Journal Article

Decreased connexin32 and a characteristic enzyme phenotype in clofibrate-induced preneoplastic lesions not shared with spontaneously occurring lesions in the rat liver

Hiroyuki Tsuda, Makoto Asamoto, Yoshio Iwahori, Takaaki Hori, Tomonori Ota, Hiroyasu Baba-Toriyama, Nobuaki Uehara, Dae Joong Kim, Vladimir A. Krutovskikh, Nobuo Takasuka, Takayuki Tsuchiya, Mamoru Mutai, Masae Tatematsu and Hiroshi Yamasaki

in Carcinogenesis

Volume 17, issue 11, pages 2441-2448
Published in print November 1996 | ISSN: 0143-3334
Published online November 1996 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.11.2441
Decreased connexin32 and a characteristic enzyme phenotype in
                    clofibrate-induced preneoplastic lesions not shared with spontaneously occurring
                    lesions in the rat liver

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Two different types of focal preneoplastic lesions, tentatively named Type I and II lesions, were recognized in the liver of rats chronically treated with clofibrate for 104 weeks. Type I lesions were characterized by mostly negative glucose-6-phosphate dehydrogenase (G6PD) activity (6 out of 10, 60%) and positive expression of succinate dehydrogenase (10 out of 10, 100%), in addition to the previously documented complete lack of expression of glutathione S-transferase, placental form (GST-P) and γ-glutamyl trans-peptidase (GGT). Furthermore, most importantly, Type I lesions exhibited a clear decrease in immunohistochemically demonstrated connexin32 (Cx32) spot counts on their hepatocyte membranes, similarly to nitrosamine-induced lesions. In contrast, Type II lesions, mostly small in size and positively expressing GST-P and/or GGT and G6PD, similarly to their previously reported nitrosamine-induced counterparts, did not exhibit a significant decrease in Cx32 count. In addition, spontaneously occurring lesions, again sharing the same enzyme phenotype, did not show a decrease in Cx32. The results indicate that: (i) a clear distinction between the two lesions, with Type I being involved in clofibrate-induced tumors and Type II being more likely to be spontaneous in nature; (ii) a decrease in Cx32 is closely linked to lesion development and possibly stage of progression, irrespective of the enzyme phenotype and the applied carcinogen; (iii) the unaltered condition of Cx32 may suggest a slow growing or non-progressive nature.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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