Résumé
AIM To explore the molecular mechanism of hydroquinone genotoxicity in human bronchial epithelial cells and investigate whether human X-ray repair cross complementing group 1 (XRCC1)was involved in protecting cells from the damage caused by hydroquinone. METHODS XRCC1 gene was knocked down by RNA interference and XRCC1-deficient cell was established by transfected recombinant plasmid pEGFP-C1-pU6-dsRNA. Normal human bronchial epithelial cells (normal cells) and cells transfected with the empty vector of pEGFP-C1 (vector cells) were used as the normal control and vector control. All cells were treated with different concentrations of hydroquinone (10-100 μmol·L-1) for 4 h. MTT assay was used to test cell viability and comet assay was used to detect the DNA damage and repairment. RESULTS MTT assay showed that hydroquinone inhibited the growth of cells in a concentration-dependant manner and the survival number of XRCC1-deficient cell was less than that of the two control groups. Comet assay revealed that different concentrations of hydroquinone caused more severe DNA damage in XRCC1-deficient cell line than in control cells and there were no significant difference in the two control groups. CONCLUSION The results suggest XRCC1 be involved in preventing cells from damage caused by hydroquinone.