Pero R W, Bryngelsson C, Bryngelsson T, Lindholm L, Scherstén B, Trell E, Janzon L, Franzén J, Johansson B W
Atherosclerosis. 1983 Aug;48(2):119-29. doi: 10.1016/0021-9150(83)90098-9.
The levels of N-acetoxy-2-acetylaminofluorene (NA-AAF)-induced unscheduled DNA synthesis (UDS) and of NA-AAF binding to DNA have been determined in resting mononuclear leukocytes from individuals with various smoking habits, heart infarct patients and subjects diagnosed for hypertension. Age-matched and blood-pressure-controlled smokers (n = 99) had significantly elevated levels of NA-AAF-induced UDS and NA-AAF binding to DNA when compared to nonsmokers (n = 75) similarly corrected for age and blood pressure. Heart infarct patients without any history of risk factors, as well as diagnosed hypertensives with normalized blood pressure, were not significantly different from matched controls when assessed by the NA-AAF method. Our results support the theory that increased mutagen sensitivity is associated with smoking and high blood pressure but not with cardiovascular disease itself via some mechanism of genetic selection.
已测定了具有不同吸烟习惯的个体、心肌梗死患者和被诊断为高血压的受试者静息单核白细胞中N-乙酰氧基-2-乙酰氨基芴(NA-AAF)诱导的非预定DNA合成(UDS)水平以及NA-AAF与DNA的结合水平。与同样根据年龄和血压进行校正的不吸烟者(n = 75)相比,年龄匹配且血压得到控制的吸烟者(n = 99)中,NA-AAF诱导的UDS水平以及NA-AAF与DNA的结合水平显著升高。通过NA-AAF方法评估时,没有任何危险因素病史的心肌梗死患者以及血压已恢复正常的已诊断高血压患者,与匹配的对照组没有显著差异。我们的结果支持这样一种理论,即诱变敏感性增加与吸烟和高血压有关,但与心血管疾病本身并无关联,这是通过某种基因选择机制实现的。