Abstract: OBJECTIVE: To investigate the role of reactive oxygen species (ROS) in isoniazid (INH)-induced DNA damage in L-02 cells and the protection by quercetin. METHODS: L-02 cells were divided into several groups:blank control,INH (10 mmol/L),quercetin low dose (10 mmol/L INH +25 μmol/L quercetin) and high dose (10 mmol/L INH +50 μmol/L quercetin). After cells were treated for 24 hours,DNA damage was detected by using the Comet test;ROS generation and mitochondrial membrane potential were evaluated by application of fluorescent probes DCFH-DA and Rhodamine123. RESULTS: Compared with the blank control group,the percentages of tail DNA,tail length and tail moment (from the Comet assay) of the INH group were significantly increased (P<0.01). Compared with the INH group,the percentages of tail DNA,tail length and tail moment of the low and high dose quercetin groups were significantly reduced (P<0.05 and P<0.01,respectively). The levels of mitochondrial ROS in cells of the INH group were significantly increased over the blank control group (P<0.01);the levels of mitochondrial ROS in the low and high dose quercetin groups were significantly decreased than that of the INH group (P<0.05 and P<0.01,respectively). The mitochondrial membrane potential of the INH group was significantly lower than that of the blank control group (P<0.01). The mitochondrial membrane potential of the low and high dose quercetin groups were significantly higher than that of the INH group (P<0.05 and P<0.01,respectively). CONCLUSION: INH can induce DNA damage in the L-02 cells and the damage may involve ROS-mediated mitochondrial damage. Quercetin has a protective effect against the INH-induction of DNA damage and the effect may be related to its inhibition of ROS-mediated mitochondrial damage.

Key words: reactive oxygen species, isoniazid, quercetin, DNA damage, reactive oxygen species, isoniazid, quercetin, DNA damage