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An Overview of Peroxisome Proliferator-Induced Hepatocarcinogenesis

M. Sambasiva Rao and Janardan K. Reddy
Environmental Health Perspectives
Vol. 93 (Jun., 1991), pp. 205-209
DOI: 10.2307/3431190
Stable URL: http://www.jstor.org/stable/3431190
Page Count: 5
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An Overview of Peroxisome Proliferator-Induced Hepatocarcinogenesis
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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 H2 O2 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.

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