论文部分内容阅读
目的研究人支气管上皮细胞(16HBE)对甲基丙烯酸环氧丙酯(GMA)所致遗传损伤的修复效应。方法 1~16μg/ml浓度范围的GMA染毒一个细胞周期(24 h),于染毒结束时、继续恢复一个细胞周期后利用胞质阻滞微核试验观察细胞遗传损伤效应及恢复情况。结果两种处理方式的双核细胞微核率(MNi)均随染毒浓度增加逐渐升高,存在剂量-效应关系(r=0.873~0.927,P<0.01)。染毒恢复组MNi曲线表现出低剂量平缓而高剂量加速升高的趋势并与染毒组曲线交叉。两种处理方式的双核细胞核桥率(NPBs)和双核细胞核芽率(NBUDs)随剂量变化的改变不明显,但染毒恢复组1、4、16μg/ml剂量的NPBs显著高于同剂量染毒组,差异有统计学意义(P<0.05),1、16μg/ml剂量的NBUDs则显著低于同剂量的染毒组,差异有统计学意义(P<0.05)。结论 GMA染毒可致明显的细胞遗传损伤,但随即启动的损伤修复机制使得遗传毒性的表现趋于减弱,细胞修复机制的及时启动在维持遗传稳定性方面发挥了关键作用。
Objective To investigate the repair effect of human bronchial epithelial cells (16HBE) on genetic damage induced by glycidyl methacrylate (GMA). Methods One cell cycle (24 h) was treated with GMA in the concentration range of 1 ~ 16μg / ml. After the cell cycle was resumed, the effects of cytogenetic damage and recovery were observed by cytosolic blockade micronucleus test. Results The micronucleus rate (MNi) of binucleated cells in both treatments increased gradually with the increase of the concentration, and there was a dose-response relationship (r = 0.873-0.927, P <0.01). MNi curve of exposure group showed a tendency of low dose and moderate dose but accelerated and crossed with that of exposure group. NPBs and NBUDs of the two treatments did not change with dose, but NPBs of 1, 4, and 16μg / ml in the recovery group were significantly higher than those of the same dose Group, the difference was statistically significant (P <0.05), 1,16μg / ml dose of NBUDs was significantly lower than the same dose of exposure group, the difference was statistically significant (P <0.05). Conclusions GMA exposure can cause obvious cytogenetic damage, however, the immediate repair mechanism of injury leads to the decrease of genotoxicity. The timely initiation of cell repair mechanism plays a key role in maintaining genetic stability.