Abstract: OBJECTIVE: To study the effects of N-acetyl cysteine (NAC) on the oxidative DNA damage and cell survival rate of malignant BERP35T-1 cells exposed to α-particles. METHODS：Western blot was used for the detection of protein expression of γH2AX in the human bronchial epithelial cell lines BEP2D，RH22 and BERP35T-1， and BERP35T-1 treated with 0-2 mmol/L NAC for 48 h. Immunocytochemistry was used to compare the different expression levels of 8-OH-dG in BERP35T-1 treated with 1 mmol/L NAC for 0-48 h. Using DCHF-DA， the generation of active oxygen radicals (ROS) in BERP35T-1 treated with 1 mmol/L NAC for 48 h was monitored by flow cytometry. MTT assay was used to examine the cell survival rate of BERP35T-1 cells treated with 1 mmol/L NAC for 48 h and/or 2 Gy γ-rays. RESULTS：Compared to BEP2D cells， increased level of γH2AX was detected in RH22 and BERP35T-1 cells (P<0.01). The protein expression of γH2AX in BERP35T-1 was higher than in RH22 cells (P<0.01). After treatment with 1-2 mmol/L NAC for 48 h， the expression level of γH2AX in BERP35T-1 was significantly decreased (P<0.01). Decreased expression of 8-OH-dG was seen in BERP35T-1 treated with 1 mmol/L NAC for 24-48 h (P<0.05 or P<0.01). After treatment by 1 mmol/L NAC for 48 h， the basal level of ROS in BERP35T-1 decreased (P<0.05). In addition，the cell survival rate of BERP35T-1 treated with NAC was reduced (P<0.01). Meanwhile， compared to BERP35T-1 treatment with γ-rays alone， increased cell survival rate was detected in BERP35T-1 when treated with γ-rays combined with NAC (P<0.05). CONCLUSION：NAC， as an antioxidant， could up-regulate the antioxidant ability of BERP35T-1， resulting in decreased ROS level and oxidative DNA damage and increased genomic stability to partially reverse the malignant phenotype of BERP35T-1，such as inhibiting the malignant proliferation，and reducing its radiosensitivity．

Key words: N-acetyl cysteine, α-particle, lung cancer, oxidative damage, cell survival rate