Wickliffe Jeffrey K, Bickham Amy M, Rodgers Brenda E, Chesser Ronald K, Phillips Carleton J, Gaschak Sergey P, Goryanaya J A, Chizhevsky I, Baker Robert J
Department of Biological Sciences, Texas Tech University, Lubbock, Texas, USA.
Environ Mol Mutagen. 2003;42(1):11-8. doi: 10.1002/em.10170.
Empirical genetic effects resulting from low-dose rate irradiation and chronic, cumulative exposure are poorly characterized. Expected effects are based on epidemiological studies and downward, linear extrapolations from nonthreshold models derived from acute, high-dose exposures. These extrapolations and their associated risk coefficients have no experimental support, and because of their inherent uncertainty they are the subject of considerable debate. The expectation of deleterious genetic effects resulting from low-dose rate irradiation and chronic exposure is in need of empirical assessment because this type of exposure is typical of those encountered in occupational, residential, and environmental settings. Recent acute low-dose (<10 cGy) studies using cytogenetic and point mutation endpoints indicate that observed effects range from those lower than spontaneous to an increase in the frequency of point mutations. Using the Big Blue assay, we examined the ability of chronic, continuous gamma-irradiation (2.3 x 10(-3) cGy/min) in the Chornobyl environment to induce point mutations. This system has demonstrated a significant point mutation sensitivity (4.5-fold increase) to acute, high-dose (1-3 Gy) gamma-radiation. Mutant frequencies and the mutation spectra were examined in exposed and reference samples of Big Blue mice following 90 days exposure (cumulative absorbed dose = 3 Gy) to the Chornobyl environment. No significant increase in the mutant frequency or bias in the mutational spectrum was observed in exposed individuals. This finding suggests that low-dose rate gamma-irradiation at Chornobyl does not induce point mutations and that cumulative, chronically absorbed doses do not induce the same genetic effects as acute doses of the same magnitude.
低剂量率辐射以及慢性累积照射所产生的经验性遗传效应目前还未得到充分表征。预期效应是基于流行病学研究以及从急性高剂量照射得出的非阈值模型进行的向下线性外推。这些外推及其相关风险系数并无实验依据，并且由于其内在的不确定性，它们成为了大量争论的主题。低剂量率辐射和慢性照射会产生有害遗传效应这一预期需要进行经验性评估，因为这种照射类型在职业、居住和环境场景中很常见。近期使用细胞遗传学和点突变终点的急性低剂量（<10 cGy）研究表明，观察到的效应范围从低于自发水平到点突变频率增加。我们使用“大蓝”检测法，研究了切尔诺贝利环境中的慢性连续伽马辐射（2.3×10⁻³ cGy/分钟）诱导点突变的能力。该系统已证明对急性高剂量（1 - 3 Gy）伽马辐射具有显著的点突变敏感性（增加4.5倍）。在将“大蓝”小鼠暴露于切尔诺贝利环境90天（累积吸收剂量 = 3 Gy）后，对暴露组和对照组样本的突变频率和突变谱进行了检测。在暴露个体中未观察到突变频率有显著增加或突变谱存在偏差。这一发现表明，切尔诺贝利的低剂量率伽马辐射不会诱导点突变，并且累积的慢性吸收剂量不会产生与相同剂量急性照射相同的遗传效应。
