Studies on energy dependency of biological effects of neutrons and risk estimation
Studies on energy dependency of biological effects of neutrons and risk estimation
批准号:
09680530
负责人:
KUBOTA Nobuo
金额:
$1.86万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1998
中文摘要
我们在中国仓鼠V79细胞中检测了hprt位点对细胞杀伤和突变诱导的中子能量依赖性。在广岛大学放射生物学研究加速器(HIRRAC)设施中产生了0.32,0.57和1.2 MeV的单能中子,并用于照射细胞。观察RBE随中子能量对细胞存活终点和hprt突变诱导的变化。与137Cs伽马射线相比,所有中子能量在细胞杀伤和诱导突变方面都更有效。在检测的中子能量范围内,我们发现细胞毒性随着能量从1.2 MeV降低到0.32 MeV而增加。与伽马射线相比,在1.2、0.57和0.32 MeV的情况下,10%存活率下的细胞致死率的rbe分别为5.7、6.7和7.6。另一方面,突变诱导在0.57 MeV时最高,在1.2和0.32 MeV时逐渐降低。1.2、0.57和0.32 mev中子诱导突变的rbe分别为9.7、19.4和13.9。我们从未经处理和中子暴露的细胞中分离出hprt位点的独立V79细胞突变体,并通过基于多重聚合酶链反应(PCR)的外显子缺失分析确定突变的遗传变化。初步结果提示了缺失模式与中子能量之间的特殊关系。
英文摘要
We have examined the neutron energy dependency of cell killing and mutation induction at hprt locus in Chinese hamster V79 cells. Monoenergetic neutrons at 0.32, 0.57, and 1.2 MeV were generated at the Hiroshima University Radiobiological Research Accelerator (HIRRAC) Facility, and were used to irradiate cells. The variation in RBE with neutron energy for the end points of cell survival and hprt mutation induction was observed. When compared to 137Cs gamma-rays, all neutron energies were more effective at both cell killing and induction of mutation. Over the range of the neutron energies examined, we found that cytotoxicity increased as the energy decreased from 1.2 to 0.32 MeV.In comparison to gamma-rays, RBEs for cell lethality at 10% survival were 5.7, 6.7, and 7.6 for 1.2, 0.57, and 0.32 MeV, respectively. Mutation induction, on the other hand, was highest at 0.57 MeV with a gradual decrease at 1.2 and 0.32 MeV.RBEs for mutation induction were 9.7, 19.4, and 13.9 for 1.2, 0.57, and 0.32 MeVneutrons.We isolated independent V79 cell mutants at the hprt locus from untreated and neutron-exposed cells and determined the genetic changes underlying the mutation by multiplex polymerase chain reaction (PCR)-based exon deletion analysis. Preliminary results are suggestive of a specific relationship between deletion patern and neutron energy.
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Kubota, et al.: "Mutation induction and RBE of low energy neutrons in V79 cells." J.Radiat.Res.in press. (1999)
Kubota 等人:“V79 细胞中低能中子的突变诱导和 RBE。”
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通讯作者:
Kubota, et al.: "The phosphatidylinositol 3-kinase inhibitor wortmannin sensitizes quiescent but not proliferating MG-63 human osreosarcoma cells to radiation." Cancer Lett.133. 161-167 (1998)
Kubota 等人:“磷脂酰肌醇 3-激酶抑制剂渥曼青霉素可使静止但不增殖的 MG-63 人类骨肉瘤细胞对辐射敏感。”
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"Mutation induction and RBE of low energy neutrons in V79 cells" J.Radiat.Res.(in press).
“V79 细胞中低能中子的突变诱导和 RBE”J.Radiat.Res.(出版中)。
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Kubota,et al.: "The phosphatidylinositol 3-kinase inhibitor wortmannin sensitizes quiescent but not proliferating MG-63 human osreosarcoma cells to radiation." Cancer Lett.133. 161-167 (1998)
Kubota 等人:“磷脂酰肌醇 3-激酶抑制剂渥曼青霉素可使静止但不增殖的 MG-63 人类骨肉瘤细胞对辐射敏感。”
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Kubota, et al.: "Induction of a particular deletion in mitochondrial DNA by X rays depends on the inherent radiosensitivity of cells." Radiat.Res.148. 395-398 (1997)
Kubota 等人:“X 射线诱导线粒体 DNA 特定缺失取决于细胞固有的放射敏感性。”
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Radiosensitization by cyclin-dependent kinase inhibitors and its molecular mechanism
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依托单位:
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Radiosensitization by inhibiting DNA-protein kinase and microenvironmental factor
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批准年份:2021
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