X射线照射Hep-2细胞对其培养基吸收光谱的影响

采用分光光度计分别测量了受不同剂量X射线照射后继续培养48h时的人上皮样喉癌细胞株Hep-2的培养基RPMI1640的紫外吸收光谱,分析了该培养基中蛋白质的紫外吸收特性.结果发现:各组培养基的吸收光谱存在明显的差别,新鲜培养基RPMI1640(10%胎牛血清)233nm处的吸收峰在细胞生长过程中位移至235nm,275nm处的吸收峰位移至278nm.反映出各组培养基中芳香族氨基酸中各种氨基酸如色氨酸、酪氨酸、苯丙氨酸的含量的变化,说明癌细胞在生长过程中对这几种氨基酸的改变不是按等量比的.实验还发现细胞培养基的吸收光谱强度与各剂量组细胞数基本成正相关,进而与细胞所受X射线照射的剂量有内在的联系.这些结果将为利用光谱技术研究人喉癌最佳X射线放射剂量奠定基础.     

Influence of X-ray on the autophagic-lysosomal system in rat pancreatic acini

Lysosomes have an important role in radiation injury of cells and tissues. Activation of autophagy is frequently observed in different types of pathological tissue degeneration. In radiation response it increases in some cases, and lysosomes are responsible for regulated degradation of the autophagic vacuoles. Lysosomes are also involved in ionizing radiation induced cell death. In apoptosis lysosomes degrade content of the phagocytotic vacuoles derived from engulfed apoptotic blebs. On the other hand lysosomal enzymes discharged from disintegrated cells have a key role in induction of necrotic changes. In this work we investigate autophagy and lysosomal protein degradation in the relatively radiation insensitive exocrine pancreatic acini in vivo and in vitro. Type of cell death induced by X-ray was also examined in relation to the changes of the lysosomal processes. In 5h after 16 Gy in vivo whole body irradiation we observed significant increase in the cytoplasmic volume fraction of autophagic vacuoles and in the number of apoptotic cells in vivo. But in the acini isolated from irradiated rats we could not detect a change in the lysosomal degradation of intracellular proteins. Therefore irradiation probably influences the autophagy in an earlier step than lysosomal degradation. Extended necrotic lesions were not observed in vivo as long as 48 h. Isolated pancreatic acini usually contain more autophagic vacuoles than in vivo, but we could not observe additional increase in autophagy after 8 Gy, in vitro irradiation. Lysosomal degradation of intracellular proteins was also unaltered after 8 Gy, in vitro irradiation. Other biochemical functional parameters of the isolated pancreatic acini, like protein synthesis and amylase secretion were not changed either after 8 Gy, in vitro X-ray treatment. These results indicate that pancreatic acinar cells in vitro have a high tolerance to irradiation. The observed in vivo radiation induced changes of the exocrine pancreas are possibly indirectly induced by injuries of more sensitive mechanisms.     

X射线和~(60)Coγ射线辐照食管癌细胞的拉曼光谱研究

食管癌细胞(EC9706)经不同剂量X射线和60Coγ射线辐照后继续培养24h,利用激光拉曼光谱分析EC9706细胞内部蛋白质、核酸、脂类等生物大分子的构象和含量变化。分析发现,两种放射源各剂量组拉曼光谱的峰强和频移与空白对照组之间都存在较大的差异。主要表现为(1)X射线辐照后,对照组光谱中存在的某些谱带,个别剂量组中该谱带却消失。蛋白质主链中骨架C-N振动引起的1114 cm-1谱带在各剂量组中普遍消失,膜脂中膜结合β-胡萝卜素的C=C振动谱带1523 cm-1仅存在于6Gy组。(2)60Coγ射线辐照后,蛋白质酰胺Ⅲ带在中等剂量(4、5Gy)组中β折叠结构向无规卷曲转化,大剂量组中DNA中的磷酸二酯(O-P-O)基团的非氢键化程度增强。拉曼特征峰在不同剂量组中的变化,为进一步从物理能级结构角度研究X射线和60Coγ射线对EC9706细胞的辐照损伤机制提供了实验依据。     

X射线辐照对发根农杆菌介导芸芥遗传转化的影响

探讨了X射线辐照对芸芥发状根诱导的影响, 为研究辐射对转基因技术的协同作用提供一定的实验依据。 以芸芥无菌苗的子叶为材料, 通过5—20 Gy的X射线辐照和不等浸染时间的联合处理, 研究苗龄、 预培养时间、 辐照剂量及其浸染时间等因素对芸芥发状根诱导的影响作用, 并通过聚合链酶式反应（PCR）对所得发状根进行了分子水平的鉴定。 15 Gy X射线辐射能提高芸芥发状根的诱导频率, 且有量效关系, 其中先浸染后辐照比先辐照后浸染效果更显著; PCR结果也表明, 发根农杆菌R1000的 rolB基因已成功地被转入并整合到该发状根的基因组中。 X射线辐照对芸芥发状根的诱导具有一定的促进作用, 且最佳推荐诱导剂量为15 Gy或稍多。     

Hep-2细胞经X射线照射后其培养基吸收光谱的研究

采用日本岛津UV-3101分光光度计测量了受不同剂量X射线照射后继续培养24,48,72h的人上皮样喉癌细胞株Hep-2的培养基RPMI1640(10%胎牛血清)的紫外吸收光谱,分析了该培养基中蛋白质的紫外吸收特性。结果发现：不同剂量组培养基的吸收光谱存在明显的差别,RPMI1640培养基(10%胎牛血清)原在233 nm处的吸收峰在受照细胞生长过程中位移至235 nm附近, 278 nm处的吸收峰随着细胞培养时间的增加而逐渐变的平滑直至消失;各剂量组细胞培养基吸收光谱强度随时间而增加,在细胞受X射线照射后继续培养24,48h时各组培养基吸收强度均低于空白对照组,但到了第72h时均超过了空白组,这反映了该培养基中芳香族氨基酸中各种氨基酸(如色氨酸、酪氨酸、苯丙氨酸)的含量及比例变化,说明癌细胞在生长过程中对芳香族氨基酸的改变不是按等量比的。这些改变与X射线照射引起Hep-2细胞的凋亡及坏死程度有密切的关系,这将为研究人喉癌最佳X射线放射剂量奠定基础。     

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.     

X-ray irradiation-induced changes in Bayfol DPF 5023 polycarbonate

Samples from sheets of the polymeric material Bayfol DPF 5023 have been exposed to X-ray radiation in the dose range 100–2300 Gy. The modifications induced in Bayfol samples due to X-ray irradiation have been studied through different characterization techniques such as X-ray diffraction (XRD), Fourier transform infrared (FTIR) spectroscopy, intrinsic viscosity, refractive index and color difference studies. The infrared spectroscopy indicated that crosslinking is the dominant mechanism at the dose range of 200–2300 Gy. The crosslinking reported by FTIR spectroscopy destroyed the degree of ordering in the Bayfol samples, as revealed by the XRD technique. Also, this crosslinking led to an increase in the value of intrinsic viscosity from 0.54 for the non-irradiated sample to 0.63 for the sample irradiated with 2300 Gy at 30 °C, indicating an increase in the average molecular mass. This was associated with an increase in the refractive index. Additionally, the non-irradiated Bayfol samples showed significant color sensitivity toward X-ray irradiation. This sensitivity appeared in the change of the blue color component of the non-irradiated Bayfol film to yellow after exposure to X-ray doses up to 2300 Gy. This is accompanied by a net increase in the darkness of the samples.     

Investigation of erythrocyte membrane damage under the action of γ radiation in a wide dose range using electroporation

Human erythrocyte membrane damage under the impact of γ radiation on blood suspension is studied in a wide dose range (2–1000 Gy, irradiation dose rate 2.75 Gy/min). It is shown that the irradiation in the absorbed dose range from 600 Gy and higher results in hemolysis of erythrocytes immediately (or within several hours) after irradiation, and the value of the hemolysis rate constant increases with increasing absorbed dose. For finding hidden membrane damage occurring several hours after irradiation with smaller doses, the suspension was affected by a high voltage pulsed electric field (PEF). It is shown that, for an absorbed dose range from 2 to ～350 Gy, no noticeable increase in the erythrocyte hemolysis rate was observed after the action of PEF on the suspension, as compared to the nonirradiated suspension. This testifies that, in this dose range, the degree of membrane damage is small and practically independent of absorbed dose value. For doses from 400 to ～550 Gy, a noticeable increase in the hemolysis rate after the action of PEF growing with increasing absorbed dose was observed.     

利用拉曼光谱研究~(60)Co γ射线对EC9706细胞的辐射损伤

将EC9706细胞经不同剂量^60Coγ射线辐照后继续培养24 h。利用激光拉曼光谱分析EC9706细胞内部蛋白质、核酸、脂类等生物大分子的构象和含量变化。分析结果发现,各剂量组拉曼谱的峰强和频移与空白对照组之间存在较大的差异,主要表现是蛋白质酰胺Ⅲ带1 244 cm^-1谱带在中等剂量组（4、5Gy）β折叠结构向无规卷曲转化;色氨酸残基的吲哚环振动谱带1 341 cm^-1在各剂量组中出现不同程度的红移;782 cm^-1谱带在大剂量组（7、8Gy）红移2～3 cm^-1,说明大剂量γ射线辐照导致DNA中的磷酸二酯（O—P—O）基团的非氢键化程度增强。脂类的CH2和CH3弯曲振动谱带1 446 cm^-1在2、4Gy组蓝移4 cm^-1,其他剂量组频移不大,这与60Coγ射线对EC9706细胞的生物膜造成一定损伤有关。拉曼特征峰在不同剂量组中的变化,为进一步研究60Coγ射线辐照损伤EC9706细胞的最佳剂量提供了一定实验依据。     

低剂量辐射诱导hepG2细胞克隆存活和细胞周期适应性反应

以低剂量γ射线(0.05 Gy)预照射人肝癌细胞hep G2, 8 h后再用高剂量(3 Gy)照射, 测定了细胞的克隆存活率和细胞周期。 结果表明, 低剂量辐射预处理可诱导hep G2细胞产生克隆存活适应性反应, 并且有助于细胞通过G2/M期阻滞; 低剂量辐射诱导的克隆存活适应性反应与增强的通过细胞周期阻滞的能力之间有一定的相关性。 Human hepatoma cells hep G2 were irradiated with 3 Gy of γ ray 8 hours after primed with 0.05 Gy of γ ray, thereafter,cell survival and cell cycle were determined. The results indicated that both survival adaptive response and the enhanced ability to overcome G2/M arrest could be induced by pre irradiation with low dose of γ ray. It is suggested that there is a certain correlation between the survival adaptive response and the enhanced ability to overcome cell cycle arrest.     

X射线和过氧化氢引起的Hela细胞染色质损伤的微区拉曼光谱研究

我们成功地用微区拉曼光谱探针技术获得了培养单个活体 Hela 细胞核中染色质的拉曼光谱。从光谱中我们看到正常 Hele 细胞核蛋白的二级结构为 a 螺旋,DNA 为 A 型构象。经10~(-3)moI/L 过氧化氢处理20分钟及8Gy x 射线照射后的 Hela 细胞核蛋白的二级结构出现反平行β折叠,DNA 出现 B 型构象。这种结果与我们的假设是相符合的。     

辐照诱导的人正常肝细胞系HL-7702细胞延迟效应

利用X射线辐照人正常肝细胞系HL-7702细胞, 运用胞质分离阻滞微核法实验检测细胞微核率,AnnexinV FITC细胞凋亡检测试剂盒检测细胞凋亡率, 细胞微核率和凋亡率随着辐照剂量的增加而显著增加。X射线照射后细胞传代培养, 第7代时不同剂量辐照后子代细胞微核率和凋亡率同未辐照细胞相比已无明显区别。 对不同剂量辐照后传代7代的细胞再次照射2.5 Gy的相同剂量,发现它们细胞微核率和凋亡率存在明显差异,即初次受辐照剂量高的细胞, 再次以相同剂量辐照后的微核率和凋亡率也高. 这些结果表明,X射线辐照导致了HL-7702细胞基因组不稳定性这一辐射延迟效应,再次辐照使得辐射的延迟效应得以明显的表现。 Human normal liver cell line HL-7702 cells were irradiated with different doses of X rays. Micronucleus and apoptosis rates in the irradiated cells were measured with cytokinesis block micronucleus method and Annexin V FITC apoptosis detection kit, respectively. Experimental data showed that the micronucleus and apoptosis rates increased obviously with increasing irradiation dose. After seven population doublings, the micronucleus and apoptosis rates of the cells surviving exposure to the X rays reduced to the same levels as non irradiated control cells; the progenies of the cells were secondly exposed to X rays at the same dose of 2.5 Gy. We found that the progenies of the cells surviving the first irradiations of the various doses showed markedly differential micronucleus frequencies and apoptotic rates. Although the same dose of 2.5 Gy was applied in the second irradiations, the micronucleus frequencies and apoptotic rates of the progenies of the cells initially exposed at higher doses were significantly higher than the others. These results indicate that X rays lead to genomic instability in HL 7702 cells, which is an important manifestation of radiation induced delayed effect, and a second radiation stimulus makes the delayed effect in the progeny of the previously irradiated cells be expressed obviously.     

P53及其相关蛋白对X射线照射肝癌细胞周期的调节

X射线照射人肝癌细胞HepG2， 照射后细胞存活随照射剂量增大明显下降。 流式细胞术分析， 不同剂量组照射后24 h均发生G2期阻滞。 照射后不同时间组的细胞周期分布也有不同， 照射后12 h， 有显著的S期延迟。 Western Blot 显示照射后24 h P53， MDM2， P21蛋白表达上升， 并有时间效应: P53在照射后24 h之内始终维持较高表达, MDM2和P21分别在照射后6和12 h的表达最高。 X射线照射通过影响P53及其相关蛋白的表达影响细胞周期。 HepG2 cells were irradiated with X ray at the doses of 0, 1.0, 2.0, 4.0 or 8.0 Gy and separately maintained in DMEM at 37 ℃ for 0, 6, 12 or 24 h. Colony forming assay showed that cell survival decreased with the irradiation dose increasing. Cell cycle was detected by FACS, the arrest of S phase was found after 12 h irradiation and arrest of G2 phase took place at 24 h after all irradiation doses, which suggested that cell cycle distribution was different in groups gathered after different maintaining time. The results of Western blotting showed that the expression of P53, MDM2 and P21 increased more after irradiation than the control. The expression of P53 remained high at 24 h after irradiation, while the levels of MDM2 or P21 arrived at the highest at 6 h or 12 h after irradiation respectively. The expressions of P21 after irradiation were in corresponding with the cell cycle distribution in the groups of different maintaining time. In conclusion, irradiation change the distribution of cell cycle by effecting the expression of P53 and its related proteins.     

辐射诱导促进AdCMV-p53 转染前列腺癌细胞

用腺病毒重组体（AdCMV p53/GFP）转染经0.5, 1.0和2.0 Gy γ射线辐射处理的前列腺癌细胞[PC 3（ nullp53）], 用克隆形成法检测细胞增殖能力, 用流式细胞分析法测定腺病毒重组体转染率和外源性p53蛋白表达。 结果提示, 辐射诱导使腺病毒重组体转染PC 3细胞提高7%—39%。 辐射联合 AdCMV p53 转染组p53表达水平提高18.5%—35.4%。 与单纯 AdCMV p53 转染组和单纯辐射组相比, 辐射联合 AdCMV-p53 转染组细胞存活率分别降低25%—64%和22%—65%。 To determine whether low dose pre irradiation could enhance adenovirus mediated p53 transfer and expression in human prostate adenocarcinoma, the PC 3 cells were pre exposed to γ rays, and then infected with replication deficient adenovirus recombinant vectors, containing human wild type p53 (AdCMV p53) or green fluorescent protein gene (AdCMV GFP) respectively (γ ray irradiation + AdCMV p53 /GFP infection). The exogenous gene transfer and expression were detected by flow cytometric analysis. The GFP transfer frequencies in γ irradiation + AdCMV GFP infection groups were 7%—39% more than those in AdCMV GFP infection groups. The p53 levels in the γ irradiation + AdCMV p53 infection groups were 18.5%—35.4% more than those in AdCMV p53 infection groups (p<0.05),suggesting that low dose (less than or equal to 1.0 Gy) irradiation could significantly promote exogenous p53 transfer and expression in the PC 3 cells. The survival fractions for the γ irradiation + AdCMV p53 infection groups were 25%—64%, 22%—65% less than those for AdCMV p53 infection, or γ irradiation groups, respectively (p<0.05).     

聚合物光纤辐照特性的实验研究

分析了聚合物受辐照后发生物理化学变化的机理,实验研究了聚苯乙烯（PS）、聚碳酸脂（PC）、聚甲级丙烯酸甲脂（PMMA）三种聚合物光纤在不同辐照剂量下光传输性能的变化以及其恢复特性.在各种辐照剂量下,光透过率有不同程度的下降,经过一段时间后也有不同程度的回复,并且恢复主要发生在停止辐照后的较短时间内.在102 Gy以下,辐照造成的光损伤经过一段时间基本可以恢复,在更高剂量的辐照下(超过5*10³ Gy),辐照对光纤造成了永久损伤,经过很长时间也只能恢复一部分.实验结果表明,PS光纤的抗辐照特性最好,PC光纤优于PMMA光纤.     

重离子束辐照对荷颊囊癌金黄地鼠血清微量元素的影响

探讨了重离子束辐照后荷颊囊癌金黄地鼠血清中微量元素含量的变化趋势。采用0, 4, 6, 8和12 Gy剂量的12C6+ 离子束对荷颊囊癌金黄地鼠辐照治疗后28 d取血, 应用原子吸收光谱仪火焰法测定血清中Fe, Cu, Zn, Mg和Ca 5种微量元素的含量。金黄地鼠成瘤后, 血清中微量Cu, Zn, Ca和Mg元素含量下降, 均明显低于正常组（P<0.05）; 不同剂量的重离子束辐照后28 d, 血清中5种微量元素在低剂量时均呈现继续下降趋势, 在6或8 Gy时恢复到正常组水平, 到12 Gy再呈降低的趋势, 存在一定的剂量-反应关系。重离子束辐照影响荷颊囊癌金地鼠血清微量元素的含量, 具有一定的临床意义。 To study the trend of the changes of trace elements in serum of golden hamster with cheek pouch carcinoma after irradiation by heavy ion beam, the cheek pouch carcinoma of golden hamster was exposed to different doses of heavy ion beam, after 4 weeks, the contents of Cu, Zn, Fe, Mg and Ca in serum were detected by flame method of Atomic Absorption Spectrometer. The contents of Cu, Zn, Ca and Mg in experimental groups with cheek pouch carcinoma were significantly lower than that of the normal group (P<0.05). After irradiated by 0, 4, 6, 8, 12 Gy heavy ion beam, the 4 Gy group showed a tendency downward, when the irradiation dose reached 6 Gy, the contents of Fe, Zn were increased, and decreased at 12 Gy. While Cu, Ca and Mg content of 8 Gy group rose to the highest, and decreased at 12 Gy. All of the results showed a dose reaction relationship (P<0.05). The irradiation of heavy ion beam maybe significantly affect the content of trace elements in serum of golden hamster with cheek pouch carcinoma.     

低剂量连续辐射引起的小鼠免疫系统的变化

为了评估低剂量X射线连续辐射对BALB/c小鼠健康机体免疫系统的影响, 实验采用X射线全身连续照射BALB/c小鼠, 照射第一天剂量为0.07 Gy, 剂量率0.2 Gy/min, 之后每天照射0.08 Gy, 共照射12 d, 累积剂量1.03 Gy, 照射后24和48 h取血、胸腺和脾脏。 流式细胞仪检测免疫细胞周期和凋亡的变化, 胸腺和脾脏指数用重量法获取。 实验结果表明, 小鼠胸腺细胞的周期在照射后24 h被阻滞在G2/M期; 外周血淋巴和胸腺细胞周期48 h被阻滞在 G0/G1期, 细胞凋亡比例在照射后两个时间点都显著增加; 脾脏淋巴细胞周期24 h被阻滞在 G0/G1期, 48 h被阻滞在 S期, 细胞凋亡比例在24和48 h显著减少; 脾脏指数在照射后48 h显著减少。 故低剂量X射线连续全身照射BALB/c小鼠可激活免疫细胞不同的周期监测点, 引起免疫细胞凋亡比例发生变化, 造成一定的辐射损伤, 且这种影响随着免疫器官的不同而不同。 For estimating the effect of low doses X ray continual irradiation to immunity system of mouse, BALB/c mice were continually irradiated to 1.03 Gy by X rays at a dose rate of 0.2 Gy/min in 13 d. At 24 or 48 h after irradiation, the immunocyte cycle and apoptosis were determined by flow cytometry, and the thymus and spleen weights were measured too. The results showed that the cycle of thymocyte were arrested in G2/M at 24 h, the number of peripheral blood lymphocytes and thymocytes in G0/G1 phase at 48 h was up and the percentage of apoptosis had a significance increase in both of time points; the cycle of spleen lymphocytes was delayed in G0/G1 at 24 h, in S phase at 48 h, the apoptosis had a significance decrase at 24 and 48 h; spleen index declined significantly at 48 h. The results suggested that low doses continual X ray whole body irradiation could activate different cell cycle checkpoints, and result in some changes of apoptosis and some damages to immunocytes. The continual X ray irradiation affects the organs differently, it might provide experiment basis for radioprotection.     

ROS enhancement by silicon nanoparticles in X-ray irradiated aqueous suspensions and in glioma C6 cells

The capability of silicon nanoparticles to increase the yield of reactive species upon 4 MeV X-ray irradiation of aqueous suspensions and C6 glioma cell cultures was investigated. ROS generation was detected and quantified using several specific probes. The particles were characterized by FTIR, XPS, TEM, DLS, luminescence, and adsorption spectroscopy before and after irradiation to evaluate the effect of high energy radiation on their structure. The total concentration of O₂ ^•−/HO₂ ^•, HO^•, and H₂O₂ generated upon 4-MeV X-ray irradiation of 6.4 μM silicon nanoparticle aqueous suspensions were on the order of 10 μM per Gy, ten times higher than that obtained in similar experiments but in the absence of particles. Cytotoxic ¹O₂ was generated only in irradiation experiments containing the particles. The particle surface became oxidized to SiO₂ and the luminescence yield reduced with the irradiation dose. Changes in the surface morphology did not affect, within the experimental error, the yields of ROS generated per Gy. X-ray irradiation of glioma C6 cell cultures with incorporated silicon nanoparticles showed a marked production of ROS proportional to the radiation dose received. In the absence of nanoparticles, the cells showed no irradiation-enhanced ROS generation. The obtained results indicate that silicon nanoparticles of <5 nm size have the potential to be used as radiosensitizers for improving the outcomes of cancer radiotherapy. Their capability of producing ¹O₂ upon X-ray irradiation opens novel approaches in the design of therapy strategies.     

Spatial and temporal distribution of γH2AX fluorescence in human cell cultures following synchrotron‐generated X‐ray microbeams: lack of correlation between persistent γH2AX foci and apoptosis

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).     

Dose effects on the long persistent luminescence properties of beta irradiated SrAl2O4:Eu2+, Dy3+ phosphor

The SrAl₂O₄:Eu²⁺, Dy³⁺ is a phosphor characterized by a long persistent luminescence (PLUM) when it is excited with UV–VIS light and ionizing radiation. In this paper, we study the PLUM behavior as a function of beta irradiation dose in the 0–650 Gy range with a fixed dose rate of 5 Gy/min. The PLUM intensity showed a complex decay behavior, exhibiting a near linear response in the 0–1.7 Gy low dose range and gradually increasing up to 160 Gy. The PLUM reached the saturation for higher doses (>275 Gy) with a slight decrease in the range of 300–650 Gy. In addition, a systematic PLUM enhancement was produced after a thermal cleaning procedure and irradiation at RT in a series of 10 cycles. The observed phenomenon may be related to a radiation-induced process of charge trapping accumulation, which is triggered by thermal stimulation during the irradiation stage. It improves the luminescent characteristics of SrAl₂O₄:Eu²⁺, Dy³⁺ phosphors rendering them suitable for permanent display and illumination devices.