可吸入颗粒物PM_(10)对细胞间隙连接通讯的抑制作用

Inhibition of Gap Junctional Intercellular Communication by PM_(10)

[目的 ]研究直径≤ 1 0 μm的可吸入大气颗粒物 (PM1 0 )对细胞间隙连接通讯的影响 ,探讨PM1 0 的非遗传毒性作用。 [方法 ]用大流量采样器 ,采集城区交通干道旁约 1 8m高度处大气中的PM1 0 。超纯水超声提取、低温真空冷冻干燥制备PM1 0 悬液。采用细胞代谢协同试验和染料划痕试验观察PM1 0 对中国仓鼠肺成纤维V79细胞以及人肺成纤维细胞间隙连接通讯的影响。 [结果 ]PM1 0 抑制V79细胞的代谢协同作用 ,使V79- 细胞的存活率增高 ,在 1 0～ 1 0 0mg/L剂量范围内 ,与对照组比较 ,克隆形成数明显增高 ,有剂量 反应关系 (r=0 94,P <0 0 5)。细胞划痕实验结果显示 ,在PM1 01 0～ 1 0 0mg/L剂量范围内 ,在人肺成纤维细胞中荧光染料扩散距离随剂量的增加而减小 (7 5～ 2 1 61mm) ,与对照组(2 6 56mm)比较 ,差异显著。 [结论 ]PM1 0 能抑制细胞间隙连接通讯 ,提示可能在癌症的发生过程中起促进作用。

Epidemiologic studies have provided strong evidence that air pollution,especially respirable particle matter (PM 10 ) is associated with increase in morbidity of respiratory diseases. The inhibition of gap junctional intercellular communication (GJIC) has been considered as an important factor for abnormal cell growth and differentiation. The objective of our study is to detect the nongenotoxic effects of PM 10 by GJIC. PM 10 was collected on glass fibre filters using a high volume sampler,located nearly urban traffic road at the height of 18 m. PM 10 suspensions were prepared by a ultrasonic disruptor. The inhibition effect of PM 10 on GJIC was studied by two assay systems,metabolic cooperation in V79 cells and scrape loading dye transfer in human lung fibroblasts. PM 10 significantly inhibited metabolic cooperation between V79 cells and the colony numbers of V79 - cells increased in a dose dependent manner in 1 0～100 mg/L. The dye transfer distances in HLF cells exposed to PM 10 decreased from 21 61 to 7 5 mm and indicated significant difference compared to control group (26 56 mm). [Conclusion] This study suggests that PM 10 may have tumor promoting activity.