The Effects of Antioxidants on Skin Tumor Initiation and Aryl Hydrocarbon Hydroxylase

Thomas J. Slags, William M. Bracken

Research output: Contribution to journalArticlepeer-review

206 Scopus citations

Abstract

Butylated hydroxytoluene, butylated hydroxyanisole, and vitamins C and E are effective inhibitors of 7, 12-dimethylbenz(a)anthracene tumor initiation in a two-stage system of tumorigenesis. These antioxidants did not significantly induce epidermal aryl hydrocarbon [benzo(a)pyrene]hydroxylase, nor did they have any effect when added directly to the in vitro aryl hydrocarbon [benzo(a)pyrene]hydroxylase assay. However, butylated hydroxytoluene and butylated hydroxyanisole, when applied topically to mice, inhibited the in vitro, epidermally mediated, covalent binding of radioactive benzo(a)pyrene and 7, 12-dimethylbenz(a)anthracene to DNA. When butylated hydroxytoluene and butylated hydroxyanisole were added in vitro, they did not inhibit the epidermally mediated covalent binding of the hydrocarbons to DNA. The inhibition of polycyclic hydrocarbon tumorigenesis by antioxidants may be related to the ability of antioxidants to prevent the in vivo activation of hydrocarbons to carcinogenic epoxides and/or other electrophilic intermediates or may be related to their ability to increase detoxification of the reactive intermediate that requires intact cells to be operational. In any event, the results suggest that the antioxidants have an indirect effect on the epidermal metabolizing system which leads to a decrease in covalent binding to DNA.

Original languageEnglish (US)
Pages (from-to)1631-1635
Number of pages5
JournalCancer Research
Volume37
Issue number6
StatePublished - Jun 1977
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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