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低剂量慢性暴露于γ射线和裂变中子对小鼠生殖系微卫星突变的诱导作用。

Induction of minisatellite mutations in the mouse germline by low-dose chronic exposure to gamma-radiation and fission neutrons.

作者信息

Dubrova Y E, Plumb M, Brown J, Boulton E, Goodhead D, Jeffreys A J

机构信息

Department of Genetics, University of Leicester, Leicester LE1 7RH, UK.

出版信息

Mutat Res. 2000 Sep 20;453(1):17-24. doi: 10.1016/s0027-5107(00)00068-3.

Abstract

Germline mutation induction at mouse minisatellite loci by paternal low-dose (0.125-1 Gy) exposure to chronic (1.66 x 10(-4) Gy min(-1)) low-linear energy transfer (low-LET) gamma-irradiation and high-LET fission neutrons (0.003 Gy min(-1)) was studied at pre-meiotic stages of spermatogenesis. Both types of radiation produced linear dose-response curves for mutation of the paternal allele. In contrast to previous results using higher doses, the pattern of induction of minisatellite mutation after chronic gamma-irradiation was similar to acute (0.5 Gy min(-1)) exposure to X-rays, indicating that the elevated mutation rate was independent of the ability of the cell to repair damage induced immediately or over a period of up to 100 h. Chronic exposure to fission neutrons was more effective than acute or chronic low-LET exposure (relative biological effectiveness, RBE=3.36). The data also provide strong support for the previous conclusion that increases in minisatellite mutation rate are not caused by radiation-induced DNA damage at minisatellite loci themselves, but rather from damage induced by ionising radiation elsewhere in the genome/cell.

摘要

在精子发生的减数分裂前期阶段,研究了父本低剂量(0.125 - 1 Gy)暴露于慢性(1.66×10⁻⁴ Gy min⁻¹)低线性能量传递(低LET)γ射线和高LET裂变中子(0.003 Gy min⁻¹)对小鼠小卫星位点种系突变的诱导作用。两种辐射均产生了父本等位基因突变的线性剂量反应曲线。与之前使用更高剂量的结果相反,慢性γ射线照射后小卫星突变的诱导模式与急性(0.5 Gy min⁻¹)X射线照射相似,表明突变率升高与细胞修复即时或长达100小时内诱导损伤的能力无关。慢性裂变中子暴露比急性或慢性低LET暴露更有效(相对生物效应,RBE = 3.36)。这些数据也为之前的结论提供了有力支持,即小卫星突变率的增加不是由小卫星位点本身的辐射诱导DNA损伤引起的,而是由基因组/细胞其他部位的电离辐射诱导的损伤引起的。

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