Modulatory effect of soy isoflavones on biochemical alterations mediated by TPA in mouse skin model

Food Chem Toxicol. 2004 Oct;42(10):1669-75. doi: 10.1016/j.fct.2004.06.003.


Exposure to various carcinogenic agents along with other contributing factors increase the risk of cancer formation. The current study assesses the effect of soy isoflavones on the biochemical events associated with tumor promotion in mouse skin. 12-O-tetradecanoyl phorbol-13-acetate (TPA), a well-known tumor promoter on topical application depletes the reduced glutathione content (GSH) and down regulates the activities of its metabolizing enzyme, glutathione-S-transferase (GST) and the activities of antioxidant enzymes. However, the ornithine decarboxylase (ODC) activity and unscheduled DNA synthesis are elevated on single topical application of TPA to the dorsal cutaneous portions of the mice. Topical applications of soy isoflavones, half-an-hour prior to the application of TPA prevented the induction of ODC activity and DNA synthesis mediated by TPA (p < 0.01). The content of GSH, GST and antioxidant enzymes (p < 0.05) was also recovered significantly by soy isoflavones in a dose dependent manner. Parallel to these effects, pretreatment with the soy isoflavones also reduced hydrogen peroxide (H2O2) content (p < 0.05) at 1.0 and 2.0 microg/0.2 ml vehicle/animal. Therefore, we conclude that soy isoflavones are potentially protective against TPA induced biochemical alterations.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anticarcinogenic Agents*
  • Antioxidants / metabolism
  • Biomarkers, Tumor
  • Carcinogens / toxicity*
  • Catalase / metabolism
  • DNA / biosynthesis
  • Dose-Response Relationship, Drug
  • Female
  • Glutathione / metabolism
  • Glutathione Peroxidase / metabolism
  • Glutathione Transferase / metabolism
  • Hydrogen Peroxide / metabolism
  • Isoflavones / pharmacology*
  • Lipid Peroxidation / drug effects
  • Mice
  • Ornithine Decarboxylase / metabolism
  • Oxidation-Reduction
  • Skin Neoplasms / chemically induced*
  • Skin Neoplasms / prevention & control*
  • Soybeans / chemistry*
  • Tetradecanoylphorbol Acetate / antagonists & inhibitors*
  • Tetradecanoylphorbol Acetate / toxicity*
  • Thymidine / metabolism


  • Anticarcinogenic Agents
  • Antioxidants
  • Biomarkers, Tumor
  • Carcinogens
  • Isoflavones
  • DNA
  • Hydrogen Peroxide
  • Catalase
  • Glutathione Peroxidase
  • Glutathione Transferase
  • Ornithine Decarboxylase
  • Glutathione
  • Tetradecanoylphorbol Acetate
  • Thymidine