论文部分内容阅读
目的研究甲基丙烯酸环氧丙酯(GMA)对人支气管上皮细胞(16HBE)染毒早期的遗传损伤效应及去除暴露因素后的恢复效应。方法 1、2、4、8、16、32 mg/L质量浓度的GMA短时间(3 h)染毒16HBE(染毒组);另选细胞经上述染毒后,于染毒结束时继续恢复1个细胞周期(染毒恢复组),利用胞质阻滞微核试验观察细胞遗传损伤效应。结果 染毒组的双核细胞微核率(MN)和双核细胞核芽率(NBUD)随染毒剂量的增加逐渐升高,并存在剂量-效应关系(决定系数分别为0.887、0.558,P<0.01),剂量达8 mg/L时核分裂指数(NDI)降低;但双核细胞核质桥率随染毒剂量增加变化趋势不明显,没有明显的剂量-效应关系。染毒后染毒恢复组的MN在低剂量时变化不明显,剂量增加后才逐渐升高,但上升速度较慢;NDI随剂量变化不明显;NBUD在4、8 mg/L时甚至出现下降。结论 GMA在染毒早期即对细胞有明显的遗传损伤效应,但暴露因素去除后损伤有被修复的趋势,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 study the genetic damage effects of glycidyl methacrylate (GMA) on early human bronchial epithelial cells (16HBE) and the recovery effect after exposure to exposure factors. Methods GMAs with concentrations of 1, 2, 4, 8, 16 and 32 mg / L were exposed to 16HBE (3 h) for a short time (exposure group). After the above selection, 1 cell cycle (exposure recovery group), the use of cytoplasmic arrest micronucleus test cell genetic damage effect. Results The numbers of MN and NBUD increased gradually with the dose increasing, and there was a dose-response relationship (the determination coefficients were 0.887,0.558, P <0.01 respectively) , And the index of mitotic index (NDI) decreased when the dose was up to 8 mg / L. However, there was no obvious dose-response relationship between the bridging rate of nucleus in nucleus and the dose of radiation. MN in the recovery group did not change significantly at low dose, but increased slowly after the dose was increased, but the increase rate was slow; NDI did not change with the dose; NBUD even decreased at 4 and 8 mg / L . Conclusions GMA has obvious genetic damage effect on cells at the early stage of exposure, but the injury tends to be repaired after the removal of exposure factors. The timely initiation of cell repair mechanism plays a key role in maintaining genetic stability.