Prevention by 1'-acetoxychavicol acetate of the induction but not growth of putative preneoplastic, glutathione S-transferase placental form-positive, focal lesions in the livers of rats fed a choline-deficient, L-amino acid-defined diet

• Published in: Carcinogenesis (New York) 1998-10, Vol.19 (10), p.1809-1814
• Main Authors: KOBAYASHI, Y, NAKAE, D, OHIGASHI, H, KONISHI, Y, AKAI, H, KISHIDA, H, OKAJIMA, E, KITAYAMA, W, DENDA, A, TSUJIUCHI, T, MURAKAMI, A, KOSHIMIZU, K
• Format: Article
• Language: English
• Subjects: Amino Acids - administration & dosage; Animals; Anticarcinogenic Agents - pharmacology; Benzyl Alcohols; Biological and medical sciences; Carcinogenesis, carcinogens and anticarcinogens; Carcinogens - pharmacology; Chemical agents; Choline - administration & dosage; Diet; Diethylnitrosamine - pharmacology; Glutathione Transferase - metabolism; Liver Neoplasms, Experimental - enzymology; Liver Neoplasms, Experimental - pathology; Liver Neoplasms, Experimental - prevention & control; Male; Medical sciences; Placenta - enzymology; Precancerous Conditions - enzymology; Precancerous Conditions - pathology; Precancerous Conditions - prevention & control; Rats; Rats, Inbred F344; Terpenes - pharmacology; Tumors
• ISSN: 0143-3334; 1460-2180; 1460-2180
• DOI: 10.1093/carcin/19.10.1809

The effects of 1'-acetoxychavicol acetate (ACA) on endogenous rat liver carcinogenesis because of chronic feeding of a choline-deficient, L-amino acid-defined (CDAA) diet were examined. Male Fischer 344 rats, 6 weeks old, received the CDAA diet containing ACA at doses of 0, 0.005, 0.010 and 0.050% for 12 weeks and were then killed. ACA decreased the numbers of putative preneoplastic, glutathione S-transferase placental form (GST-P)-positive, focal lesions developing in the livers of rats fed the CDAA diet but did not alter their sizes. At the same time, ACA reduced the levels of 8-hydroxyguanine, a parameter of oxidative DNA damage, but did not significantly affect generation of 2-thiobarbituric acid-reacting substances, indicators of oxidative extra-DNA damage, or hepatocyte proliferation. Furthermore, ACA did not exert any significant effects on the numbers or sizes of GST-P-positive lesions in the livers of rats when administered between weeks 2 and 8 after initiation with a single i.p. dose of 200 mg/kg body wt of N-nitrosodiethylamine. These results indicate that ACA prevents the CDAA diet-associated induction of putative preneoplastic lesions by reduction of oxidative DNA damage but does not affect their subsequent growth.