Carcinogenesis, Vol 18, 1663-1668, Copyright © 1997 by Oxford University Press
GA Clawson, CM Benedict, MR Kelley and J Weisz
Rats were treated with low doses of the hepatocarcinogen thioacetamide.
Forty-eight hours following this treatment, microscopic foci of hepatic
injury were observed, which were surrounded by a peripheral rim of
histologically normal hepatocytes. These peripheral hepatocytes generally
contained enlarged nuclei, and showed nuclear staining for 4-
hydroxynonenal-protein adducts, indicative of nuclear oxidative damage. In
these same hepatocytes, we also observed specific focal nuclear induction
of mu-class glutathione-S-transferase and alcohol dehydrogenase I, two
enzymes which are important in metabolism of 4- hydroxynonenal. Of
particular interest was the concurrent nuclear induction of APE/ref-1, a
multifunctional DNA repair enzyme which can function as a redox factor, and
of the transcription factor Jun, whose DNA binding is facilitated by
APE/ref-1. These results document an orchestrated focal nuclear response to
oxidative damage produced by thioacetamide administration, and may relate
to the permanent effects produced by this treatment.
ARTICLES
Focal nuclear hepatocyte response to oxidative damage following low dose thioacetamide intoxication
Department of Pathology, Biochemistry & Molecular Biology, The Pennsylvania State University School of Medicine, Milton S. Hershey Medical Centre, Hershey 17033, USA.
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