Physiological concentrations of (-)-epigallocatechin-3-O-gallate (EGCg) prevent chromosomal damage induced by reactive oxygen species in WIL2-NS cells.

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 micromol/L. This damage was due to the production of H(2)O(2) by EGCg. In contrast, EGCg at < 10 micromol/L did not induce chromosomal damage and did not produce H(2)O(2). In addition, EGCg at < 10 micromol/L dose-dependently prevented chromosomal damage induced by H(2)O(2), 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 micromol/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 H(2)O(2) were detected. These findings suggest that physiological concentrations of EGCg (< 1 micromol/L) are not genotoxic but rather, can prevent ROS-induced chromosomal damage.