Antioxidant properties of (-)-epicatechin-3-gallate and its inhibition of Cr(VI)-induced DNA damage and Cr(IV)- or TPA-stimulated NF-κB activation

Xianglin Shi, Jianping Ye, Stephen S. Leonard, Min Ding, Val Vallyathan, Vincent Castranova, Yon Rojanasakul, Zigang Dong

Research output: Contribution to journalArticlepeer-review

101 Scopus citations

Abstract

Electron spin resonance (ESR) spin trapping was utilized to investigate the scavenging effects on hydroxyl radicals (OH) and superoxide radicals (O2-) by (-)-epigallocatechin-3-gallate (EGCG), one of the major anticancer compounds in tea. The spin trap used was 5,5-dimethyl-pyrroline N-oxide (DMPO). The Fenton reaction (Fe2+ + H2O2 → Fe3+ + OH + OH-) was used as a source of OH radicals. EGCG efficiently scavenges OH radicals with reaction rate of 4.62 x 1011 M-1 sec-1, which is an order of magnitude higher than several well recognized antioxidants, such as ascorbate, glutathione and cysteine. It also scavenges O2-radicals as demonstrated by using xanthine and xanthine oxidase system as a source of O2- radicals. Through its antioxidant properties, EGCG exhibited a protective effect against DNA damage induced by Cr(VI). EGCG also inhibited activation of nuclear transcription factor NF-κB induced by Cr(IV) and 12-o- tetradecanoylphorbol-13-acetate (TPA). The present studies provide a mechanistic basis for the reported anticarcinogenic properties of EGCG and related tea products.

Original languageEnglish
Pages (from-to)125-132
Number of pages8
JournalMolecular and Cellular Biochemistry
Volume206
Issue number1-2
DOIs
StatePublished - 2000

Bibliographical note

Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.

Keywords

  • Antiooxidants
  • Cancer
  • Epigallocatechin- 3-gallate
  • Oxygen derived free radicals
  • Tea

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Fingerprint

Dive into the research topics of 'Antioxidant properties of (-)-epicatechin-3-gallate and its inhibition of Cr(VI)-induced DNA damage and Cr(IV)- or TPA-stimulated NF-κB activation'. Together they form a unique fingerprint.

Cite this