An overview of peroxisome proliferator-induced hepatocarcinogenesis

M. S. Rao, J. K. Reddy

Research output: Contribution to journalArticlepeer-review

103 Scopus citations

Abstract

Peroxisome proliferators are hepatocarcinogens in rats and mice. Chronic administration of these compounds results in the development of altered areas and neoplastic nodules followed by hepatocellular carcinomas. All three types of hepatic lesions do not express γ-glutamyltranspeptidase, glutathione s-transferase-P, and α-fetoprotein and are resistant to iron accumulation after overload. The mechanism by which nongenotoxic peroxisome proliferators induce hepatic tumors is not well understood. It has been proposed that with continuous administration of peroxisome proliferators, liver cells are subjected to persistent oxidative stress resulting from marked proliferation of peroxisomes and a differential increase in the levels of H2O2 producing (20- to 30-fold) and degrading (2-fold) enzymes. Free oxygen radicals lead to DNA damage (both directly and through lipid peroxidation) and thus may cause initiation and promotion of the carcinogenic process.

Original languageEnglish (US)
Pages (from-to)205-209
Number of pages5
JournalEnvironmental health perspectives
Volume93
DOIs
StatePublished - 1991

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Health, Toxicology and Mutagenesis

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