Sister-chromatid exchanges (SCEs) induced by
mitomycin C (MMC),
4-nitroquinoline-1-oxide (4NQO) or UV-light in cultured Chinese hamster ovary cells (CHO K-1 cells) were enhanced by
cinoxate (2-ethoxyethyl p-methoxycinnamate) or
methyl sinapate (methyl 3,5-dimethoxy 4-hydroxycinnamate). Both substances are
cinnamate derivatives and
cinoxate is commonly used as a cosmetic UV absorber.
Methyl sinapate also increased the frequency of cells with
chromosome aberrations in the CHO K-1 cells treated with MMC, 4NQO or UV. These increasing effects of
methyl sinapate were critical in the G1 phase of the cell cycle and the decline of the frequencies of UV-induced SCEs and
chromosome aberrations during liquid holding was not seen in the presence of
methyl sinapate. Both compounds were, however, ineffective in cells treated with X-rays. In cells from a normal human embryo and from a
xeroderma pigmentosum (XP) patient, MMC-induced SCEs were also increased by the post-treatment with
methyl sinapate. The SCE frequencies in UV-irradiated normal human cells were elevated by
methyl sinapate, but no SCE-enhancing effects were observed in UV-irradiated XP cells. Our results suggest that the test substances inhibit
DNA excision repair and that the increase in the amount of unrepaired DNA damage might cause the enhancement of induced SCEs and
chromosome aberrations.