【摘 要】
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OBJECTIVE To investigate the cellular pathways or proteins involved in DNA damage repair induced by low concentration formaldehyde in human bronchial epithelial (HBE) cells.METHODS The cell counting K
【机 构】
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Key Laboratory of Chemical Safety and Health, National Institute for Occupational Health and Poison
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OBJECTIVE To investigate the cellular pathways or proteins involved in DNA damage repair induced by low concentration formaldehyde in human bronchial epithelial (HBE) cells.METHODS The cell counting Kit-8 was used to measure the cytotoxic effects of formaldehyde on HBE cells.An alkaline COMET assay was conducted to test DNA damage by formaldehyde.The protein expression level was assessed by Western Blot.We used RNA interference cell to test the role of ATM in formaldehydeinduced DNA damage repair and NBS1 and p-p53 expression.RESULTS In the results, we found that the formaldehyde could induce the single-strand breaks (SSBs) in low concentration of 5 μmol· L-1.Interestingly, the SSB is accompanied with increased expression of ataxia telangiectasia mutated (ATM),Nbs1 and p-p53.In addition, formaldehyde-induced SSBs were quickly repaired in ATM siRNA depleted cells, demonstrating that ATM is not required for efficient completion of SSBs.Moreover, consistent with knocking down of ATM, expressions of Nbs1 were significantly decreased, and p-p53 expression was showed a slight decrease.Formaldehyde was also found to trigger up-regulation of poly(ADP-ribose)polymerase (PARP).Furthermore, pretreatment of cells with PJ34, a specific PARP-1inhibitor, we found a high level of DNA damage and delayed repair in PARP-1 inhibited cells, as reflected by a significant increase of the three COMET parameters compared with controls.CONCLUSION In summary, our results indicate that low concentration FA-induced DNA damage repair may be through PARP-1 pathway, but not ATM pathway.These findings will help us to understand the signal transduction mechanisms involved in the carcinogenic effects of FA at DNA damage repair level.
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