Aspirin shares a short-term effect, inhibition of pyruvate kinase activity with tumor-promoting agents, but fails to promote rat liver carcinogenesis.
Since aspirin was found to cause a persistent decrease in pyruvate kinase activity, which is a prominent characteristic of the hepatic promoters, the effect of aspirin on hepatic tumorigenesis in the rat has been studied. Male Wistar rats were initiated with a diet containing 0.06% 3'-methyl-4-dimethylamino-azobenzene for 4 weeks. They were divided into 3 groups and each group was fed one of the following diets containing either 0, 0.5 or 1% aspirin. At the end of a 58-week experimental period, no differences were observed in the incidence of hepatic lesions and hepatocellular carcinomas among the groups. Thus, it was concluded that aspirin does not promote nor inhibit the postinitiation step of hepatic tumorigenesis in the rat.
Yanagi
S
S
Department of Biochemistry, Nara Medical College, Japan.
Yamashita
M
M
Hiasa
Y
Y
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D003043:Cocarcinogenesis; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced*; D008297:Male; D008749:Methyldimethylaminoazobenzene; D009929:Organ Size / Q000187:drug effects; D011770:Pyruvate Kinase / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D008749:Methyldimethylaminoazobenzene; D002784:Cholesterol; D011770:Pyruvate Kinase; D001241:Aspirin