Abstract
Using the placental form of glutathione S‐transferase (GST‐P) as a marker of carcinogen‐initiated hepatocytes, we investigated how a choline‐deficient (CD) diet and BR931, a carcinogenic hypolipidemic agent, modify populations of single GST‐P‐positive hepatocytes. The liver of male Fischer rats (6‐7 weeks old) fed a CS or basal diet contained mostly single or double GST‐P‐positive hepatocytes. Feeding a CD diet for 2–4 weeks led to increases in the number of aggregates of two and three GST‐P‐positive hepatocytes. By 8–12 weeks, there was an emergence of discrete foci of GST‐P‐positive hepatocytes consisting of more than 20 hepatocytes. Feeding a BR931 diet for 4–8 weeks resulted in no significant change in the number of single GST‐P‐positive hepatocytes in the liver as compared to feeding a basal diet. It is suggested that single GST‐P‐positive hepatocytes in the liver of relatively young rats maintained on a commercial diet may represent endogenously initiated cells. A CD diet promotes endogenously initiated cells to form larger aggregates or foci of GST‐P‐positive cells.
Keywords: Choline deficiency, Hypolipidemic agent, Liver carcinogenesis, GST‐P‐positive cells
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