和厚朴酚对非小细胞肺癌细胞的辐射增敏效应

研究了和厚朴酚（HNK）对非小细胞肺癌（NSCLC）细胞系A549和H1299对低线性能量转移（LET） X射线和高LET碳离子的辐射增敏效应。首先用CCK-8检测了HNK对A549和H1299细胞的生长抑制情况,发现20 μmol/L的HNK处理对细胞的生长抑制作用较弱。用该浓度HNK预处理细胞2 h后给予不同剂量X射线或碳离子的照射,克隆存活法检测细胞的辐射敏感性,Annexin-PI双染法检测细胞凋亡,γH2AX焦点法检测DNA的双链断裂（DSB）损伤。实验结果显示:与X射线相比,NSCLC细胞对碳离子更敏感,HNK预处理仅对碳离子照射有辐射增敏作用;与碳离子单独照射相比,HNK预处理联合碳离子照射诱导了更明显的细胞凋亡;在照射后24 h,HNK预处理联合碳离子照射引起的细胞γH2AX焦点阳性率维持在较高水平,而X射线照射没有这些效应。实验结果表明,HNK预处理抑制了NSCLC细胞DNA的DSB修复,诱导了细胞凋亡的发生,从而提高了细胞对碳离子的辐射敏感性。The radiosensitizing effect of Honokiol (HNK) on non-small cell lung carcinoma (NSCLC) cell lines A549 and H1299 to low-linear energy transfer (LET) X-rays and high-LET carbon ions was investigated in this study. First, the inhibitory effects of HNK on the growth of A549 and H1299 cells were detected by CCK-8 assay, and 20 μmol/L HNK treatment was found to induce a growth inhibitory effect slightly in these two cell lines. Cells were pre-treated with HNK and then irradiated with X-rays and carbon ions of different doses. Cellular radiosensitivity, apoptosis and DNA damage were analyzed by clonogenic survival, Annexin-PI staining and γH2AX foci, respectively. The results showed the cells were more sensitive to carbon ion irradiation compared to X-rays and the radiosensitization of HNK was only observed after carbon ion irradiation. Furthermore, the co-treatment led to higher apoptosis rate 48 h after irradiation and increased the positive rate of γH2AX foci 24 h after irradiation in A549 and H1299 cells compared with those in the groups treated with carbon ion irradiation alone. These phenomena were not observed after X-ray irradiation. Our data suggest that the pre-treatment with HNK inhibited DNA DSB repair, induced apoptosis and then enhanced the cellular radiosensitivity to carbon ions in NSCLC cells.     

辐照诱导人正常肝细胞系HL-7702 细胞远后的微卫星不稳定性

采用高传能线密度(LET) 的12C6+离子束和低LET 的X 射线辐照人正常肝细胞系HL-7702 细胞,利用微卫星不稳定性(MSI) 检测来分析直接受照射细胞和通过转移培养基方式旁细胞传代八代子细胞以MSI 表征的远后效应。实验结果表明,12C6+离子束诱导的远后效应较X射线的低;旁细胞的远后效应较直接受照射细胞的高;辐射引起的MSI 与杂合性丢失(LOH) 的发生率具有位点特异性。结果提示,重离子放射治疗较X 射线放射治疗对正常组织引发的辐射风险要小,可通过对MSI 高发位点的筛选来评估放疗后患者长期生存状况和二次癌症发生风险。Human normal liver cell line HL-7702 cells were irradiated with high linear energy transfer (LET) 12C6+ ions and low-LET X-rays, respectively. Delayed effect in terms of microsatellite instability (MSI) in progenies of the directly irradiated cells and bystander cells, obtained in the way of medium transfer at the 8th passage postirradiation,were examined. The delayed effect induced by the high-LET 12C6+ ions was different from that induced by the low-LET X-rays, and a higher incidence of MSI was observed in the progenies of the cells after exposure to the X-rays than to the 12C6+ ions. We also found that the delayed effect in the progenies of the bystander cells was much more severe than thoseof directly irradiated cells. Furthermore, the events of MSI and loss of heterozygosity (LOH) induced by the ionizing radiations were not randomly distributed throughout the genome and specific loci existed indeed. These results imply that the radiation risk to normal tissues is lower in heavy ion therapy than in conventional X-ray radiotherapy, and the analysis of microsatellite loci with MSI high frequency occurrence can be applied to access long-term survival condition and second cancer risk for the patients after radiotherapy.     

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.     

C离子辐照引起细胞分泌旁效应信号因子浓度随时间的变化

信号因子通常能介导旁效应的发生。 利用高LET C离子辐照体外培养的人肝癌QGY-7703细胞, 检测辐照后不同时刻培养基中信号因子TGF-β1和NO的浓度, 并通过转移培养基法检测照射后不同时刻转移培养基对人肝L02旁细胞存活率和代谢活力的影响, 发现受照射细胞在时间与空间上调控着周围信号因子的浓度, 并且通过信号因子浓度的变化影响旁细胞的各种效应发生。 实验为旁效应的解释提供了新的实验数据。 Signaling factors usually play an important role in bystander effect. In this work, human hepatoma QGY 7703 cells in vitro were irradiated with high LET carbon ions. Concentrations of signaling factors such as TGF-β1 and NO were measured in the media of the irradiated QGY-7703 cells at different time points after irradiation. The conditioned media harvested at various times post irradiation were transferred to human hepatocyte L02 cells as bystander cells and then the influence of the conditioned media on survival fraction and cell viability of the bystander cells were determined. The results show that the irradiated cells regulate the concentration of the signaling factors released nearby themselves temporally and spatially, and the bystander cells response to the signaling factors differentially according to the concentration change. This work provides new basic data for exploring the bystander effect, especially caused by high LET radiation.     

碳离子辐射诱导秀丽隐杆线虫生殖细胞凋亡研究

重离子辐射具有独特的深度剂量分布和较高的相对生物学效应,被认为是理想的放疗手段。重离子的生物学效应在径迹形成过程中由多个物理参量共同决定,而这些物理参量和离子入射深度紧密相关,因此明确离子不同入射深度的生物学效应对重离子肿瘤放疗方案的设计和优化有着重要的理论和应用价值。使用兰州重离子研究装置HIRFL-CSRe 终端的碳离子束作为辐射源,以活体模式动物线虫作为实验对象,以线虫生殖细胞的凋亡水平作为生物学检测终点,研究了10 和20 Gy 碳离子辐射在辐射的入口、坪区和峰区的当代生物学效应和对后代个体基因组不稳定性的影响。结果表明:10 和20 Gy 碳离子辐射在三个不同的辐照区域内均显著增加了辐射当代的线虫生殖腺细胞的凋亡水平,并表现出一定的辐射区域和辐射剂量依赖性。同时,辐射诱导的后代个体基因组不稳定性也表现出一定的辐射区域和辐射剂量相关性。Heavy ion irradiation is a perfect means in radio-therapy due to its special depth dose distribution and high relative biological effects. The biological effects of heavy ion irradiation are determined by some major physical parameters, and vary along the tracks of heavy ions. Therefore, it is very significant for the tumor radio-therapy to investigate the biological effects along whole range of heavy ion radiation. In the present study, Caenorhabditis elegans, a model in vivo, was irradiated by carbon ion beams from HCRFL-CSRe, The level of germ cell apoptosis of worms was used as a checking endpoint for DNA damage, the effects of carbon irradiation located in the entrance, plateau and peak regions on the genomic instability of the irradiated worm and their progeny were detected. The results showed that the 10 and 20 Gy of carbon ion radiations led to the increased germ cell apoptosis in irradiated worms and these effects depend on the worm location along the range of carbon ions and the irradiation dosage. The results also suggested that heavy ion irradiation induced the up-regulated genomic instability in their progeny, and might be related to both the irradiation dose and the irradiated location.     

乏氧细胞线粒体与肿瘤辐射抗性

综述了乏氧环境对细胞整体和对线粒体的影响,正常细胞线粒体呼吸链在乏氧环境下的损伤及其与肿瘤的关系,并对肿瘤细胞适应乏氧环境的机制进行了阐述。总结了线粒体作为供能细胞器,对肿瘤细胞在乏氧条件下生长、侵袭和转移及获取能量过程中的作用,并介绍了中国科学科院近代物理研究所利用重离子辐照所做的相关研究成果,包括不同剂量重离子对线粒体DNA超螺旋构象及线粒体功能的影响,同一剂量不同时间重离子辐照后对线粒体DNA 4 977 大片段损伤累积的影响。The hypoxia environment on the cells and mitochondria, and the damage of normal cells mitochondrial respiratory chain in hypoxia and its relationship with tumors are reviewed. In addition, the tumor radiation resistance mechanism in hypoxia are summarized. It also expounds that mitochondria, as energy supply organelles for cells, are related to tumor cells growth, invasion and metastasis in hypoxia environment, besides, it gives a brief introduction to the mitochondria study of the Institute of Modern Physics, Chinese Academy of Sciences with heavy ion irradiation, including effects of different dose of heavy ion on mitochondrial DNA superhelix conformation and function of mitochondria,and the influence on mitochondrial DNA 4 977 damage cumulation in different time after the same dose of heavy ion irradiation.     

Copper Ion Beam Irradiation-Induced Effects on Structural,Morphological and Optical Properties of Tin Dioxide Nanowires

The 0.8 MeV copper(Cu) ion beam irradiation-induced effects on structural,morphological and optical properties of tin dioxide nanowires(SnO_2 NWs) are investigated.The samples are irradiated at three different doses5 × 10~(12) ions/cm~2,1 × 10~(13) ions/cm~2 and 5 × 10~(13) ions/cm~2 at room temperature.The XRD analysis shows that the tetragonal phase of SnO_2 NWs remains stable after Cu ion irradiation,but with increasing irradiation dose level the crystal size increases due to ion beam induced coalescence of NWs.The FTIR spectra of pristine SnO_2NWs exhibit the chemical composition of SnO_2 while the Cu-O bond is also observed in the FTIR spectra after Cu ion beam irradiation.The presence of Cu impurity in SnO_2 is further confirmed by calculating the stopping range of Cu ions by using TRM/SRIM code.Optical properties of SnO_2 NWs are studied before and after Cu ion irradiation.Band gap analysis reveals that the band gap of irradiated samples is found to decrease compared with the pristine sample.Therefore,ion beam irradiation is a promising technology for nanoengineering and band gap tailoring.     

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.     

Survivin表达在高LET射线诱导细胞凋亡中

先前的研究表明, 肿瘤细胞中survivin的高表达与细胞对高传能线密度(LET)射线的辐射抗性相关。 研究了survivin表达在高LET射线诱导的细胞凋亡中的作用, 发现抑制survivin表达对高LET C离子辐射诱导的Bcl-2和Bax表达没有明显的影响。 在高LET射线辐照中, survivin可能通过抑制caspase-3和-9活性的途径, 抑制了细胞凋亡。It has been proven that over expression of survivin in cancerous cell lines is related to the radioresistance of cells to high LET radiation in previous work. In this study, action mechanisms of survivin gene in apoptosis induced by high LET radiation were investigated. We found that inhibiting survivin by siRNA had no notable influence on Bcl-2 and Bax expressions induced by carbon ions. Survivin depressed cell apoptosis through the inhibition of the activities of caspase-3 and -9 possibly in cell apoptosis induced by high LET radiation.     

X射线诱导的HeLa细胞旁效应中ROS和NO关系研究

活性氧(ROS)和一氧化氮（NO)是辐射诱导的旁效应信号通路中的两个重要信号分子。 实验研究了这两种信号分子在HeLa细胞旁效应信号通路中的关系。 通过微核实验, 发现X射线辐照过的HeLa细胞及其旁观者细胞微核形成明显增加, 而二甲亚砜（DMSO）预处理显著抑制了微核形成。 另外还发现, 接受条件培养基的旁观者细胞的增殖速率增加, 而DMSO预处理产生条件培养基的受辐照细胞则使旁观者细胞的增殖速率降低。 以上的结果从不同角度证实了HeLa细胞存在X射线诱导的旁效应, 且其可以被DMSO预处理所抑制。Western blotting和DAF FM DA荧光探针检测分别显示出辐照后细胞的诱导型一氧化氮合酶（iNOS）和NO水平均升高, 而DMSO预处理则降低其水平。 因此, 可以推测X射线诱导的HeLa旁效应当中ROS是NO的上游信号。 Accumulating evidence indicates that irradiated cells can release signals which induce a series of biological responses in non exposed cells. This is known as irradiation induced bystander effects. Both reactive oxygen species(ROS) and nitric oxide(NO) play important roles in bystander effects. In this study, we determined the relationship of ROS and NO in the signaling pathway of bystander effects. HeLa cells were treated with or without dimethye sulfoxide(DMSO) before X ray irradiation, and micronuclei formation as well as cell proliferation rate was detected in both irradiated and bystander cells. In addition, we also detected inducible nitric oxide synthase(iNOS) expression and NO level in irradiated cells using Western blotting and DAF FM DA fluorescent probe, respectively. Our results showed that micronuclei were induced in irradiated and bystander cells while DMSO treatment significantly suppressed the formation of micronuclei in both of them. We also found that when cells were irradiated their proliferation rate was suppressed while DMSO treatment eliminated this inhibition effect. In contrast, the cells received conditioned medium from irradiated cells proliferated more quickly than the cells received medium from non irradiated cells while DMSO treatment reduced the difference. Finally, we found that irradiated cells had higher level of iNOS and NO compared to non irradiated controls, whereas DMSO treatment decreased their levels. These results suggest that ROS is the upstream signal of NO in X ray induced bystander effects in HeLa cells.     

重离子辐照对人肝癌HepG2细胞蛋白质组图谱的影响

分别制备经1 Gy C离子辐照和未经辐照人肝癌HepG2细胞的总蛋白样品, 采用固相pH梯度双向凝胶电泳技术进行蛋白分离, 用ImageMaster 2D双向电泳凝胶图像分析软件分析数字化图谱。 结果显示, 差异表达的蛋白质点为17个, 其中1个仅在未经C离子辐照的HepG2细胞中表达, 8个蛋白质点在辐照后的细胞中表达上调, 8个蛋白质点在辐照后的细胞中表达下调。 建立了重复性较好和分辨率较高的分离HepG2细胞总蛋白的双向电泳技术。 实验结果表明, C离子辐照HepG2细胞后其蛋白质组发生了改变。     

Differential expression of cancer pathway-related genes in low-versus high-dose-rate-irradiated AKR/J mice

To understand the biological effects of ionizing radiation on lymphomagenesis, we reared AKR/J mice for 130 days with exposure to either high-dose-rate (HDR, 0.8 Gy/min, a single dose of 4.5 Gy) or low-dose-rate (LDR, 0.7 mGy/h, a cumulative dose of 2.1 Gy) irradiation. After 130 days, we compared the mean thymus weight, analyzed the histological changes, and measured apoptotic cell numbers using the terminal deoxynucleotidyl transferase-mediated dUTP-end labeling (TUNEL) assay. We also used microarrays and quantitative polymerase chain reaction analysis (qPCR) to analyze the expression profiles of cancer pathway-related genes in the thymuses of the mice. The mean thymus weight of the LDR-irradiated mice decreased relative to Sham- and HDR-irradiated mice. Histopathological examination revealed that the neoplastic cells in the thymuses of the Sham- and HDR-irradiated mice were pleomorphic, with marked anisocytosis and anisokaryosis, whereas the cells and their nuclei were relatively small and uniform in size in the LDR-irradiated mice. Furthermore, TUNEL assays showed that the number of apoptotic cells was higher in the LDR-irradiated mice than in the Sham- and HDR-irradiated mice. Microarray analysis showed differentially expressed genes according to carcinogenic stage (DNA repair/genomic instability, DNA damage signaling pathway, cell cycle, cancer pathway, p53 signaling pathway, apoptosis, and T- and B-cell activation). qPCR data for cancer pathway-related genes showed that Cds1 gene expression was upregulated in the LDR-irradiated mice, whereas expression of the Itga4, Myc, and Itgb1 genes was upregulated in the irradiated mice. However, the functions of cancer pathway-related genes require further study and validation.     

内质网应激对碳离子辐照宫颈癌HeLa 细胞的影响

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。To investigate the effect of endoplasmic reticulum stress on HeLa cells to 12C6+ ion irradiation,HeLa cells were pretreated with 2.5 mmol/L dithiothreitol and irradiated by 12C6+ ions with different doses.The results showed that, compared with IR alone, dithiothreitol combined with carbon ion irradiation caused HeLa cell survival decreased, and the apoptosis increased. Moreover, dithiothreitol and carbon ion radiation combination treatment led to a significant increase of G2/M phase, and autophagy was activated obviously in combination treatment group. The results imply that continuous endoplasmic reticulum stress can change the response of HeLa cells to 12C6+ irradiation, and dithiothreitol may affect HeLa cells through the autophagy cell death pathway.     

模拟微重力效应对辐射致细胞DNA损伤修复效应的影响

在地面模拟微重力的情况下, 应用碱性单细胞凝胶电泳（SCGE）技术对80 MeV/u Ne离子辐射诱发人血淋巴细胞DNA损伤修复效应进行了研究。 在不同时刻对相同剂量辐照后的淋巴细胞经单细胞电泳处理后显示, 在模拟微重力下孵育的彗星尾更长, 彗星头面积更小。 这表明, 相对地面环境而言, 模拟微重力环境对淋巴细胞的DNA损伤修复有一定的抑制作用。 Effect of the modeled microgravity (MMG) on heavy ion induced lymphocytes DNA repair by using single cell gel electrophoresis (SCGE) has been studied. The results showed that residual DNA damage induced by Ne ions irradiation increased more in cultures incubated in MMG than in 1 g, which indicated that MMG incubation after Ne ions irradiation reduce the DNA damage repair capacity.     

MicroRNA-19b通过下调BTG1增加重离子辐射诱导的基因组不稳定性

重离子束放疗可有效杀死肿瘤细胞。研究表明:重离子束能引起癌细胞的基因异常,引发基因组不稳定性。BTG1作为一个重要的G0/G1期相关蛋白,具有强烈的抗细胞增殖能力。以碳离子辐射为手段,通过蛋白质印迹杂交技术发现:人肾癌786-O细胞中BTG1能够对重离子辐射应激产生应答。同时,荧光定量PCR结果显示碳离子辐照后,BTG1转录本与micro RNA-19b的表达水平呈负相关变化。瞬时转染micro RNA-19b类似物于人肾癌786-O细胞中,能够抑制由碳离子辐射引起的BTG1蛋白上调,并增加细胞的微核发生率。因此micro RNA-19b能够通过抑制BTG1的表达,增加重离子辐射诱导的细胞基因组不稳定性。     

彗星电泳检测 12C6+离子束辐照人类肝L02细胞的DNA损伤效应

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。     

两种保护剂对C离子诱导小鼠急性肝损伤的应答

比较了N-乙酰半胱氨酸(NAC)及乙酰左旋肉毒碱(ALCAR)对12C6+离子照射小鼠的损伤效应,并探讨了其可能的作用机制。利用4Gy剂量的12C6+离子束对预先给予NAC(100mg/kg)和ALCAR(100mg/kg)保护的昆明小鼠进行单次全身照射。随后检测肝组织中总抗氧化能力(TAC)、DNA单链断裂和细胞凋亡率。结果显示,与照射对照组相比,提前给予NAC和ALCAR均极显著地增强了肝组织的抗氧化能力(P0.001),减轻了12C6+离子导致的肝组织中DNA断裂(P0.001)和细胞凋亡(P0.001)。此外,还发现ALCAR组抗重离子辐照损伤的能力显著地高于NAC组(P0.05)。实验结果提示了NAC和ALCAR可通过抵御组织内的氧化胁迫,阻止DNA链的断裂和细胞的凋亡,实现对C离子辐照损伤的保护效应。而且ALCAR比NAC可能更适合成为有潜力、有希望的抗C重离子辐射药物。