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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #173410
Title: EFFECTS OF CHRONIC ETHANOL FEEDING ON HEPATIC CELL PROLIFERATION, ERK ACTIVATION AND ALTERED HEPATIC FOCI FORMATION IN DIETHYLNITROSAMINE-INITIATED RATS

Author
item CHAVEZ, POLLYANNA - TUFTS/HNRCA
item Russell, Robert
item Mason, Joel
item Ordovas, Jose
item Wang, Xiang-Dong

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 11/3/2004
Publication Date: 4/1/2005
Citation: Chavez, P.R., Russell, R., Mason, J.B., Ordovas, J.M., Wang, X. 2005. Effects of chronic ethanol feeding on hepatic cell proliferation, ERK activation and altered hepatic foci formation in diethylnitrosamine-initiated rats [abstract]. Journal of Federation of American Societies for Experimental Biology. 19:A78.

Interpretive Summary:

Technical Abstract: The role of ethanol in the development of liver cancer independent of hepatitis infection, cirrhosis, or aflatoxin exposition is not well defined. The present study was carried out to determine the effect of long-term ethanol feeding (1, 6 and 10 months) on the hepatocarcinogenesis in a chemical carcinogen (diethylnitrosamine) initiated rat model. Results showed that ethanol feeding significantly decreased the number of altered hepatic foci (AHF) and the expression of Ki-67 in the livers of rats over a 10 months period, as compared with the non-ethanol fed rats. Further analysis of the levels of extracellular-regulated kinase (ERK), p53 and cyclin D1 showed that ethanol feeding for 6 months increased phosphorylated ERK, as well as phosphorylated p53 (serine 15), whereas it had no effect on total protein level of ERK and p53. Moreover, ethanol feeding decreased the protein levels of cyclin D1 in the livers of rats. Collectively, these data indicate that long-term ethanol feeding in this rat model arrest cell cycle progression, via activation of ERK signaling and decreases in cyclin D1 levels, which possibly allows for a repair mechanism to take place, thereby decreasing the number of AHF in the liver.