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1.
以0, 0.05, 0.1, 0.25, 0.5 Gy 12C6+ 离子全身预辐照昆明小鼠, 间隔4 h后再对小鼠进行4 Gy全身辐射。 辐照后12 h用流式细胞仪检测小鼠胸腺脾脏细胞在各细胞周期时相的百分率, 同时用单细胞电泳检测受辐射小鼠胸腺脾脏细胞DNA损伤程度。 结果显示, 相对于大剂量预照射组, 各低剂量预照射组胸腺细胞S期细胞百分率显著减少; 脾脏细胞G0/G1期细胞百分率明显减少; 同时胸腺脾脏细胞的拖尾率及拖尾长度明显减少, 以0.1 Gy预辐照效果最为明显。 这些结果表明, 低剂量预辐射处理可以减弱胸腺细胞的S期阻滞及脾脏细胞的G1期阻滞, 并明显减轻胸腺脾脏细胞的DNA损伤程度。  相似文献   

2.
采用高传能线密度(LET)重离子辐照人胃癌SGC7901细胞,应用流式细胞技术、蛋白质印迹法(Western blot)及反转录聚合酶链式反应(RT-PCR)观察重离子诱导人胃癌SGC7901细胞周期、凋亡和MSH2表达状况。结果表明:与对照组相比,SGC7901细胞在辐射后72 h G2/M期所占细胞比率(33.26±0.08)和凋亡率(24.16±0.64)均达到峰值,且呈时间依赖性增加;经重离子照射后,DNA错配修复基因MSH2 m RNA和蛋白表达水平在6 h最高。结果提示:重离子在体外诱导SGC7901细胞周期阻滞和凋亡,且具有显著的时间依赖性效应;重离子在一定剂量和时间下,诱导了SGC7901细胞MSH2基因表达。DNA错配修复基因MSH2可能参与了重离子辐照诱导胃癌细胞DNA损伤的修复应答。  相似文献   

3.
研究大蒜素重要活性成分二烯丙基二硫( Diallyl disulfide, 简称DADS) 对12C6+离子束辐照损伤小鼠的保护作用。利用4 Gy 剂量12C6+离子束对不同浓度DADS 预处理的雄性昆明小鼠进行单次全身照射。随后检测骨髓细胞微核率和肝组织中丙二醛(MDA) 含量、蛋白质总羰基含量、总抗氧化能力( TAOC)及谷丙转氨酶(ALT ) 活性。结果显示,与单纯照射组相比,低浓度DADS 预处理组骨髓细胞微核率和肝组织ALT 活性均显著降低(p<0.001),而肝组织T-AOC明显增强( p < 0.05 );中浓度DADS 预处理组肝组织中MDA 含量和蛋白质总羰基含量均显著减少( p < 0.05 )。结果提示,DADS通过抑制氧化应激,有效地保护了脂质、蛋白质和遗传物质免受12C6+离子束辐照引起的损伤。The radioprotective effect of Diallyl disulfide (DADS) on 12C6+ ion irradiation was studied. Pretreated with DADS of different concentration, male Kung-Ming mice were exposed to whole body irradiation with dosage of 4 Gy 12C6+ ion. The animals were sacrificed after irradiation. Then the bone marrow cells micronucleus rate, malondialdehyde (MDA) levels, content of protein carbonylation, total antioxidant capacity ( T-AOC) and alanine aminotransferase ( ALT ) activity were measured. As compared with those in irradiated group, the ratio of micronucleus cells in marrow and the hepatic ALT activity in the pretreatment group with low dose DADS decreased significantly ( p < 0.001 ). Similarly,the content of protein carbonylation and the levels of MDA droped dramatically in the group with middle dose DADS treatment ( p < 0.05 ). On the contrary, the hepatic T-AOC increased markedly in the group of pretreatment with low dose DADS ( p < 0.05 ). The results showed that DADS protect lipoid, protein and genetic material from 12C6+ ion irradiation by right of resisting oxidative stress.  相似文献   

4.
本研究旨在探讨羧甲基-β-1,3葡聚糖(CMG)对人肝癌HepG2细胞X射线或12C6+离子束辐射敏感性的影响。首先用CCK-8法检测CMG对HepG2细胞的生长抑制情况,得到半数抑制浓度(IC50)为120.6μg/mL。用浓度为0.1×IC50的CMG预处理HepG2细胞24 h,再给予2 Gy X射线或12C6+离子束辐照(CMG+辐照组);CMG未处理组直接接受2 Gy X射线或12C6+离子束辐照(辐照组)。对比分析辐照组和CMG+辐照组细胞的克隆存活、DNA损伤、凋亡与周期分布、细胞内活性氧(ROS)水平。发现:与X射线辐照组相比,相同剂量的12C6+离子辐照组克隆存活率更小,DNA损伤和周期阻滞更加严重,细胞凋亡率和细胞内ROS水平也更高。与单独X射线或12C6+离子束辐照组相比,CMG+辐照组克隆存活率明显降低,细胞凋亡率随辐照后CMG作用时间的延长而明显增加,CMG使辐照后细胞内ROS维持在一个较高的水平,同时CMG明显加重了单独辐照诱导的DNA损伤和周期阻滞。结果表明,与X射线相比,HepG2细胞对相同剂量的12C6+离子辐射更敏感;CMG可增加HepG2细胞对X射线或12C6+离子辐射的敏感性;CMG可能通过增加受照HepG2细胞内的ROS水平,加剧辐照诱导的DNA损伤,促进辐射诱导细胞凋亡而起到辐射增敏作用。This study aims to investigate the effect of carboxymethy-β-1, 3-glucan (CMG) on the sensitivity of human hepatoma HepG2 cells to X-rays or 12C6+ ions irradiation. First, the inhibitory effect of CMG on the growth of HepG2 cells was detected by CCK-8 assay, and the half maximal inhibitory concentration (IC50) was 120.6 μg/mL. HepG2 cells were pretreated with CMG at a concentration of 0.1×IC50 for 24 h and then irradiated with 2 Gy X-ray or 12C6+ ion beams (CMG + irradiation group). CMG untreated group was directly irradiated by 2 Gy X-rays or 12C6+ ions beam (irradiation group). The clone survival, DNA damage, cell apoptosis, cell cycle distribution, and intracellular reactive oxygen species (ROS) levels in irradiation group and CMG + irradiation group were comparatively analyzed. The results showed that the clone survival rate was lower, DNA damage and cycle arrest were more serious, and the rate of apoptosis and intracellular ROS levels were higher in 12C6+ ions irradiation group than those in the same dose of X-rays irradiation group. Compared with X-rays or 12C6+ ions irradiation group, the clone survival rate of CMG + irradiation group was significantly decreased, and the apoptosis rate significantly increased with the prolongation of CMG treatment post-irradiation; CMG maintained intracellular ROS at a higher level after irradiation, CMG also significantly aggravated radiation-induced DNA damage and cycle arrest. These results indicated that HepG2 cells were more sensitive to 12C6+ ions radiation than those at the same dose of X-rays. CMG increased the sensitivity of HepG2 cells to X-rays or 12C6+ ions irradiation by increasing intracellular ROS level, exacerbating radiation-induced DNA damage and promoting radiation-induced apoptosis in irradiated HepG2 cells.  相似文献   

5.
利用30,90,180Gy3种剂量的12C6+重离子束辐照大葱种子,研究其在细胞水平和农艺性状的诱变效应并进行RAPD分析。通过与M1代的研究结果比较后表明:经过不同剂量12C6+重离子照射后能有效地诱导大葱细胞形成微核和染色体畸变,这种诱变效应,在M2代仍然有所表现。M1代大葱结果期的株高、白长、花序直径和种子产量随辐照剂量增加产生明显差别,其中30Gy辐照组增幅最大。大葱总水溶性蛋白质和维生素C的含量在30Gy组中积累最多,在90Gy组有明显下降。与M1代一致,M2代中大葱染色体微核率及RAPD分析所得的DNA多态性比率仍然与辐照剂量呈正相关,但比率整体下降;说明高能量重离子辐照造成的DNA变异在M2代被修复和淘汰。  相似文献   

6.
用高传能线密度(LET)的12C离子束和低LET的X射线辐照体外培养的非小细胞肺癌H1299(p53基因缺失), 研究它们的辐照生物学效应的差异。 用克隆形成率法测定了细胞对射线的辐射敏感性; 用AnnexinV/PI试剂盒检测了细胞早期凋亡; 用流式细胞仪检测了细胞周期变化。 实验结果表明, 12C离子束辐照H1299细胞的存活率明显低于用X射线辐照的; 12C离子束引起H1299细胞的早期凋亡率明显高于X射线辐照引起的, 且持续时间更长; 12C离子束引起的H1299细胞G2/M期的抑制更明显。 说明H1299细胞对高LET的12C离子束的辐射敏感性高于对X射线的, 重离子对p53基因缺失型肿瘤的治疗可实施较低的照射剂量、 较少的照射次数和较长的时间间隔。  相似文献   

7.
以传能线密度为30 keV/μm的12C6+离子束辐照人类肝L02细胞, 利用彗星电泳技术检测了以DNA链断裂为生物终点的DNA辐射损伤效应。 CASP软件分析彗星图像, 主要检测尾部DNA(TDNA%)、 彗星全长(CL)、 尾长(TL)、 尾矩(TM)和Olive尾矩(OTM)等指标, SPSS 11.5软件进行统计学分析, 绘制并拟合TM\|剂量曲线。 结果显示, 辐照以剂量依赖的方式引起L02细胞彗星图像各指标的增大, 且TM值与剂量线性正相关。 说明12C6+离子束对DNA有较强的致损伤效应, 且与剂量正相关。 研究为正确评价重离子对人体正常组织的辐射风险及危害提供了一定的基础数据和依据。  相似文献   

8.
用高传能线密度(LET)的^12C离子束和低LET的X射线辐照体外培养的非小细胞肺癌H1299(p53基因缺失),研究它们的辐照生物学效应的差异。用克隆形成率法测定了细胞对射线的辐射敏感性;用AnnexinV/PI试剂盒检测了细胞早期凋亡;用流式细胞仪检测了细胞周期变化。实验结果表明,^12C离子束辐照H1299细胞的存活率明显低于用X射线辐照的;^12C离子束引起H1299细胞的早期凋亡率明显高于X射线辐照引起的,且持续时间更长;^12C离子束引起的H1299细胞G2/M期的抑制更明显。说明H1299细胞对高LET的^12C离子束的辐射敏感性高于对X射线的,重离子对p53基因缺失型肿瘤的治疗可实施较低的照射剂量、较少的照射次数和较长的时间间隔。  相似文献   

9.
研究了一种新的恶唑酮类衍生物GANRA-5对于人胚肺细胞MRC-5的辐射防护作用。以MTT评价其对于细胞的毒性,以γH2AX foci形成法检测其对于辐照后细胞中双链断裂的影响,发现其对于受到X射线和12C6+离子照射的细胞具有较强的辐射防护作用,并进一步发现其能够显著清除辐照后细胞内的自由基。这些结果表明,GANRA-5具有较低的细胞毒性,并能够通过清除自由基发挥较强的针对X射线和12C6+离子的辐射防护作用,有望开发为高效的辐射防护药物。  相似文献   

10.
探讨姜黄素(Curcumin,简称Cur)对重离子辐射损伤小鼠睾丸组织的防护作用。小鼠灌胃不同剂量的Cur后给予4 Gy剂量~(12)C~(6+)离子束全身单次照射。24 h后对小鼠睾丸组织形态学变化进行观察,并测定丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和过氧化氢酶(CAT)活性。结果显示:中、高浓度Cur预处理组对小鼠睾丸组织的形态具有较好的保护作用;低、中浓度Cur预处理组MDA含量显著降低(P0.05);与单纯照射组相比,低浓度Cur预处理组SOD活性水平和中浓度Cur预处理组CA了活性水平显著提高(P0.05)。结果表明:Cur对重离子全身辐射小鼠的抗氧化系统有一定的激活效应,对辐射损伤有一定的防护作用,其机制可能与Cur清除自由基,保护脂质和蛋白质有关。  相似文献   

11.
以人肝癌细胞系和正常肝细胞系为材料,报道了不同传能线密度射线辐射引发细胞染色体原初断裂及24 h内的修复情况。 计算了相对生物学效应的值。 以L02染色体总断裂数量得出的RBE值96.05 keV/μm的12C6+ 为3.6, 512 keV/μm 36Ar18+ 为2.9。 而以7721染色体总断裂数量得出的RBE值: 96.05 keV/μm的12C6+ 为3.5,512keV/μm 36Ar18+也为2.9。用产生等点染色单体断裂计算,则RBE更高。对比得出,高LET对增加等点染色单体断裂量的作用要远远大于对增加染色单体断裂量的作用。等点染色单体的断裂修复难度要远远大于染色单体断裂的修复难度, 这也是高LET高致死率的一个重要原因。 Human hepatoma SMMC 7721 and normal liver L02 cells were irradiated with γ rays,12C6+ and 36Ar18+ ion beams at the Heavy Ion Research Facility in Lanzhou(HIRFL). We reported the kinetic repair of chromosome breaks of L02 and SMMC 7721 cells in 24 h of post irradiation time. The relative biological effectiveness(RBE) for inducing chromatid breaks were 3.6 for L02 and 3.5 for SMMC 7721 cell lines at the linear energy transfer(LET) peak of 96.55 keV/μm 12C6+ ions, and 2.9 (both of the two cell lines) at 512 keV/μm 36Ar18+ ions.It suggested that the RBE of isochromatid type breaks induced by 36Ar18+ was higher than those by 12C6+. We concluded that the high production of isochromatid type breaks, induced by the densely ionizing track structure, could be regarded as a signature of high LET radiation exposure.  相似文献   

12.
Interaction of ionizing radiation with plasmid DNA can lead to formation of single strand breaks, double strand breaks and clustered lesions. We have investigated the response of the synthetic plasmid pBR322 in aqueous solution upon irradiation with 12C ions under spread-out Bragg peak conditions (densely ionizing) and with 137Cs γ-photons (sparsely ionizing) as a function of dose. To evaluate the relevance of indirect effects, i.e. influences of diffusion limited radical induced DNA damage triggered by water radiolysis, the experiments were performed at various concentrations of the radical scavenger mannitol. Agarose gel electrophoresis was employed to quantify the DNA damage. At low scavenger concentration for a given dose DNA damage is higher for γ-photons than for 12C. For the latter, the microscopic dose distribution is inhomogeneous, with very high dose deposited along the few tracks through the solution. This is in agreement with the concept that scavengers efficiently reduce damage for γ-photons, implying that the underlying damage mechanism is single strand break induction by OH radicals. For 12C induced damage, the fraction of SSB and DSB that is unaffected by radical scavengers and thus due to direct effect is quantified.  相似文献   

13.
Irradiation caused DNA single-strand breaks in S180 cells in the presence oflaser-hematoporphyrin derivative(HPD).The number of single strand breaks was 3.69 ×10~(10)break dolton~(-1).The analysis of base composition of DNA showed that the effect of laser-HPDirradiation on guanine was the highest,being 5-12 times as high as those of the three others(adenine,cytosine and thymine).It was different from the nature of DNA damage caused by γ-ray irradiation.  相似文献   

14.
选取对数生长期人肺癌细胞A549接受0—6.0 Gy 碳离子照射, 用克隆形成法检测细胞的存活率; 并于照射后12和24 h收集细胞, 用流式细胞术检测细胞周期各时相的细胞百分比, 观察不同剂量碳离子辐照对A549细胞周期进程的影响。 结果显示: 0—6.0 Gy 碳离子照射后细胞存活率显著下降; 照射后12 h细胞发生G0/G1期阻滞, 而照射后24 h, 1.0 Gy 照射组细胞在G0/G1期阻滞, 2.0—6.0 Gy 照射组细胞在G2/M期阻滞。 上述结果表明, 在A549细胞接受碳离子照射后的12 和24 h内, 1.0 Gy 照射可持续激活细胞G1期检查点, 而2.0—6.0 Gy 碳离子照射后其细胞周期进程是随时间变化的。 To investigate the effects of cell cycle progression of A549 cell induced by 12C6+ ion irradiation at different doses, the survival fractions of the A549 cells were determined by colony forming assay; cell cycles were analyzed by FACS at 12 h or 24 h after irradiation. The results showed that the percentage of survival in the A549 cells decreased with irradiation doses. Compared with control group, the percentage of the cells in G0/G1 phase significantly increased at 12 h after irradiation with different doses of 12C6+ ions. However, at 24 h after irradiation the percentage of the cells in G0/G1 phase significantly increased with 1.0 Gy 12C6+ ions, while the cells showed increasing percentage in G2/M phase with 2.0, 4.0 or 6.0 Gy 12C6+ ions. The results suggested that G1 cell cycle checkpoint was activated in 12—24 h after irradiation with 1.0 Gy 12C6+ ions, but after irradiation with 2.0—6.0 Gy 12C6+ ions, the cell cycle progression of the A549 cells changed with time.  相似文献   

15.
利用不同剂量的碳离子辐照二硫苏糖醇(2.5 mmol/L)预处理的HeLa细胞,探讨了内质网应激反应对碳离子辐照宫颈癌HeLa细胞的影响。实验发现:与单独辐照组相比,二硫苏糖醇联合碳离子辐照后细胞的存活率下降,而凋亡率增加;二硫苏糖醇联合碳离子辐照加重了碳离子辐照引起的细胞周期阻滞;且联合辐照组的自噬被明显激活。结果表明,持续的内质网应激可改变宫颈癌HeLa细胞对碳离子辐照反应,且二硫苏糖醇可能通过影响HeLa细胞的自噬性细胞死亡通路发挥作用。  相似文献   

16.
Formation of γH2AX foci (a marker of DNA double‐strand breaks), rates of foci clearance and apoptosis were investigated in cultured normal human fibroblasts and p53 wild‐type malignant glioma cells after exposure to high‐dose synchrotron‐generated microbeams. Doses up to 283 Gy were delivered using beam geometries that included a microbeam array (50 µm wide, 400 µm spacing), single microbeams (60–570 µm wide) and a broad beam (32 mm wide). The two cell types exhibited similar trends with respect to the initial formation and time‐dependent clearance of γH2AX foci after irradiation. High levels of γH2AX foci persisted as late as 72 h post‐irradiation in the majority of cells within cultures of both cell types. Levels of persistent foci after irradiation via the 570 µm microbeam or broad beam were higher when compared with those observed after exposure to the 60 µm microbeam or microbeam array. Despite persistence of γH2AX foci, these irradiation conditions triggered apoptosis in only a small proportion (<5%) of cells within cultures of both cell types. These results contribute to the understanding of the fundamental biological consequences of high‐dose microbeam irradiations, and implicate the importance of non‐apoptotic responses such as p53‐mediated growth arrest (premature senescence).  相似文献   

17.
7Li和12C离子致DNA链断裂的研究   总被引:6,自引:0,他引:6  
选用HI-13串列加速器产生的不同传能线密度的7Li和12C重离子,以不同的剂量对纯化的质粒DNA水溶液进行了辐照.利用原子力显微镜对这两种重离子诱发的DNA损伤进行了纳米水平的结构分析,并用ScionImage分析软件完成了DNA碎片长度的测量.得到了DNA分子超螺旋、开环和线性三种形态随剂量的变化情况以及DNA碎片长度的分布函数,并用Tsallis熵统计理论对实验结果进行了拟合.  相似文献   

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