Different effects of genistein and resveratrol on oxidative DNA damage in vitro

William Win, Zhuoxiao Cao, Xingxiang Peng, Michael A. Trush, Yunbo Li

Research output: Contribution to journalArticlepeer-review

Abstract

Previous studies have demonstrated that phenolic compounds, including genistein (4′,5,7-trihydroxyisoflavone) and resveratrol (3,4′,5-trihydroxystilbene), are able to protect against carcinogenesis in animal models. This study was undertaken to examine the ability of genistein and resveratrol to inhibit reactive oxygen species (ROS)-mediated strand breaks in φX-174 plasmid DNA. H2O2/Cu(II) and hydroquinone/Cu(II) were used to cause oxidative DNA strand breaks in the plasmid DNA. We demonstrated that the presence of genistein at micromolar concentrations resulted in a marked inhibition of DNA strand breaks induced by either H2O2/Cu(II) or hydroquinone/Cu(II). Genistein neither affected the Cu(II)/Cu(I) redox cycle nor reacted with H2O2 suggest that genistein may directly scavenge the ROS that participate in the induction of DNA strand breaks. In contrast to the inhibitory effects of genistein, the presence of resveratrol at similar concentrations led to increased DNA strand breaks induced by H2O2/Cu(II). Further studies showed that in the presence of Cu(II), resveratrol, but not genistein was able to cause DNA strand breaks. Moreover, both Cu(II)/Cu(I) redox cycle and H2O2 were shown to be critically involved in resveratrol/copper-mediated DNA strand breaks. The above results indicate that despite their similar in vivo anticarcinogenic effects, genistein and resveratrol appear to exert different effects on oxidative DNA damage in vitro.

Original languageEnglish (US)
Pages (from-to)113-120
Number of pages8
JournalMutation Research - Genetic Toxicology and Environmental Mutagenesis
Volume513
Issue number1-2
DOIs
StatePublished - Jan 15 2001

Keywords

  • Copper
  • DNA strand breaks
  • Genistein
  • Hydrogen peroxide
  • Hydroquinone
  • Reactive oxygen species
  • Resveratrol

ASJC Scopus subject areas

  • Genetics
  • Health, Toxicology and Mutagenesis

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