FIGURE 6.

ROS contributed to sevoflurane-induced DNA damage in neuronal cells. (A) Fluorescence intensity using DCFH-DA showed that ROS was excessively generated in SH-SY5Y cells, HT22 cells, and hippocampal neurons when exposed to 4 and 8% sevoflurane for 12 h. Pretreatment of antioxidant NAC at 5 mmol/L significantly inhibited sevoflurane-induced overproduction of intracellular ROS. (B–G) Western blotting and quantitative analysis showed that 4 and 8% sevoflurane for 12 h significantly upregulated the levels of protein 8-OHdG, γH2AX, and p-ATM in SH-SY5Y cells, HT22 cells, and hippocampal neurons, which were markedly attenuated by pretreatment of NAC. Compared with the control group, ^∗∗p < 0.01; Compared with sevoflurane group, pretreatment of NAC prior to sevoflurane exposure significantly decreased the ratio of 8-OHdG, γH2AX, and p-ATM to histone (p < 0.01). Data are represented as mean ± SD from five independent experiments.