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Department of Food Science Research for Health, National Institute of Health and Nutrition, Tokyo, 162-8636, Japan
1To whom correspondence should be addressed. E-mail: umegaki{at}nih.go.jp.
We investigated the effects of (-)-epigallocatechin-3-O-gallate (EGCg) on chromosomal damage, which was evaluated by a cytokinesis-block micronucleus (CBMN) assay using WIL2-NS cells. EGCg itself induced chromosomal damage at 100 µmol/L. This damage was due to the production of H2O2 by EGCg. In contrast, EGCg at < 10 µmol/L did not induce chromosomal damage and did not produce H2O2. In addition, EGCg at < 10 µmol/L dose-dependently prevented chromosomal damage induced by H2O2, tert-butyl hydroperoxide (tert-BuOOH) and superoxide, all of which are reactive oxygen species (ROS). A large amount of EGCg was present in cells after they were incubated with 0.3 µmol/L EGCg. When extracellular EGCg was removed and EGCg was present only inside of cells, the preventive effect of EGCg against tert-BuOOH-induced chromosomal damage was diminished but not that against the other two ROS tested. Direct interactions of EGCg with tert-BuOOH and superoxide but not with H2O2 were detected. These findings suggest that physiological concentrations of EGCg (< 1 µmol/L) are not genotoxic but rather, can prevent ROS-induced chromosomal damage.
KEY WORDS: EGCg reactive oxygen species WIL2-NS cells chromosomal damage oxidative stress
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