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为探讨细胞信号转导系统在吸烟与石棉联合致癌过程中的作用，本研究采用体外细胞培养技术，对香烟烟雾溶液（ＣＳＳ）和温石棉（ＣＨ）单独及联合作用于人胚肺（ＨＥＬ）细胞后细胞内蛋白激酶Ｃ（ＰＫＣ）活性的变化进行了观察。结果表明，ＣＳＳ与ＣＨ单独作用均可使胞浆ＰＫＣ（ＰＫＣ－Ｃ）和胞膜ＰＫＣ（ＰＫＣ－Ｍ）活性增强；当二者联合作用时可协同增强ＰＫＣ－Ｃ和ＰＫＣ－Ｍ的活性，提示吸烟与温石棉可能通过改变细胞内ＰＫＣ的活性进一步促进肿瘤的发生。
In order to explore the role of cell signal transduction system in carcinogenesis associated with smoking and asbestos, we studied the effects of cigarette smoke solution (CSS) and chrysotile (CH) alone and in combination on human embryo lung (HEL) Changes in cellular intracellular protein kinase C (PKC) activity were observed. The results showed that both the cytoplasmic PKC (PKC-C) and the membrane-derived PKC (M-PKC-M) activity were enhanced by CSS and CH alone. Tip smoking and chrysotile may further promote tumorigenesis by changing the activity of intracellular PKC.