Carcinogenesis · 1984 · 80 citations · 0 references
MedicinePharmacologyToxicologyCarcinogenesisNeoplasiaToxicologic PathologyCarcinogenicity AssessmentCarcinogenicity Of Dietary ExposuresHepatic ToxicityHepatocellular CarcinomaLiver CancerCarcinogenic Hepatic EffectsGamma-glutamyl TransferaseHepatic TumorsLiver NeoplasmsMechanisms Of CarcinogenicityNeoplastic DiseaseNitrosamine CarcinogenesisNitrosamine Exposure
Studies were made on the effects of butylated hydroxyanisole (BHA), ethoxyquin (EQ) and acetaminophen (AAP) on the induction of neoplastic lesions in the liver and kidney of rats initiated by N-ethyl-N-hydroxyethylnitrosamine (EHEN). The number and area of histochemical gamma-glutamyltranspeptidase-positive (gamma-GT+) foci per unit area of liver section in rats given BHA, EQ or AAP were significantly less than in rats given EHEN alone. Similarly, the number of hyperplastic nodules (HN) in groups given BHA or AAP and their area in groups given BHA, EQ or AAP were significantly less than in control groups. Induction of hepatocellular carcinoma (HCC) was also clearly inhibited by these three chemicals. No liver lesions were found in any animals given BHA, EQ or AAP orally without EHEN. In contrast, the incidence and quantitative values of preneoplastic lesions and renal cell adenoma were significantly increased in groups given BHA, EQ or AAP. The results clearly demonstrated that BHA, EQ and AAP inhibited the development of gamma-GT+ foci, HN and HCC, whereas they enhanced the appearance of preneoplastic and neoplastic lesions in the kidney.