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高功率微波辐射后下丘脑神经元凋亡和线粒体膜电位与Ca^(2+)的变化 被引量:8

Changes of apoptosis,mitochondrion membrane potential and Ca^(2+) of hypothalamic neurons induced by high power microwave
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摘要 目的探讨高功率微波辐射后下丘脑神经元凋亡、线粒体膜电位与Ca^(2+)的变化。方法以10与30 mW/cm^2高功率微波辐射原代培养的下丘脑神经元,于辐射后6 h采用倒置显微镜和流式细胞术检测细胞的凋亡、线粒体膜电位与胞浆钙离子的变化。结果辐射后6 h,10与30 mW/cm^2组凋亡率与假辐射组相比均明显增加;30 mW/cm^2组辐射后坏死率与假辐射组比较亦明显升高,差异有统计学意义(P<0.05)。辐射后6 h,30 mW/cm^2组Ca^(2+)明显升高,膜电位性明显下降,差异均有统计学意义(P<0.01)。结论细胞凋亡是下丘脑神经元死亡的主要方式之一,胞浆内Ca^(2+)超载及线粒体膜电位的下降参与其损伤过程。 Objective To explore the injury effect and mechanism of hypothalamic neurons after high power microwave(HPM) exposure. Methods Primarily cultured hypothalamic neurons were exposed to 10 and 30 mW/cm^2 HPM, and the inverted phase contrast microscope(IPCM) and flow cytometry(FCM) were employed to detect the injury of cells and change of mitochondrion membrane potential(MMP) and Ca^2+ in the cytoplasm of neurons. Results The ratio of apoptosis was significantly higher than that of the sham exposure( P 〈0.05) induced by 10 and 30 mW/cm^2 HPM and necrosis increased significantly( P 〈0.05) in the group of 30 mW/cm^2 at 6 h after exposure. The content of Ca^2+ in the cytoplasm of neuron cells increased( P 〈 0.01 ) while MMP decreasedsignificantly(P〈0.01) after radiation of 30 mW/cm^2 HPM at 6 h after exposure. Condusion Apoptosis is one of the major death ways of hypothalamic neurons. The overloading of Ca^2+ and the decline of MMP axe involved in the process.
出处 《中华劳动卫生职业病杂志》 CAS CSCD 北大核心 2006年第12期739-741,共3页 Chinese Journal of Industrial Hygiene and Occupational Diseases
关键词 微波 神经元 细胞凋亡 膜电位 Microwave Neurons Cell apoptosis Calcium Membrane potential
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  • 1Maxwell SRJ.Prospects for the use of antioxidant therapies.Drugs,1995;49(3):345~61
  • 2Sujata MK,Priyadarsini KI,Venkatesan P et al.Free radicals cavenging ability and antioxidant efficiency of curcumin and its substituted analogue.Biophys Chem,1999;80(2):83~9
  • 3Rajakrishnan V,Viswanathan P,Rajasekharan KN et al.Neuroprotective role of curcumin from curcuma longa on ethanol-induced brain damage.Phytother Res,1999;13(7):571~4
  • 4Timothy JS,William DA.Transmitter,ionchannel and receptor properties of pheochromocytoma (PC12) cells:A model for neurotoxicological studies.Neurotoxicology,1991;12(3):473~92
  • 5Chopp M,Li Y,Jiang N et al.Antibodies against adhesion molecules reduce apoptosis after transient middle cerebral artery occlusion in rat brain.J Cereb Blood Flow Metab,1996;16(4):578~84
  • 6Mattson MP,Zhang Y,Bose S.Growth factors prevent mitochondrial dysfunction,loss of calcium homeostasis,and cell injury,but not ATP depletion in hippocampal neurons deprived of glucose.Exp Neurol,1993;121(1):1~13
  • 7Walarand S,Vaeix S,Rodriguez C et al.Flow cytometry study of polymorphonuclear neutrophil oxidative burst: A comparison of three fluorescent probes.Clinica Chimica Acta,2003;331(1~2):103~10
  • 8Motterlini R,Foresti R,Bassi R et al.Curcumin,an antioxidant and anti-inflammatory agent,induces heme oxygenase-1 and protects endothelial cells against oxdative stress.Free Radical Biol Med,2000;28(8):1303~12
  • 9Nieminen AL,Saylor AK,Tesfai SA et al.Contribution of the mitochondrial permeability transition to lethal injury after exposure of hepatocytes to t-butyl-hydroperoxide.Biochem J,1995; 307(Pt1):99~106
  • 10Zamzami N,Marchetti P,Castedo M et al.Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo.J Exp Med,1995;181(5):1661~72

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