the National Cancer Institute
Volume77
Issue number4
StatePublished - 1986

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Fingerprint

Dive into the research topics of 'Peroxisome proliferator-induced hepatocarcinogenesis: Histochemical analysis of ciprofibrate-induced preneoplastic and neoplastic lesions for γ-glutamyl transpeptidase activity'. Together they form a unique fingerprint.

Cite this