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IMMUNOHISTOCHEMICAL ANALYSIS OF DICHLOROACETIC ACID (DCA)-INDUCED HEPATOCARCINOGENESIS IN MALE FISCHER (F344) RATS
Citation:
Richmond, R., J. Carter, H. Carter, F. Daniel, AND A.B. DeAngelo. IMMUNOHISTOCHEMICAL ANALYSIS OF DICHLOROACETIC ACID (DCA)-INDUCED HEPATOCARCINOGENESIS IN MALE FISCHER (F344) RATS. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-95/388, 1995.
Description:
Treatment of male B6C3F1 mice with DCA induced hepatoproliferative lesions (HP) including; hyperplastic nodules (HN), adenomas (HA), and carcinomas (HC). ur previous studies have suggested that HN are the putative preneoplastic lesions. ere, we studied DCA-induced liver tumors in F344 rats treated with 0. 05, 0.5 and 2.4 g/l DCA in the drinking water. o assess the sequence of HP lesions, immunohistochemical methods were used to detect six markers, the oncoproteins, p21 ras, p39 c-jun, and p55 c-fos, as well as tumor associated aldehyde dehydrogenase, alpha fetoprotein, and glutathione s-transferase (GST-p). arker expression was examined in formalin-fixed sections of normal liver and HP lesions from rats killed at 15, 30, 45, 60 and 104 weeks. igh incidence of (GST-p)+ altered hepatic foci (AF) occurred in control and DCA treated rats. here were no significant differences between the number of AF/cmz suggesting that AF incidence was not increased by DCA treatment. F did not express any of the other five markers. N, HA, and HC which did not stain for GST-P expressed the other markers. ur data support the concept that AF might not be related to the development of HN, HA, or HC in the rat consistent with observations in the mouse and suggest a similarity between the two.