Nelson R, Holian O
Department of Surgery, University of Illinois College of Medicine, Chicago 60680.
Anticancer Res. 1991 Jan-Feb;11(1):157-60.
The activity and subcellular distribution of Protein Kinase C (PKC) was determined in the colons of Sprague-Dawley rats that were fed either a low fat rat chow or rat chow supplemented with 17% corn oil (40% ingested calories as fat). Rats given the high fat diets were either given no carcinogen or treated prior to or subsequent to the initiation of the test diets with 1,2 dimethylhydrazine (DMH). Rats were sacrificed and PKC activity determined in the soluble and particulate fractions of the colonic tissue 13 weeks after the initiation of the diets or DMH treatment, which was before tumor induction. In addition several rats were maintained on their diets until colon tumor formation occurred and PKC activity determined in the colonic tumor and compared to age matched control colonic tissue. In the absence of DMH, fish oil and corn oil equally augmented PKC activity and decreased the ratio of soluble/particulate PKC. With DMH treatment, corn oil augmented PKC as above, but fish oil supplementation resulted in a pattern of PKC activity and distribution more typical of a low fat diet, particularly when fish oil supplementation preceded DMH treatment. PKC activity in DMH induced colonic carcinomas was markedly depressed regardless of the fat source in the diet, when compared to colonic tissue from a non-DMH treated age matched low fat control.
测定了喂食低脂大鼠饲料或添加17%玉米油(40%摄入热量来自脂肪)的大鼠饲料的斯普拉格-道利大鼠结肠中蛋白激酶C(PKC)的活性和亚细胞分布。给予高脂饮食的大鼠要么不给予致癌物,要么在开始试验饮食之前或之后用1,2-二甲基肼(DMH)处理。在饮食或DMH处理开始13周后(即在肿瘤诱导之前),处死大鼠并测定结肠组织可溶性和颗粒部分的PKC活性。此外,将几只大鼠维持在其饮食上,直到结肠肿瘤形成,并测定结肠肿瘤中的PKC活性,并与年龄匹配的对照结肠组织进行比较。在没有DMH的情况下,鱼油和玉米油同样增强了PKC活性并降低了可溶性/颗粒性PKC的比例。用DMH处理时,玉米油如上述增强了PKC活性,但补充鱼油导致PKC活性和分布模式更典型于低脂饮食,特别是当补充鱼油先于DMH处理时。与未用DMH处理的年龄匹配的低脂对照的结肠组织相比,无论饮食中的脂肪来源如何,DMH诱导的结肠癌中的PKC活性均明显降低。