卷烟烟气抽提物对细胞遗传毒性及茶多酚干预作用

Hereditary toxicity of cigarette smoke extraction and protection of tea polyphenols on the toxicity in BEAS-2B cells

目的探讨卷烟烟气抽提物(CSE)对支气管上皮细胞(BEAS-2B)遗传毒性及茶多酚干预作用。方法以高、中、低3个浓度对支气管上皮细胞进行染毒,同时设立茶多酚干预组和空白对照组;采用彗星实验及γ-H2AX蛋白表达检测DNA损伤,以微核实验检测染色体损伤,并检测HPRT基因突变率。结果高剂量染毒组BE-AS-2B细胞彗星细胞数(130.5±1.6)个、彗星尾长(134.33±3.56)μm、尾部面积(7 798.43±43.45)μm2,均明显高于空白对照组(P<0.05),并呈剂量—效应关系;CSE低、中、高剂量染毒组BEAS-2B细胞中微核细胞分别为(22.4±3.2)、(38.6±1.8)、(79.6±2.4)个,均明显多于空白对照组的(6.2±1.5)个(P<0.05);CSC中、高剂量染毒组BEAS-2B细胞HPRT基因突变率分别为(0.802±0.040)‰、(1.058±0.002)‰,均明显高于空白对照组的(0.330±0.002)‰(P<0.05)。茶多酚对CSE诱发的DNA链断裂及微核细胞增多有明显抑制作用,并可有效降低HPRT基因突变率。结论 CSE具有细胞遗传毒性,茶多酚对其遗传毒性具有干预作用。

Objective To study the genetic toxicity in human bronchial epithelial cells（BEAS-2B） induced by cigarette smoke extraction（CSE） and protective effect of tea polyphenols（TPs） on the toxicity.Methods The BEAS-2B cells were exposed to high,moderate,and low concentration of CSE in culture medium and a tea polyphenols protection group and a control group were set up.Comet assay and H2AX phosphorylation were adopted to detect DNA damage and micronucleus assay was used to estimate chromosomal damage and hypoxanthine phosphoribosyl（HPRT） gene mutation.Results Compared to those of the control group,the number of comet cells（130.5 ± 1.6）,tail length（134.33±3.56 μm）,the tail area（7 798.43 ± 43.45 μm2） for BEAS-2B cells of high dose CSE exposure group increased significantly（P〈0.05 for all） in a dose-effect manner.The number of cells with micronucleus in 1 000 BEAS-2B cells exposed to low,moderate,and high CSE were 22.4±3.2,38.6±1.8,and 79.6±2.4,respectively,and significantly higher than that of the control group（6.2±1.5）（P〈0.05 for all）.The CSE significantly inbihit the increases of HPRT gene mutation rate,DNA chain break and number of cells with micronucleus induced by CSE exposure in BEAS-2B cells.Conclusion CSE has genotoxicity and tea polyphenols could inhibit the genetic toxicity of CSE.