Yokota K, Singh U, Shinozuka H
Department of Pathology, University of Pittsburgh School of Medicine, PA 15261.
Jpn J Cancer Res. 1990 Feb;81(2):129-34. doi: 10.1111/j.1349-7006.1990.tb02538.x.
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.
我们以胎盘型谷胱甘肽S-转移酶(GST-P)作为致癌物引发的肝细胞标志物,研究了胆碱缺乏(CD)饮食和致癌性降血脂药物BR931如何改变单个GST-P阳性肝细胞群体。喂食CS或基础饮食的雄性Fischer大鼠(6 - 7周龄)肝脏中大多是单个或双个GST-P阳性肝细胞。喂食CD饮食2 - 4周导致两个和三个GST-P阳性肝细胞聚集体数量增加。到8 - 12周时,出现了由20多个肝细胞组成的离散的GST-P阳性肝细胞灶。与喂食基础饮食相比,喂食BR931饮食4 - 8周导致肝脏中单个GST-P阳性肝细胞数量无显著变化。研究表明,维持商业饮食的相对年轻大鼠肝脏中的单个GST-P阳性肝细胞可能代表内源性引发的细胞。CD饮食促进内源性引发的细胞形成更大的GST-P阳性细胞聚集体或病灶。