Catechol is a genotoxic agent assumed to induce DNA damage via the oxidative pathway. Using the comet assay and the repair-specific
enzymes formamido
pyrimidine glycosylase (Fpg) and
endonuclease III (Endo III), we examined the ability of
catechol to induce DNA damage in extended-term cultures of human lymphocytes and mouse
lymphoma cells. Our results suggest that mouse
lymphoma cells are somewhat more sensitive towards
catechol-induced DNA damage than the extended-term cultures of human lymphocytes. At high concentrations, the
catechol-induced damage seemed to be independent of both Fpg and Endo III, possibly indicating a non-oxidative pathway for the DNA damage (involving, for example, a bulky adduct). The fact that Endo III, but not Fpg, enhanced the
DNA damaging effect of
catechol, suggests that this metabolite of
benzene either mediates oxidation of
pyrimidines rather than
purines, or that oxidised
purines are repaired more efficiently, at least in human lymphocytes. In the latter cells, low concentrations of
catechol were found to reduce the
DNA migration. Considering the role of Fpg and it's adduct specific detection of
8-oxoguanine, this suggests that a low concentration of
catechol has an antioxidative effect reducing the background levels of oxidized
purines.