Numerous preclinical studies have shown that the
naturally-occurring polyphenol resveratrol may
produce health-beneficial effects in a variety of
disorders, including cancer, diabetes, Alzheimer, and
cardiovascular diseases. Resveratrol has entered
clinical trials for the prevention and treatment of
several of these disorders. This polyphenol is also
available in the market as a dietary supplement.
Experimental data have shown, however, that
resveratrol induces DNA damage in a variety of cells.
Here we review such evidence and evaluate the
cytotoxicity of resveratrol (MTT assay) in cells deficient
in several major DNA repair pathways (i.e.,
homologous recombination, non-homologous end
joining, base excision repair, nucleotide excision repair,
mismatch repair, and Fanconi anemia repair). Cells
deficient in base excision repair (EM9), nucleotide
excision repair (UV4 and UV5) and Fanconi Anemia
(KO40) were slightly hypersensitive to
resveratrol-induced cytotoxicity with respect to their
parental cells (AA8). Our results suggest that these
pathways may participate in the repair of the DNA
damage induced by resveratrol and that deficiencies in
these pathways may confer hypersensitivity to the
genotoxic activity of this dietary constituen