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dependent cytotoxicity, and the cytotoxic eect was signicantly decreased by co-treatment withN-acetylcystein (NAC), an antioxidant,suggesting involvement of oxidative stress in cell death caused by UDMA. The preventive eects of NAC were also observed in UDMA-induced apoptosis in RPC-C2A pulp like cell line. A fragmented DNA ladder pattern, characteristic of apoptosis, was shown by treat-ment with UDMA, but NAC blocked the DNA fragmentation. The preventive eects of NAC on apoptosis were also conrmed byBy applying the same analysis, AH26, a resin-based root canal sealer, was found to cause oxidative stress and apoptosis. NAC low-ered cytotoxicity and DNA fragmentation of AH26, suggesting that oxidative stress is involved in apoptotic cell death caused by AH26.