分子辐射生物剂量计发展潜势

穆蕊 陈英

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分子辐射生物剂量计发展潜势

Development potential on molecular radiation biological dosimeter

  • 摘要: 生物剂量估算无论在辐射事故或职业流行病学调查等方面都是不可缺少的重要手段。以细胞遗传学方法为代表的生物剂量计经过半个多世纪的发展已经非常成熟,并被广泛应用。为了更好地应对辐射突发事件,寻找具有快速、简便、适合大范围人群应用的新型分子水平生物剂量计成为目前研究的热点。为此,着重介绍近年来研究期望价值比较高的分子水平生物指示剂。
  • [1] Marhetti F, Coleman MA, Jones IM, et al. Candidate protein biodosimeters of human exposure to ionizing radiation[J]. Int J Radiat Biol, 2006, 82(9):605-639.
    [2] Snyder AR, Morgan WF. Gene expression profiling after irradiation:clues to understanding acute anti persistent responses?[J]. Cancer Metastasis Rev, 2004, 23(3-4):259-268.
    [3] Hildesheim J, Bulavin DV, Anver MR, et al. Gadd45a protects against UV irradiation-induced skin tumors, and promotes apoptosis and stress signaling via MAPK and p53[J]. Cancer Res, 2002, 62(24):7305-7315.
    [4] Takekawa M, Saito H. A family of stress-inducible GADD45-like proteins mediate activation of the stress-responsive MTK1/MEKK4/MAPKKK[J]. Cell, 1998, 95(4):521-530.
    [5] Gupta M, Gupta SK, Hoffman B, et al. Gadd45a and Gadd45b protect hematopoietie cells from UV-induced apoptosis via distinct signaling pathways, including p38 activation and JNK inhibition[J]. J Biol Chem, 2006, 281(26):17552-17558.
    [6] Gupta SK, Gupta M, Hoffman B,et al. Hematopoietic cells from gadd45a-deficient and gadd45b-deficient mice exhibit impaired stress responses to acute stimulation with cytokines, myeloablation and inflammation[J]. Oncogene, 2006, 25(40):5537-5546.
    [7] Hildesheim J, Belova GI, Tyner SD, et al. Gadd45a regulates matrix metalloproteinases by suppressing DeltaNp63alpha and beta-catenin via p38 MAP kinase and APC complex activation[J]. Oncogene, 2004, 23(10):1829-1837.
    [8] Tront JS, Hoffman B, Liebermann DA. Gadd45a suppresses Ras-Driven mammary tumorigenesis by activation of c-Jun NH2-terminal kinase and p38 stress signaling resulting in apoptosis and senescence[J]. Cancer Res, 2006, 66(17):8448-8454.
    [9] Zhan Q. Gadd45a, a p53-and BRCA1-regulated stress protein, in cellular response to DNA damage[J]. Mutat Res, 2005, 569(1-2):133-143.
    [10] Amundson SA, Bittner M, Chen Y, et al. Fluorescent cDNA microarray hybridization reveals complexity and heterogeneity of cellular genotoxic stress responses[J]. Oncogene, 1999, 18(24):3666-3672.
    [11] Gajdusek C, Onoda K, London S, et al. Early molecular changes in irradiated aortic endothelium[J]. J Cell Physiol, 2001, 188(1):8-23.
    [12] Grace MB, McLeland CB, Blakely WF. Real-time quantitative RT-PCR assay of GADD45 gene expression changes as a biomarker for radiation biodosimetry[J]. Int J Radiat Biol, 2002, 78(11):1011-1021.
    [13] Jen KY, Cheung VG. Transcriptional response of lymphoblastoid cells to ionizing radiation[J]. Genome Res, 2003, 13(9):2092-2100.
    [14] Akerman GS, Rosenzweig BA, Domon OE, et al. Alterations in gene expression profiles and the DNA-damage response in ionizing radiation-exposed TK6 Cells[J]. Environ Mol Mutagen, 2005, 45(2-3):188-205.
    [15] Amundson SA,Do KT, Shahab S, et al. Identification of potential mRNA hiomarkers in peripheral blood lymphocytes for human exposure to ionizing radiation[J]. Radiat Res, 2000, 154(3):342-346.
    [16] Stassen T, Port M, Nuyken I, et al. Radiation-induced gene expression in MCF-7 cells[J]. Int J Radiat Biol, 2003, 79(5):319-331.
    [17] Marko NF, Dieffenbach PB, Yan G, et al. Does metabolic radiolabeling stimulate the stress response? Gene expression profiling reveals differential cellular responses to internal beta vs. external gamma radiation[J]. FASEB J, 2003, 17(11):1470-1486.
    [18] Fernandez-Capetillo O, Lee A, Nussenzweig M, et al. H2AX:the histone guardian of the genome[J]. DNA Repair, 2004, 3(8-9):959-967.
    [19] Wang H, Wang M, Wang H, et al. Complex H2AX phosphorylation patterns by multiple kinases including ATM and DNAPK in human cells exposed to ionizing radiation and treated with kinase inhibitors[J]. J Cell Physiol, 2005, 202(2):492-502.
    [20] Stiff T, O'Driscoll M, Rief N, et al. ATM and DNA-PK function redundantly to phosphorylate H2AX after exposure to ionizing radiation[J]. Cancer Res, 2004, 64(7):2390-2396.
    [21] Lowndes NF, Toh GW. DNA repair:the importance of phosphorylating histone H2AX[J]. Curr Biol, 2005, 15(3):99-102.
    [22] Celeste A, Petersen S, Romanienko PJ, et al. Genomic instability in mice lacking histone H2AX[J]. Science, 2002, 96(5569):922-927.
    [23] Paul T, Rogakou EP, Yamazaki V, et al. A critical role for histone H2AX in recruitment of repair factors to nuclear foei after DNA damage[J]. Curr Biol, 2000, 10(15):886-895.
    [24] Rogakou EP, Pilch DR, Orr AH, et al. DNA double-stranded breaks induce histone H2AX phosphorylation on serine 139[J]. J Biol Chem, 1998, 273(10):5858-5868.
    [25] 王会平,周平坤.组蛋白H2AX与DNA损伤的分子感应[J].癌变.畸变.突变,2006,18(4):334-336.
    [26] 闵锐,倪瑾.H2AX活化与DNA双链断裂及辐射剂量的关系[J].生命的化学,2006,26(5):427-429.
    [27] Ding LH, Shingyoji M, Chen F, et al. Gene expression profiles of normal human fibroblasts after exposure to ionizing radiation:A comparative study of low and high doses[J]. Radiat Res, 2005, 164(1):17-26.
    [28] Azzam El, de Toledo SM, Little JB. Direct evidence for the participation of gap junction-mediated intercellular communication in the transmission of damage signals from alpha-particXe irradiated to nonirradiated cells[J]. Proc Natl Acad Sci USA, 2001, 98(2):473-478.
    [29] Shao C, Furusawa Y, Aoki M, et al. Role of gap junctional intercellular communication in radiation-induced bystander effects in human fibroblasts[J]. Radiat Res, 2003, 160(3):318-323.
    [30] Azzam El, de Toledo SM, Little JB. Expression of connexin43 is highly sensitive to ionizing radiation and other environmental stresses[J]. Cancer Res, 2003, 63(21):7128-7135.
    [31] Glover D, Little JB, Lavin MF, et al. Low dose ionizing radiation-induced activation of connexin 43 expression[J], Int J Radiat Biol 2003, 79(12):955-964.
  • [1] 周平坤夏寿萱 . 真核基因损伤修复和基因表达的辐射兴奋效应. 国际放射医学核医学杂志, 1996, 20(5): 223-226.
    [2] 王平关华顺吕玉民 . 外周血核基因表达评价辐射生物剂量方法研究进展. 国际放射医学核医学杂志, 2014, 38(6): 416-420, 432. doi: 10.3760/cma.j.issn.1673-4114.2014.06.016
    [3] 龙贤辉周平坤 . 缝隙连接蛋白43基因及其辐射诱导表达反应. 国际放射医学核医学杂志, 2005, 29(6): 269-271.
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    [5] 赵红光蔡露龚守良 . 低剂量辐射与糖尿病. 国际放射医学核医学杂志, 2006, 30(1): 59-62.
    [6] 杨岩王娟王冠军 . 低剂量辐射对人骨髓间充质干细胞影响的研究. 国际放射医学核医学杂志, 2008, 32(3): 183-187.
    [7] 闵锐 . 电离辐射生物剂量研究现状. 国际放射医学核医学杂志, 2004, 28(3): 121-127,145.
    [8] 赵欣然姜恩海李进刘强邢志伟江波王晓光姜立平 . 低剂量辐射兴奋效应的研究及临床应用. 国际放射医学核医学杂志, 2008, 32(2): 114-117.
    [9] 杨春平卢圣栋 . 基因表达的序列分析. 国际放射医学核医学杂志, 1999, 23(3): 131-134.
    [10] 唐刚华 . 基因表达正电子发射断层显像. 国际放射医学核医学杂志, 2001, 25(6): 241-245.
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  • 收稿日期:  2007-10-22

分子辐射生物剂量计发展潜势

  • 100850 北京, 军事医学科学院放射与辐射医学研究所放射毒理与辐射危害评价研究室

摘要: 生物剂量估算无论在辐射事故或职业流行病学调查等方面都是不可缺少的重要手段。以细胞遗传学方法为代表的生物剂量计经过半个多世纪的发展已经非常成熟,并被广泛应用。为了更好地应对辐射突发事件,寻找具有快速、简便、适合大范围人群应用的新型分子水平生物剂量计成为目前研究的热点。为此,着重介绍近年来研究期望价值比较高的分子水平生物指示剂。

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