Inhibition of the prenatal dimethylbenz[a]anthracene-induced tumour initiation in mice by prior administration of 7,8-benzoflavone

Carcinogenesis. 1986 Jul;7(7):1187-9. doi: 10.1093/carcin/7.7.1187.

Abstract

7,8-Benzoflavone (BF) was applied orally via stomach tube in doses of 50, 100, 200 and 400 mg/kg body weight to pregnant NMRI mice on the 18th day of gestation. BF application was followed 1 h later by oral administration of 60 mg/kg body weight dimethylbenz[a]anthracene (DMBA). As a rule this dose of DMBA does not lead to prenatal secondary effects and is not carcinogenic to either the mother animals or the F1 generation. Subsequent promotion of the F1 generation with the tumour promoter 12-O-tetradecanoylphorbol-13-acetate over a period of 12 weeks resulted in a high yield of skin papillomas and lung adenomas when no BF had been applied. With prior application of BF, the tumour yield could be significantly reduced.

MeSH terms

  • 9,10-Dimethyl-1,2-benzanthracene / antagonists & inhibitors*
  • Adenoma / chemically induced
  • Administration, Oral
  • Animals
  • Benzoflavones / pharmacology*
  • Cocarcinogenesis
  • Female
  • Flavonoids / pharmacology*
  • Lung Neoplasms / chemically induced
  • Mice
  • Neoplasms, Experimental / chemically induced*
  • Papilloma / chemically induced
  • Pregnancy
  • Prenatal Exposure Delayed Effects*
  • Skin Neoplasms / chemically induced
  • Tetradecanoylphorbol Acetate

Substances

  • Benzoflavones
  • Flavonoids
  • 9,10-Dimethyl-1,2-benzanthracene
  • alpha-naphthoflavone
  • Tetradecanoylphorbol Acetate