DNA damage in human pleural mesothelial cells and lung epithelial cells induced by exposure to carbon nanotubes

我们研究了单壁碳纳米管（SWCNT）和多壁碳纳米管（MWCNT）暴露于人胸膜间皮细胞的潜在风险。使用台盼蓝排斥试验测定CNT细胞毒性，使用碱性彗星试验检测DNA损伤。采用高效液相色谱电化学检测法测定DNA中8-OHdG的含量。通过免疫印迹分析估计细胞中碱基切除修复酶的表达。我们观察到细胞增殖的抑制作用和诱导的DNA损伤后，细胞暴露于纯化的碳纳米管悬浮在分散介质中。此外，碳纳米管处理24 h后，MeT-5A细胞中hOGG 1、hMTH 1和MYH相关的碱基切除酶的表达水平保持不变。CNT显著抑制人胸膜间皮细胞的细胞增殖并减少DNA损伤。我们的研究结果表明，CNT诱导的遗传毒性的机制是不同的暴露于活性氧，这导致氧化DNA修饰和8-OHdG的生产。需要进一步研究以表征CNT暴露后的特定DNA突变。

We investigated the potential risk of single-walled carbon nanotube(SWCNT) and multi-walled carbon nanotube(MWCNT) exposure in human pleural mesothelial cells. CNT cytotoxicity was determined using a trypan blue exclusion assay, and DNA damage was detected using an alkaline comet assay. The concentration of 8-oxodeoxyguanosine(8-OHdG) in DNA was measured using HPLC with electrochemical detection. The expression of base excision repair enzymes in the cell was estimated by immunoblot analysis. We observed inhibitory effects on cell proliferation and induction of DNA damage following exposure of cells to purified CNTs that were suspended in dispersion medium. However, accumulation of 8-OHdG in DNA was not found. In addition, the expression levels of base excision enzymes that are involved in hOGG1, hMTH1 and MYH in MeT-5A cells remained unchanged for 24 h after carbon nanotube exposure. CNTs significantly inhibit cell proliferation and decrease DNA damage in human pleural mesothelial cells. Our results indicate that the mechanism of CNT-induced genotoxicity is different from that of exposure to reactive oxygen species, which causes oxidative DNA modifications and 8-OHdG production. Further investigation is required to characterize the specific DNA mutations following CNT exposure.