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使用未标记的铜-吡哆醛-5'-甲基肟增强肿瘤细胞中的染色体畸变并进行铜K壳层单色X射线照射。

Enhancement of chromosomal aberrations in tumor cells with a non-labeled Cu-PTSM and irradiation with Cu K-shell monochromatic X rays.

作者信息

Takakura Kaoru, Yaguchi Satoshi, Kanansugi Yuichi, Kobayashi Katsumi, Okayasu Ryuichi, Fujibayashi Yasuhisa

机构信息

Physics Department, Division of Natural Sciences, International Christian University, Mitaka-shi, Tokyo 181-8585, Japan.

出版信息

Radiat Prot Dosimetry. 2006;122(1-4):188-94. doi: 10.1093/rpd/ncl476. Epub 2007 Jan 17.

Abstract

This study aims to clarify the enhancement effect on chromosomal aberrations via selective energy absorption by Cu atoms in cultured bone cancer cells with non-labelled Cu-pyruvaldehyde-bis(N(4)-methylsemicarbazone) (Cu-PTSM) and monochromatic X rays. The X rays having the energy of the Cu K-shell absorption edge arising from synchrotron radiation (KEK-PF) was used as radiation source. Cu-PTSM labelled with copper radionuclides has been developed for medical imaging using positron emission tomography (PET). Evidence clearly showed that the absorption of X rays in the Cu K-shell caused this enhancement. After cells were treated with 1000 nM Cu-PTSM, the enhancement ratio of the initial yield of isochromatid breaks caused by CuK-H X-ray irradiation to that by 200 kV(p) X rays was approximately 2.8. About 5.6 times of the remaining isochromatid breaks were observed at 4 h in Cu-PTSM treated samples irradiated with CuK-H X rays comparing to that with 200 kV(p) X rays. In this study, uniqueness in physical property such as Cu atom K-shell ionisation was applied for the enhancement of biological effects in cancer cells.

摘要

本研究旨在通过未标记的铜-丙酮醛双(N(4)-甲基氨基脲)(Cu-PTSM)和单色X射线在培养的骨癌细胞中通过铜原子的选择性能量吸收来阐明对染色体畸变的增强作用。使用同步辐射产生的具有铜K壳层吸收边能量的X射线(KEK-PF)作为辐射源。用铜放射性核素标记的Cu-PTSM已被开发用于正电子发射断层扫描(PET)医学成像。有证据清楚地表明,铜K壳层对X射线的吸收导致了这种增强。在用1000 nM Cu-PTSM处理细胞后,由CuK-H X射线照射引起的等臂染色单体断裂的初始产率与由200 kV(p)X射线照射引起的等臂染色单体断裂的初始产率的增强比约为2.8。与200 kV(p)X射线相比,在用CuK-H X射线照射的Cu-PTSM处理样品中,在4小时时观察到的剩余等臂染色单体断裂约为其5.6倍。在本研究中,利用铜原子K壳层电离等物理性质的独特性来增强癌细胞中的生物学效应。

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