Objective To observe the impact of mitochondrial DNA partial knockout on the injury of human bronchial epithelial cells exposed to radon gas.
Methods Bronchial epithelial cells with (ρ-HBE cells) or without (ρ+HBE cells) mitochondrial DNA partial knockout were exposed to 20 000 Bq/m3 radon and radon daughters to observe the changes in cell proliferation, cell cycle, and intracellular reactive oxygen species (ROS) levels of cells at 10 passages (low-dose groups:ρ+HBE-Rn10 and ρ-HBE-Rn10) and 30 passages (high-dose groups:ρ+HBE-Rn30 and ρ-HBE-Rn30).
Results After radon exposure, the plating efficiency (PE) and the survival fraction (SF) of the ρ-HBE-Rn10 and ρ-HBE-Rn30 cells were higher than those of the ρ+HBE cells (P<0.05). PE and SF were lower in the ρ+HBE-Rn30 cells than the ρ+HBE-Rn10 cells (P<0.05), while higher in the ρ-HBE-Rn30 cells than the ρ-HBE-Rn10 cells (P<0.05). S phase decreased and G2/M phase of the ρ+HBE-Rn10 cells increased, while the ρ+HBE-Rn30 cells showed the opposite effects. The ROS levels were increased in all exposure groups.
Conclusion Compared to the ρ+HBE cells, the ρ-HBE cells have a significant change in cell proliferation, cell cycle, and intracellular ROS generation after radon exposure, indicating that the radon induced cell injury is associated with mitochondrial structure and impairment.
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