碳离子辐照对人肺癌细胞A549细胞周期进程的影响

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.     

离子辐照与碳纳米结构体的合成

阐述了在离子辐照下生成各种碳纳米结构体研究的发展现状,探讨了相应的生长机制和一些相变机理 ,提出了一些有待解决的问题 ,并对其发展方向作了展望. The synthesis of carbon nanostructures, such as fullerenes, nanotubes, onions and diamond, by using ion irradiation, has been reviewed and the growth mechanisms of these carbon nanostructures as well as their phase transitions are simply discussed. It shows that high density plasma engendered by ion irradiation plays an important role in the growing of carbon nanostructures. In addition, it indicates that ion irradiation, due to its great flexibility of experimental parameters, is enormously convenient in...     

碳离子辐照细胞的相对生物学效率

研究了传能线密度(LET)≥125.5keV/μm的碳离子辐照小鼠黑色素瘤B16、人的宫颈癌HeLa、中国仓鼠肺V79、人的肝癌SMMC-77214种细胞的相对生物学效率(RBE).得到了当LET=125.5keV/μm时,RBE依赖于细胞种类并随细胞存活水平的升高而增加的关系,以及当LET≥125.5keV/μm时,RBE随着LET的增大而变小的关系.     

离子辐照对聚苯乙烯低温导电特性的影响

室温下用3MeV的硅离子对聚苯乙烯(PS)进行辐照,对辐照后的样品在室温至液氮温度范围的导电特性进行了测量.结果表明,当辐照剂量在1×1012cm-2附近,PS的室温电阻发生突变.随着温度的降低,PS电阻增大,在低辐照剂量下,电阻在155K附近急剧增加.对于高辐射剂量样品,在较高的温度下呈现热激活导电,在低温下电子通过隧穿传导.分析认为,PS电阻随温度的变化是由于不同剂量辐照离子在聚合物中形成的对电子传导有贡献的导电中心密度不同.通过拟合样品的渗流临界特性,分析了样品电阻随辐照剂量的变化 关键词： 聚苯乙烯 硅离子辐照 低温导电     

C20富勒烯的Ar+离子辐照合成

Ar⁺离子辐照聚乙烯靶表面在室温情况下合成的C₂₀,已采用高分辨率透射电子显微镜/电子衍射装置、飞行时间质谱、红外和拉曼谱仪进行了研究.结果认为,辐照诱发的微晶体由笼式C₂₀组成. 关键词：     

离子辐照对磷烯热导率的影响及其机制分析

通过离子辐照产生缺陷,可以非常有效地调控磷烯诸多物理性质.本文应用分子动力学方法模拟离子辐照磷烯的过程,给出了缺陷的形成概率与入射离子能量、离子种类以及离子入射角度之间的关系,并且应用非平衡态分子动力学计算辐照后磷烯热导率的变化.以缺陷形成概率为切入点,系统地研究了辐照离子的能量、辐照剂量、离子的种类以及离子的入射角度对磷烯热导率的影响.应用晶格动力学方法研究了空位缺陷对磷烯声子参与率的影响,并计算了声子局域模式的空间分布.基于量子微扰和键弛豫理论,指出空位缺陷明显降低磷烯热导率的最重要物理机制是空位缺陷附近的低配位原子对声子强烈散射.本文研究可为缺陷工程调控磷烯的热输运性质提供理论参考.     

高能氩离子辐照硅产生的缺陷研究

在室温下750MeV氩离子对本征单晶硅进行辐照,通过用正电子湮没寿命测量技术、电子顺磁共振技术以及红外光吸收方法研究了辐照产生的缺陷.结果表明:电中性双空位是辐照产生的主要空位团;在4.3×10¹⁴ions/cm²的高剂量下未见样品发生非晶化转变;虽然在离子射程末端双空位的浓度随剂量的增加而显著增大,但在以电离激发过程为主要能损方式的区域里双空位的浓度基本不变.据此可以认为,电子能损过程对辐照产生的缺陷有退人作用.     

非晶合金的离子辐照效应

非晶合金作为一种快速凝固形成的新型合金材料,引起了材料研究者的极大兴趣.微观结构上长程无序、短程有序的特征使其具有独特的物理、化学和力学性能,在许多领域展现出良好的应用前景,尤其是有望成为核反应堆、航空航天等强辐照环境下的备选结构材料.本文深入探讨非晶合金的辐照效应,主要讨论离子辐照对非晶合金微观结构、宏观力学性能以及其他物理化学性能的影响,可为进一步理解非晶合金的微观结构和宏观力学性能之间的关系提供有效的实验和理论基础,也可为非晶合金在强辐照环境下的服役性能预测提供实验依据,对推进非晶合金这一先进材料的工程化应用具有重要的理论与实际意义.     

离子辐照聚乙烯合成小于C60的富勒烯分子晶体

通过荷能离子（包括团簇离子）辐照聚乙烯首次合成了小于C60的富勒烯－C20和C26分子晶体。在此基础之上，进一步探索其他小富勒烯分子晶体（如C32，C38和C24）存在的确凿证据。     

离子辐照石墨生成的纳米尺寸Ar泡

用60keV的Ni⁺和Ar⁺在相同实验条件下,先后分别辐照同一块石墨靶,剂量均为10¹⁸/cm².带能量色散X射线分析和电子衍射分析的高分辨透射电子显微镜观察和分析发现,尺寸不同的纳米Ar泡嵌在类玻璃碳薄片中,部分泡内的Ar可能已形成固体结构.     

二烯丙基二硫对12C6+离子束辐照损伤小鼠的保护作用研究

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.     

12C6+离子预辐射对小鼠胸腺脾脏细胞周期进程的影响

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。     

12C6+ 离子束辐照对大鼠离体主动脉环内皮依赖性舒张功能的影响

利用兰州重离子研究装置(HIRFL) 提供的高能12C6+离子束(能量为300 MeV/u,剂量率为0.5 Gy/min) 辐照大鼠离体胸主动脉环,考察了12C6+离子束辐照对主动脉环内皮依赖性舒张功能的影响,并采用NBT 还原法测定血管环生成超氧阴离子(O2􀀀) 水平,加入外源性超氧化物歧化酶(SOD) 干预探讨了O2􀀀在内皮功能损伤中的作用。研究结果表明,2.0,4.0 和6.0 Gy 的12C6+离子束辐照大鼠胸主动脉环后,可致血管内皮依赖性舒张功能的剂量依赖性明显受损(P <0.01 vs control group),并可致血管环NBT 还原能力剂量依赖性增加(4.0 Gy 时,P <0.05;6.0 Gy 时,P <0.01 vs control group)。辐照前加入外源性SOD 对6.0 Gy 12C6+离子束辐照所致血管环NBT 还原能力升高有明显抑制作用(P <0.01),对血管环内皮依赖性舒张功能也有明显的保护作用(P<0.01),但辐照后10 min 加入外源性SOD,其保护作用明显不及前者。结论显示,12C6+ 离子束辐照大鼠胸主动脉环可致血管内皮功能受损,O2 清除剂SOD 对内皮功能受损有保护作用,说明O2􀀀介导了辐照所致内皮功能损伤。Heavy ion beam has many characteristics,and it is expected to be the most suitable radiation therapy technique for malignant tumor. It is lack of depth-understanding on the potential adverse reactions caused by using this technique, because heavy ion radiotherapy is applied to clinical for a short time. Studies have shown that the vascular injury plays a pivotal role in normal tissue damage induced in the conventional radiation therapy, but there was no research report on heavy ion beam irradiation-induced vascular injury. In the present study, the isolated aortic rings of rats were irradiated by 12C6+ ion beam (300 MeV/u, 0.5 Gy/min) delivered by HIRFL(Heavy Ion Research Facility in Lanzhou), the effects of 12C6+ ion beam irradiation on aortic rings with endothelium dependent diastolic function have been investigated.NBT reduction method was used for assaying the vascular ring formation of superoxide anion (O2􀀀) level, and the involvement of superoxide anion in endothelial function injury in rats was investigated through the intervention test of exogenous superoxide dismutase (SOD) on O2. The results showed that, the vascular endothelial dependent vasodilation was impaired significantly (P < 0:01 vs control group) by irradiation with 2.0, 4.0 and 6.0 Gy 12C6+ ion beam in a dosedependent manner, and the NBT reduction of vascular rings increased dose-dependently (P <0.05 at 4.0 Gy, P <0.01 at 6.0 Gy vs control group). Adding exogenous SOD before irradiation could significantly inhibit the increasing of NBT reduction (P<0.01), and also had protective effect on vascular endothelium dependent diastolic function (P<0.01), but 10 min after irradiation with exogenous SOD, its protective function was significantly less than before. Conclusion indicated that 12C6+ ion beam irradiation could cause endothelial function impaired, O2􀀀 scavenger SOD has a protective effect on endothelial dysfunction, suggesting that O2􀀀 mediates endothelial injury induced by heavy ion irradiation.     

真空、低能离子注入对人宫颈癌（HeLa）细胞中 p53及c-fos mRNA的表达影响

在具有高效护水功能石蜡油的保护下进行了人宫颈癌细胞(HeLa细胞)的低能离子注入及真空处理, 用荧光定量PCR的方法分别研究了真空和30 keV N+的不同注入剂量下, 细胞中p53基因和c-fos基因的mRNA表达变化。 结果表明, 上述两个基因的表达与真空及低能离子注入之间存在着剂量关系。     

低剂量电离辐射预处理对不同肿瘤细胞周期的影响

实验研究了低剂量γ射线预照射对人肝癌细胞系hepG2和人宫颈癌细胞系HeLa的细胞周期进程的影响.结果显示(1)低剂量(5cGy)辐射后,两种细胞的G2/M期细胞短暂累积;(2)低剂量辐射促进肿瘤细胞的生长;(3)高剂量(3Gy)辐射后,hepG2细胞发生G2期阻滞,HeLa细胞发生S期和G2期阻滞;(4)与单纯高剂量照射相比,低剂量辐射预处理后4h,再给予高剂量辐射,可进一步促进hepG2细胞在G2/M期累积,但是预照射对HeLa细胞的周期进程没有明显影响.因此,低剂量辐射预处理对高剂量诱导的细胞周期阻滞的影响依赖于肿瘤细胞的类型.     

不同LET 12C6+离子对生防菌BJ1的辐射诱变效应

选取高低两个LET点(40和60keV/m),剂量点分别为50,100,200,400,600Gy进行辐照处理,研究了生防菌的存活率与突变率的关系,抑菌谱以及活性等。结果表明,在高LET条件下,低剂量辐照就可以得到较多的突变体,并且BJ1有较高的存活率和突变谱,有利于筛选优良的正突变体。因此高LET较低LET有更为明显的辐射诱变效应。     

12C6+离子束辐照番茄种子当代效应

利用辐射能量为80 MeV/u 的12C6+重离子束辐照番茄种子, 辐照剂量分别为30, 60, 90, 120和160 Gy研究其对番茄M1代的生物学效应。结果表明, 随着辐照剂量的增大, 番茄的发芽率和成苗率降低, 且成苗率明显低于发芽率, 发现辐照损伤主要抑制了根的生长; MDA和脯氨酸含量变化的总体趋势为随着辐照剂量的增大先升后降再升高, 说明高剂量C离子辐照对生物膜造成更严重的损伤; APX活性随着辐照剂量的增大呈先升后降再升高的趋势, 表明APX在清除活性氧中起主要作用; POD和SOD活性的总体趋势是随着辐照剂量的增大而降低, 且明显低于对照组。综合分析表明, 12C6+重离子束辐照番茄种子, 对M1代具有明显的损伤效应, 高剂量辐照对番茄种子造成的损伤更大, 使酶的活性降低, 抑制植株生长。 To investigate the M1 biological effects of heavy ions irradiation on Lycopersicon esculentum Mill., its seeds were irradiated by 12C6+heavy ions (80 MeV/u) with the dosages of 30, 60, 90, 120 and 160 Gy respectively . The results showed that with doses increased gradually, germination rate and seedling rate of Lycopersicon esculentum Mill. were decreased, and the latter was lower than the former, mainly due to the inhibition of root growth. The irradiation increased the content of MDA and proline evidently, showing irradiation could damage biomembrane, and also decreased the activities of POD and SOD with distinct inhibition pattern. However, the low dose and high dose irradiation promoted APX activity, illustrating APX was induced to protect irradiation injury. In brief, exposure to 12C6+ heavy ions had obvious injury effects on the seeds of Lycopersicon esculentum Mill.. Heavy ions irradiation damaged biomembrane, inhibited activities of enzymes, and finally inhibited the growth of the first generation of these seeds.     

羧甲基-β-1,3-葡聚糖对人肝癌HepG2细胞的放射增敏作用

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.     

灵芝酸A对人肝癌细胞的辐射增敏效应的初步研究

本研究旨在初步探讨灵芝酸A(GAA)对人肝癌细胞系HepG2在高LET中子和低LET的γ射线条件下的辐射敏感性的影响及差异。研究中,我们用CCK-8方法检测不同浓度GAA对HepG2增殖抑制作用。选取低浓度(5μmol/L)GAA预处理细胞24 h,分别给予不同剂量的中子辐照或γ射线辐照,分别检测克隆存活率、细胞凋亡和γH2AX蛋白的foci的形成。结果表明:在不加GAA的情况下,高LET中子辐射比低LET的γ射线对细胞产生的凋亡比例高;在添加了GAA后,与未加GAA对照组相比,诱导细胞凋亡的比例明显增加;另外,加GAA处理后,细胞增殖抑制率也随着辐照剂量的增加而增高。即GAA能增加HepG2细胞的辐射敏感性,而在同样GAA剂量下,HepG2细胞对高LET中子辐射比低LET的γ射线更敏感。由此,这项研究说明灵芝酸或可开发成为一种天然辐射增敏剂,从而为癌症特别是肝癌的放疗提供新的辅助治疗方法。