Shahidi Maryam, Mozdarani Hossein, Mueller Wolfgang-Ulrich
Dept. of Medical Physics, Tarbiat Modares University, Tehran, Iran.
Dept. of Biochemistry and Biophysics, Mazandaran University of Medical Sciences, Sari, Iran.
Iran Biomed J. 2010 Jul;14(3):67-75.
Impaired DNA repair mechanism is one of the main causes of tumor genesis. Study of intrinsic radiosensitivity of cancer patients in a non-target tissue (e.g. peripheral blood) might show the extent of DNA repair deficiency of cells in affected individuals and might be used a predictor of cancer predisposition.
Initial radiation-induced DNA damage (ratio of Tail DNA/Head DNA), dose-response curves and kinetics of DNA repair in leukocytes from healthy volunteers and prostate cancer patients were assessed using alkaline comet assay after exposure to 60Co gamma rays.
Results showed that higher levels of baseline and gamma rays induced DNA damage in leukocytes of prostate cancer cases than in controls. A similar dose response was obtained for both groups. After a repair time of 24 h following in vitro irradiation, samples from the healthy individuals showed no residual DNA damage in their leukocytes, whereas prostate cancer patients revealed more than 20 percent. Although similar initial radiosensitivity was observed for both groups, the repair kinetics of radiation induced DNA damage of leukocytes from prostate cancer cases and healthy subjects were statistically different.
These results support the hypothesis that men affected by prostate cancer may have a constitutional genomic instability.
DNA修复机制受损是肿瘤发生的主要原因之一。研究癌症患者非靶组织（如外周血）的内在放射敏感性，可能会显示受影响个体细胞的DNA修复缺陷程度，并可作为癌症易感性的预测指标。
在健康志愿者和前列腺癌患者的白细胞中，通过碱性彗星试验评估在暴露于60Coγ射线后初始辐射诱导的DNA损伤（尾DNA/头DNA比率）、剂量反应曲线和DNA修复动力学。
结果表明，前列腺癌患者白细胞中基线和γ射线诱导的DNA损伤水平高于对照组。两组获得了相似的剂量反应。体外照射后24小时的修复时间后，健康个体的样本白细胞中未显示残留DNA损伤，而前列腺癌患者显示超过20%。虽然两组观察到相似的初始放射敏感性，但前列腺癌患者和健康受试者白细胞辐射诱导的DNA损伤修复动力学在统计学上存在差异。
这些结果支持了受前列腺癌影响的男性可能存在先天性基因组不稳定的假设。
