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영어

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging and also contributes to theirunfavorable effects in cultured cells and animal tissues. This study was conducted to investigate the effect of ionizingradiation (IR) on mtDNA deletion and the involvement of reactive oxygen species (ROS) in this process in human lungfibroblast (IMR-90) cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated with 137Cs -rays and theintracellular ROS level was determined by 2',7'-dichlorofluorescein diacetate (DCFH-DA) and mtDNA common deletion(4977bp) was detected by nested PCR. Old cells at PD 55 and H2O2-treated young cells were compared as the positivecontrol. IR increased the intracellular ROS level and mtDNA 4977 bp deletion in IMR-90 cells dose-dependently.Theincreases of ROS level and mtDNA deletion were also observed in old cells and H2O2-treated young cells. To confirmtheincreased ROS level is essential for mtDNA deletion in irradiated cells, the effects of N-acetylcysteine (NAC) on IR-induced ROS and mtDNA deletion were examined. 5 mM NAC significantly attenuated the IR-induced ROS increaseand mtDNA deletion. These results suggest that IR induces the mtDNA deletion and this process is mediated by ROS inIMR-90 cells.