Paigen B, Gurtoo H L, Minowada J, Houten L, Vincent R, Paigen K, Parker N B, Ward E, Hayner N T
N Engl J Med. 1977 Aug 18;297(7):346-50. doi: 10.1056/NEJM197708182970702.
To test whether the genetically determined trait, aryl hydrocarbon hydroxylase inducibility, affects susceptibility to lung cancer, we measured this trait in cultured lymphocytes from a normal population, patients with lung cancer and progeny of such patients. We found very low aryl hydrocarbon hydroxylase activity (19 per cent of normal) in about half the patients with lung cancer. Only part of this activity can be accounted for by reduced cell growth and by reduced protein synthesis. In an indirect assessment of inducibility, both 57 progeny and 27 matched controls had a mean inducibility of 2.95 and a similar distribution into low, intermediate and high groups (chi-square = 0.3 P = 0.9). No differences in basal or induced activity were observed. Thus, if patients with lung cancer possess altered aryl hydrocarbon hydroxylase inducibility or activity these characteristics are not transmitted to their progeny.
为了检测由基因决定的芳烃羟化酶诱导性这一性状是否影响肺癌易感性，我们在来自正常人群、肺癌患者及其后代的培养淋巴细胞中测量了这一性状。我们发现约一半肺癌患者的芳烃羟化酶活性非常低（为正常人的19%）。这种活性降低只有部分原因可归结为细胞生长减慢和蛋白质合成减少。在一项诱导性的间接评估中，57名后代和27名匹配的对照者的平均诱导性均为2.95，且在低、中、高分组中的分布相似（卡方检验=0.3，P=0.9）。未观察到基础活性或诱导活性存在差异。因此，如果肺癌患者存在芳烃羟化酶诱导性或活性改变，这些特征不会遗传给他们的后代。
