Subhashree M, Venkateswarlu R, Karthik K, Shangamithra V, Venkatachalam P
Department of Human Genetics, Sri Ramachandra University, Porur, Chennai, 600 116, India.
Department of Human Genetics, Sri Ramachandra University, Porur, Chennai, 600 116, India.
Mutat Res Genet Toxicol Environ Mutagen. 2017 Sep;821:20-27. doi: 10.1016/j.mrgentox.2017.06.007. Epub 2017 Jul 5.
Monolayer and suspension cultures of tumor (BMG-1, CCRF-CEM), normal (AG1522, HADF, lymphocytes) and ATM-mutant (GM4405) human cells were exposed to X-rays at doses used in radiotherapy (high dose and high dose-rate) or radiological imaging (low dose and low dose-rate). Radiation-induced DNA damage, its persistence, and possible bystander effects were evaluated, based on DNA damage markers (γ-H2AX, p53) and cell-cycle-specific cyclins (cyclin B1 and cyclin D1). Dose-dependent DNA damage and a dose-independent bystander response were seen after exposure to high dose and high dose-rate radiation. The level of induced damage (expression of p53, γ-H2AX) depended on ATM status. However, low dose and dose-rate exposures neither increased expression of marker proteins nor induced a bystander response, except in the CCRF-CEM cells. Bystander effects after high-dose irradiation may contribute to stochastic and deterministic effects. Precautions to protect unexposed regions or to inhibit transmission of DNA damage signaling might reduce radiation risks.
将肿瘤（BMG-1、CCRF-CEM）、正常（AG1522、HADF、淋巴细胞）及ATM突变型（GM4405）人类细胞的单层培养物和悬浮培养物，分别以放射治疗中使用的剂量（高剂量和高剂量率）或放射成像剂量（低剂量和低剂量率）进行X射线照射。基于DNA损伤标志物（γ-H2AX、p53）和细胞周期特异性细胞周期蛋白（细胞周期蛋白B1和细胞周期蛋白D1），评估辐射诱导的DNA损伤、其持续性以及可能的旁观者效应。在暴露于高剂量和高剂量率辐射后，观察到剂量依赖性DNA损伤和剂量非依赖性旁观者反应。诱导损伤水平（p53、γ-H2AX的表达）取决于ATM状态。然而，低剂量和低剂量率照射既未增加标志物蛋白的表达，也未诱导旁观者反应，但CCRF-CEM细胞除外。高剂量照射后的旁观者效应可能导致随机效应和确定性效应。保护未暴露区域或抑制DNA损伤信号传导传递的预防措施可能会降低辐射风险。
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