Skin tumor promotion by Vitamin E in mice: amplification by ionizing radiation and Vitamin C

Cancer Detect Prev. 2003;27(2):102-8. doi: 10.1016/s0361-090x(03)00028-x.

Abstract

We have shown previously that Vitamin E acts as a tumor promoter in 7,12-dimethylbenz(a)anthracene (DMBA) initiated mouse skin. We now show that high concentrations (80 micromol) of Vitamin E are required for promotion, and that 10-fold lower concentrations do not promote tumor formation. The same high concentration of the water-soluble anti-oxidant Vitamin C did not act as a tumor promoter, but did amplify the promoting effect of high, but not low, concentrations of Vitamin E. Oxidizing free radicals generated by beta-radiation exposure of the skin at the time of Vitamin E treatment also enhanced promotion by high (but not low) concentrations of Vitamin E. The results are consistent with a process whereby tumor promotion by the lipid-soluble Vitamin E occurs as a result of alpha-tocopherol acting as a free radical scavenger, with the formation and subsequent transfer of the alpha-tocopherol free radical center to the surrounding lipids, resulting in lipid oxidations.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 9,10-Dimethyl-1,2-benzanthracene / toxicity
  • Administration, Topical
  • Animals
  • Antioxidants / toxicity*
  • Ascorbic Acid / toxicity*
  • Beta Particles
  • Carcinogens / toxicity
  • Cocarcinogenesis*
  • Female
  • Free Radical Scavengers
  • Mice
  • Mice, Inbred SENCAR
  • Oxidation-Reduction
  • Radiation, Ionizing
  • Skin / drug effects*
  • Skin / radiation effects*
  • Skin Neoplasms / chemically induced*
  • Skin Neoplasms / drug therapy
  • Skin Neoplasms / pathology
  • Vitamin E / toxicity*

Substances

  • Antioxidants
  • Carcinogens
  • Free Radical Scavengers
  • Vitamin E
  • 9,10-Dimethyl-1,2-benzanthracene
  • Ascorbic Acid