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目的 探讨丙烯腈 (ACN)对中国仓鼠肺细胞 (CHL)细胞活力及细胞间隙连接通讯(GJIC)功能的影响。方法 镜下观察细胞形态学改变 ,采用MTT法测定细胞生长半数抑制浓度(IC50 ) ,应用荧光染料示踪技术观测ACN对CHL细胞GJIC的影响。结果 ACN染毒 12和 2 4h ,细胞生长IC50 分别为 435 73和 2 5 1 0 9μg/ml。低剂量组 (12 5和 2 5 0 μg/ml)细胞形态与对照组相比无明显改变 ,较高剂量组 (5 0 0～ 2 0 0 0 μg/ml)细胞轻度受损 (0～Ⅰ级 ) ,高剂量组 (80 0 0 μg/ml)细胞明显受损 (Ⅲ级 )。ACN原形在无明显细胞毒性剂量 (10 0～ 5 0 0 μg/ml)时即可抑制GJIC ,并呈持续抑制作用 ,存在剂量 效应和时间 效应关系。ACN经代谢活化后 ,可加重对细胞GJIC的抑制作用和细胞受损程度 ,但在染毒 12h后停止接触 ,该作用在一定程度上可逆转。牛磺酸作为一种重要的抗氧化剂 ,预处理细胞 (牛磺酸剂量为 10和 2 0mmol/L)可明显抑制ACN对细胞GJIC的下调作用。结论 ACN在较高剂量时对CHL细胞具有毒性作用 ,但在无明显细胞损伤剂量时即能明显抑制细胞GJIC功能 ,该抑制作用在停止接触ACN或有抗氧化剂存在时可逆转 ,提示氧化应激在ACN所致细胞GJIC功能下调中具有重要作用。
Objective To investigate the effect of acrylonitrile (ACN) on cell viability and GJIC function of Chinese hamster lung cells (CHL). Methods The morphological changes of the cells were observed under microscope and the half concentration (IC50) of cell growth was determined by MTT assay. The effect of ACN on the GJIC of CHL cells was observed by fluorescent dye tracing technique. Results The IC50 of ACN was 12 and 24 h. The IC50 of cell growth was 435 73 and 2 5 109 μg/ml, respectively. The cell morphology of the low-dose group (12 5 and 250 μg/ml) was not significantly different from that of the control group, and the cells in the higher dose group (500-2000 μg/ml) were slightly impaired (0- Grade I), cells in the high-dose group (80 0 μg/ml) were significantly impaired (grade III). ACN prototypic inhibits GJIC without significant cytotoxicity (100-500 μg/ml) and shows sustained inhibitory effect. There is a dose-effect and time-effect relationship. After metabolic activation of ACN, it can aggravate the inhibitory effect of GJIC on cells and the degree of cell damage, but the contact is stopped after 12 hours of exposure, and this effect can be reversed to a certain extent. Taurine, an important antioxidant, pretreated cells (taurine doses of 10 and 20 mmol/L) significantly inhibited the down-regulation of GJIC by ACN. Conclusions ACN has a toxic effect on CHL cells at higher doses, but it can significantly inhibit GJIC function when there is no obvious cell injury dose. This inhibition can be reversed when cessation of exposure to ACN or presence of antioxidants, suggesting that oxidative stress It plays an important role in the down-regulation of GJIC function in cells caused by ACN.