Hopkin J M
Basic Life Sci. 1984;29 Pt B:927-37. doi: 10.1007/978-1-4684-4892-4_32.
This paper presents evidence that cigarette smoke condensate (CSC) is a potent inducer of sister chromatid exchanges (SCEs) in cultured human lymphocytes; that benzo(a)pyrene (BP) contributes very little to this activity; that smokers have higher SCE rates than nonsmokers; that smokers with untreated lung cancer have consistently higher basal and CSC-induced SCE rates than their matched heavy smoking controls; and that, on a weight-for-weight basis, CSCs from different tar categories of cigarettes induce similar numbers of SCEs. These results are in keeping with the evidence that many smokers die of lung cancer, and that the basis of malignant transformation may be an alteration in cellular DNA. The results raise questions about possible innate differences in individuals' responses to cigarette smoke, and about the "safeness" of lower tar cigarettes.
香烟烟雾浓缩物（CSC）是培养的人淋巴细胞中姐妹染色单体交换（SCE）的强力诱导剂；苯并(a)芘（BP）对此活性贡献极小；吸烟者的SCE率高于不吸烟者；未经治疗的肺癌吸烟者的基础SCE率和CSC诱导的SCE率始终高于与之匹配的重度吸烟对照者；并且，按重量计算，不同焦油类别的香烟的CSC诱导的SCE数量相似。这些结果与许多吸烟者死于肺癌以及恶性转化的基础可能是细胞DNA改变的证据一致。这些结果引发了关于个体对香烟烟雾反应可能存在的先天差异以及低焦油香烟“安全性”的问题。
