| Objective: Tabacco smoke and residential radon are the first and second leading cause of lung cancer in the world. This paper is to study the redox damage of lung ang blood in rats inhaled radon and tabacco smoke.Methods: Male Wistar rats were exposed to radon and its progeny with the cumulative dose up to 27, 52, 105 working level month(WLM) , as well as radon and smoke to either alone or jointly. The change of intracellular ROS content in BALF (Bronchoalveolar lavage fluid) cell and PBMC (Peripheral blood mononuclear cell) were investigated in rats inhaled radon. The lever of SOD (superoxide dismutase ) and MDA(malondialdehyde) in blood and lung tissue were also measured. The express of Nuclear factor-κBp65 (NF-κBp65) in lung tissures and bronchial epithelial cells in rats were tested with immunohistochemistry method.Results: The lever of SOD in blood and lung tissues significantly decreased and the lever of MDA increased. The content of intracellular ROS in BALF cell and PBMC also increased remarkably. There was no difference between the rats inhaled radon of 105wlm and 35% tabacco smoke. The express of Nuclear factor-κBp65 (NF-κBp65) in lung tissue and bronchial epithelial cells were also elevated. The results indicate that combined exposure of rats to radon and tobacco smoke can disturb the redox balance more seriousely than the exposures alone.The activation of NF-κBp65 and ROS may be related to the adverse effects.Conclusion:The inhalation of radon and its progeny can disturb the redox balance in rats in a dose-response manner. SOD and MDA can be used as early biomarkers of low dose radon exposure. The blood SOD in lung tissures may be a indicative index of the redox damage.
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