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共培养的转化和未转化C3H 10T1/2细胞:低剂量率照射对转化细胞的优先杀伤作用。

Co-cultured transformed and untransformed C3H 10T1/2 cells: preferential killing of transformed cells by low dose rate irradiation.

作者信息

Zeman E M, Bedford J S

出版信息

Int J Radiat Oncol Biol Phys. 1986 Jan;12(1):51-8. doi: 10.1016/0360-3016(86)90415-3.

DOI:10.1016/0360-3016(86)90415-3
PMID:3943992
Abstract

Co-cultured C3H 10T1/2 cells, in which transformed cells were grown as discrete colonies on top of density-inhibited monolayers of untransformed cells, were used to determine the potential usefulness of a short term assay system for the study of differential radiation effects as they may apply to cell populations with differing turnover rates, but in close physical contact. Mixed cultures were exposed to either an acute dose of 20 Gy of Cs-137 gamma rays, or a dose of 72 Gy delivered at a low dose rate of 0.34 Gy per hour. These treatments resulted in approximately equal levels of damage to the untransformed monolayers. At 10-day intervals after treatment, representative flasks from each dose group were examined for evidence of degeneration, and subsequent regrowth, if any, of the transformed colonies and untransformed monolayers. For comparable amounts of visible damage to the untransformed monolayers, the low dose rate irradiation was more effective at delaying regrowth of, or even eradicating, transformed colonies. These results are consistent with expectations based on previous results in which dose-rate or dose fractionation isoeffect curves were compared for these two cell types, grown independently in plateau phase cultures.

摘要

共培养的C3H 10T1/2细胞(其中转化细胞在未转化细胞的密度抑制单层细胞上形成离散集落生长)用于确定短期检测系统在研究不同辐射效应方面的潜在用途,这些效应可能适用于具有不同更新率但紧密物理接触的细胞群体。将混合培养物暴露于20 Gy的Cs-137γ射线急性剂量,或每小时0.34 Gy的低剂量率下给予72 Gy的剂量。这些处理对未转化的单层细胞造成的损伤程度大致相同。在处理后的10天间隔期,检查每个剂量组的代表性培养瓶,以寻找退化的证据,以及转化集落和未转化单层细胞随后是否有再生长(如果有的话)。对于未转化单层细胞相当程度的可见损伤,低剂量率照射在延迟转化集落的再生长甚至根除转化集落方面更有效。这些结果与基于先前结果的预期一致,在先前的结果中,比较了这两种细胞类型在平台期培养中独立生长时的剂量率或剂量分割等效效应曲线。

相似文献

1
Co-cultured transformed and untransformed C3H 10T1/2 cells: preferential killing of transformed cells by low dose rate irradiation.共培养的转化和未转化C3H 10T1/2细胞:低剂量率照射对转化细胞的优先杀伤作用。
Int J Radiat Oncol Biol Phys. 1986 Jan;12(1):51-8. doi: 10.1016/0360-3016(86)90415-3.
2
Dose fractionation effects in plateau-phase cultures of C3H 10T1/2 cells and their transformed counterparts.C3H 10T1/2细胞及其转化细胞的平台期培养物中的剂量分割效应。
Radiat Res. 1985 Feb;101(2):373-93.
3
Survival and oncogenic transformation of C3H/10T1/2 cells after extended X irradiation.延长X射线照射后C3H/10T1/2细胞的存活与致癌转化
Radiat Res. 1985 Nov;104(2 Pt 1):214-23.
4
Response of plateau-phase C3H 10T1/2 cells to radiation and concurrent administration of bleomycin.
Radiat Res. 1989 Nov;120(2):306-12.
5
Lack of inverse dose-rate effect on fission neutron induced transformation of C3H/10T1/2 cells.裂变中子诱导C3H/10T1/2细胞转化不存在剂量率反比效应。
Int J Radiat Biol. 1988 Oct;54(4):531-6. doi: 10.1080/09553008814551971.
6
Lack of dose rate modification (0.0049 vs. 0.12 Gy/min) of fission-neutron-induced neoplastic transformation in C3H/10T1/2 cells.在C3H/10T1/2细胞中,裂变中子诱导的肿瘤转化缺乏剂量率修正(0.0049与0.12戈瑞/分钟)。
Int J Radiat Biol. 1991 Apr;59(4):1017-26. doi: 10.1080/09553009114550901.
7
Loss of repair capacity in density-inhibited cultures of C3H 10T1/2 cells during multifraction irradiation.C3H 10T1/2细胞密度抑制培养物在多次分割照射期间修复能力的丧失。
Radiat Res. 1985 Oct;104(1):71-7.
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Oncogenic transformation of C3H 10T1/2 cells by acute and protracted exposures to monoenergetic neutrons.通过急性和长期暴露于单能中子使C3H 10T1/2细胞发生致癌转化。
Radiat Res. 1991 Oct;128(1 Suppl):S60-4.
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Radiation-induced adaptive response for protection against micronucleus formation and neoplastic transformation in C3H 10T1/2 mouse embryo cells.辐射诱导的适应性反应对C3H 10T1/2小鼠胚胎细胞中微核形成和肿瘤转化的防护作用
Radiat Res. 1994 Apr;138(1 Suppl):S28-31.
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Evidence for reduced capacity for damage accumulation and repair in plateau-phase C3H 10T1/2 cells following multiple-dose irradiation with gamma rays.γ射线多剂量照射后处于平台期的C3H 10T1/2细胞中损伤积累和修复能力降低的证据。
Radiat Res. 1986 Jun;106(3):380-95.