The aim of the present study was to evaluate the protective effect of (+)-
catechin and (-)-
epicatechin against 2-amino-3,8- dimethylimidazo[4,5-f]
quinoxaline (8-MeIQx), 2-amino-3,4,8-trimethylimidazo[4,5-f]-
quinoxaline (4,8-diMeIQx) and 2-amino-1-methyl-6-phenyl-imidazo[4,5-
b]pyridine (
PhIP)-induced DNA damage in human
hepatoma cells (HepG2). DNA damage (strand breaks and oxidized
purines/
pyrimidines) was evaluated by the alkaline single-cell gel electrophoresis or comet assay. Increasing concentrations of 8-MeIQx,
4,8-diMeIQx and
PhIP induced a significant increase in
DNA strand breaks and oxidized
purines and
pyrimidines in a dose-dependent manner. Among those,
PhIP (300 µm) exerted the highest genotoxicity. (+)-
Catechin exerted protection against oxidized
purines induced by 8-MeIQx,
4,8-diMeIQx and
PhIP. Oxidized
pyrimidines and
DNA strand breaks induced by
PhIP were also prevented by (+)-
catechin. Otherwise, (-)-
epicatechin protected against the oxidized
pyrimidines induced by
PhIP and the oxidized
purines induced by 8-MeIQx and
4,8-diMeIQx. One feasible mechanism by which (+)-
catechin and (-)-
epicatechin exert their protective effect towards heterocyclic
amines-induced oxidative DNA damage may be by modulation of phase I and II
enzyme activities. The
ethoxyresorufin O-deethylation (
CYP1A1) activity was moderately inhibited by (+)-
catechin, while little effect was observed by (-)-
epicatechin. However, (+)-
catechin showed the greatest increase in
UDP-
glucuronyltransferase activity. In conclusion, our results clearly indicate that (+)-
catechin was more efficient than (-)-
epicatechin in preventing DNA damage (strand breaks and oxidized
purines/
pyrimidines) induced by
PhIP than that induced by 8-MeIQx and
4,8-diMeIQx.