Clofibrate-induced neoplastic development in the rat liver is associated with decreased connexin 32 expression but not with a co-ordinated shift in expression of marker enzymes

Toxicology Letters
H TsudaH Yamasaki

Abstract

Altered enzyme phenotype and expression of connexin 32 (Cx32), a gap junction protein were studied during the development of rat liver tumors induced by the non-genotoxic carcinogen, clofibrate. (1) In contrast to previous findings for nitrosamine-induced lesions, preneoplastic enzyme-altered foci (EAF) and neoplastic nodules (NN) lacked any clear association with degree of altered enzyme expression because of an almost complete negativity for GST-P and GGT. (2) Immunohistochemically demonstrated Cx32 spots on the hepatocyte membranes showed a clear decrease in clofibrate-induced lesions. (3) Naturally occurring EAF demonstrating GST-P and/or GGT positivity did not show a significant decrease of Cx32 counts suggesting a reversible nature. Therefore, the Cx32 decrease appears closely linked to progression of hepatocarcinogenesis irrespective of the enzyme phenotype of neoplastic focal lesions and the carcinogens used for their induction.

References

Nov 1, 1991·Proceedings of the Society for Experimental Biology and Medicine·J E Klaunig
Oct 1, 1989·Journal of Cellular Biochemistry·D J FitzgeraldH Yamasaki
Apr 1, 1989·Proceedings of the National Academy of Sciences of the United States of America·J C SáezM V Bennett
May 1, 1987·Carcinogenesis·M S Rao, J K Reddy

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Citations

Jul 27, 2007·The Journal of Membrane Biology·Maria Lúcia Zaidan Dagli, Francisco Javier Hernandez-Blazquez
Jul 18, 2008·Histochemistry and Cell Biology·Takahiro GotowYasuo Uchiyama
Mar 3, 2004·Journal of Cellular Biochemistry·Magnus EdlundLeland W K Chung
Jul 29, 2009·Critical Reviews in Biochemistry and Molecular Biology·Mathieu VinkenVera Rogiers
Sep 27, 2000·American Journal of Physiology. Gastrointestinal and Liver Physiology·S Gupta Kerr

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