Lack of initiating activity of the peroxisome proliferator ciprofibrate in two-stage hepatocarcinogenesis.
The peroxisome proliferator ciprofibrate was examined for its ability to initiate hepatocarcinogenesis in rats. Ciprofibrate was fed in the diet at levels of 0%, 0.01% and 0.025% for 2 weeks in order to induce steady-state peroxisome proliferation. Rats were then subjected to partial hepatectomy and then maintained for 6 months on a basal diet or one containing 0.05% phenobarbital. Ciprofibrate treatment did not increase the number or volume of altered hepatic foci (putative preneoplastic lesions). However, ciprofibrate treatment increased liver weights in a dose-dependent manner in rats which did not receive phenobarbital. It is concluded that ciprofibrate-induced peroxisome proliferation is not sufficient to induce initiation, but that a permanent change is produced which results in an increased liver weight.
Glauert
H P
HP
Department of Nutrition and Food Science, Veteran's Administration Hospital, Lexington.
Clark
T D
TD
D000818:Animals; D002994:Clofibrate / Q000031:analogs & derivatives*; D002995:Clofibric Acid / Q000031:analogs & derivatives*; D003043:Cocarcinogenesis; D004032:Diet; D004305:Dose-Response Relationship, Drug; D005260:Female; D058607:Fibric Acids; D008099:Liver / Q000187:drug effects; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced*; D008830:Microbodies / Q000187:drug effects*; D009929:Organ Size / Q000187:drug effects; D010634:Phenobarbital; D051381:Rats; D011919:Rats, Inbred Strains
D058607:Fibric Acids; D002995:Clofibric Acid; C019304:ciprofibrate; D002994:Clofibrate; D010634:Phenobarbital