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Chromosomal aberrations induced by ionizing radiation at different doses  [cached]
Anisoara Nevoie,Mihaela Pascariu,Ivanov Iuliu,Daniela Jitaru
Analele ?tiin?ifice Ale Universit??ii Alexandru Ioan Cuza din Ia?i,Sectiunea II A : Genetica si Biologie Moleculara , 2010,
Abstract: The present study was designed to evaluate the in vitro effect of ionizing radiation in human peripheral blood mononuclear cell cultures. We studied the chromosomal aberration induced by X ray in normal human peripheral blood mononuclear cell cultures. Different doses (0.8 Gy, 2 Gy and 5 Gy) for irradiation of human cell cultures were used for this study. Chromosome aberration analysis was carried out at 48 and 72 hours from irradiation. Radiation- induced chromosomal modifications were detected by karyotyping. The obtained results strongly suggest that normal cells can repair at low doses.
Low Doses of Ionizing Radiation Promote Tumor Growth and Metastasis by Enhancing Angiogenesis  [PDF]
Inês Sofia Vala,Leila R. Martins,Natsuko Imaizumi,Raquel J. Nunes,José Rino,Fran?ois Kuonen,Lara M. Carvalho,Curzio Rüegg,Isabel Monteiro Grillo,Jo?o Taborda Barata,Marc Mareel,Susana Constantino Rosa Santos
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011222
Abstract: Radiotherapy is a widely used treatment option in cancer. However, recent evidence suggests that doses of ionizing radiation (IR) delivered inside the tumor target volume, during fractionated radiotherapy, can promote tumor invasion and metastasis. Furthermore, the tissues that surround the tumor area are also exposed to low doses of IR that are lower than those delivered inside the tumor mass, because external radiotherapy is delivered to the tumor through multiple radiation beams, in order to prevent damage of organs at risk. The biological effects of these low doses of IR on the healthy tissue surrounding the tumor area, and in particular on the vasculature remain largely to be determined. We found that doses of IR lower or equal to 0.8 Gy enhance endothelial cell migration without impinging on cell proliferation or survival. Moreover, we show that low-dose IR induces a rapid phosphorylation of several endothelial cell proteins, including the Vascular Endothelial Growth Factor (VEGF) Receptor-2 and induces VEGF production in hypoxia mimicking conditions. By activating the VEGF Receptor-2, low-dose IR enhances endothelial cell migration and prevents endothelial cell death promoted by an anti-angiogenic drug, bevacizumab. In addition, we observed that low-dose IR accelerates embryonic angiogenic sprouting during zebrafish development and promotes adult angiogenesis during zebrafish fin regeneration and in the murine Matrigel assay. Using murine experimental models of leukemia and orthotopic breast cancer, we show that low-dose IR promotes tumor growth and metastasis and that these effects were prevented by the administration of a VEGF receptor-tyrosine kinase inhibitor immediately before IR exposure. These findings demonstrate a new mechanism to the understanding of the potential pro-metastatic effect of IR and may provide a new rationale basis to the improvement of current radiotherapy protocols.
Infrared investigation of hard human teeth tissues exposed to various doses of ionizing radiation from the 1986 Chernobyl accident  [PDF]
L. A. Darchuk,L. V. Zaverbna,V. G. Bebeshko,A. Worobiec,E. A. Stefaniak,R. Van Grieken
Spectroscopy: An International Journal , 2008, DOI: 10.3233/spe-2008-0336
Abstract: Infrared spectroscopy (IR) was applied to study changes in solid teeth tissues of persons exposed to low (0.12–0.20 Gy) and high (0.5–1.7 Gy) doses of ionizing radiation during their work in the Chernobyl zone after the accident. Changes in the inorganic and organic matrix of teeth were noted for both high and low radiation doses. The obtained results demonstrated that high doses of radiation lead to imbalance between phosphate–carbonate phases level (because of increasing of CO32? content) and accumulation of soluble phosphates in the mineral part of the teeth. These changes have an effect on dental matrix strength. Low doses of radiation do not induce appreciable negative changes in the mineral part of all tooth tissues but lead to changes in organic matrix of teeth (in collagen).
Membrane Signaling Induced by High Doses of Ionizing Radiation in the Endothelial Compartment. Relevance in Radiation Toxicity  [PDF]
Isabelle Corre,Ma?va Guillonneau,Fran?ois Paris
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms141122678
Abstract: Tumor areas can now be very precisely delimited thanks to technical progress in imaging and ballistics. This has also led to the development of novel radiotherapy protocols, delivering higher doses of ionizing radiation directly to cancer cells. Despite this, radiation toxicity in healthy tissue remains a major issue, particularly with dose-escalation in these new protocols. Acute and late tissue damage following irradiation have both been linked to the endothelium irrigating normal tissues. The molecular mechanisms involved in the endothelial response to high doses of radiation are associated with signaling from the plasma membrane, mainly via the acid sphingomyelinase/ceramide pathway. This review describes this signaling pathway and discusses the relevance of targeting endothelial signaling to protect healthy tissues from the deleterious effects of high doses of radiation.
High and Low Doses of Ionizing Radiation Induce Different Secretome Profiles in a Human Skin Model  [PDF]
Qibin Zhang, Melissa Matzke, Athena A. Schepmoes, Ronald J. Moore, Bobbie-Jo Webb-Robertson, Zeping Hu, Matthew E. Monroe, Wei-Jun Qian, Richard D. Smith, William F. Morgan
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0092332
Abstract: It is postulated that secreted soluble factors are important contributors of bystander effect and adaptive responses observed in low dose ionizing radiation. Using multidimensional liquid chromatography-mass spectrometry based proteomics, we quantified the changes of skin tissue secretome – the proteins secreted from a full thickness, reconstituted 3-dimensional skin tissue model 48 hr after exposure to 3, 10 and 200 cGy of X-rays. Overall, 135 proteins showed statistical significant difference between the sham (0 cGy) and any of the irradiated groups (3, 10 or 200 cGy) on the basis of Dunnett adjusted t-test; among these, 97 proteins showed a trend of downregulation and 9 proteins showed a trend of upregulation with increasing radiation dose. In addition, there were 21 and 8 proteins observed to have irregular trends with the 10 cGy irradiated group either having the highest or the lowest level among all three radiated doses. Moreover, two proteins, carboxypeptidase E and ubiquitin carboxyl-terminal hydrolase isozyme L1 were sensitive to ionizing radiation, but relatively independent of radiation dose. Conversely, proteasome activator complex subunit 2 protein appeared to be sensitive to the dose of radiation, as rapid upregulation of this protein was observed when radiation doses were increased from 3, to 10 or 200 cGy. These results suggest that different mechanisms of action exist at the secretome level for low and high doses of ionizing radiation.
Effects of Low Doses of Ionizing Radiation Exposures on Stress-Responsive Gene Expression in Human Embryonic Stem Cells  [PDF]
Mykyta Sokolov,Ronald Neumann
International Journal of Molecular Sciences , 2014, DOI: 10.3390/ijms15010588
Abstract: There is a great deal of uncertainty on how low (≤0.1 Gy) doses of ionizing radiation (IR) affect human cells, partly due to a lack of suitable experimental model systems for such studies. The uncertainties arising from low-dose IR human data undermine practical societal needs to predict health risks emerging from diagnostic medical tests’ radiation, natural background radiation, and environmental radiological accidents. To eliminate a variability associated with remarkable differences in radioresponses of hundreds of differentiated cell types, we established a novel, human embryonic stem cell (hESC)-based model to examine the radiobiological effects in human cells. Our aim is to comprehensively elucidate the gene expression changes in a panel of various hESC lines following low IR doses of 0.01; 0.05; 0.1 Gy; and, as a reference, relatively high dose of 1 Gy of IR. Here, we examined the dynamics of transcriptional changes of well-established IR-responsive set of genes, including CDKN1A, GADD45A, etc. at 2 and 16 h post-IR, representing “early” and “late” radioresponses of hESCs. Our findings suggest the temporal- and hESC line-dependence of stress gene radioresponses with no statistically significant evidence for a linear dose-response relationship within the lowest doses of IR exposures.
Phosphoproteomics and Lung Cancer Research  [PDF]
Elena López,William C. S. Cho
International Journal of Molecular Sciences , 2012, DOI: 10.3390/ijms131012287
Abstract: Massive evidence suggests that genetic abnormalities contribute to the development of lung cancer. These molecular abnormalities may serve as diagnostic, prognostic and predictive biomarkers for this deadly disease. It is imperative to search these biomarkers in different tumorigenesis pathways so as to provide the most appropriate therapy for each individual patient with lung malignancy. Phosphoproteomics is a promising technology for the identification of biomarkers and novel therapeutic targets for cancer. Thousands of proteins interact via physical and chemical association. Moreover, some proteins can covalently modify other proteins post-translationally. These post-translational modifications ultimately give rise to the emergent functions of cells in sequence, space and time. Phosphoproteomics clinical researches imply the comprehensive analysis of the proteins that are expressed in cells or tissues and can be employed at different stages. In addition, understanding the functions of phosphorylated proteins requires the study of proteomes as linked systems rather than collections of individual protein molecules. In fact, proteomics approaches coupled with affinity chromatography strategies followed by mass spectrometry have been used to elucidate relevant biological questions. This article will discuss the relevant clues of post-translational modifications, phosphorylated proteins, and useful proteomics approaches to identify molecular cancer signatures. The recent progress in phosphoproteomics research in lung cancer will be also discussed.
Low doses of gamma ionizing radiation increase hprt mutant frequencies of TK6 cells without triggering the mutator phenotype pathway
Ayres, Flávio Monteiro;Cruz, Aparecido Divino da;Steele, Patricia;Glickman, Barry W.;
Genetics and Molecular Biology , 2006, DOI: 10.1590/S1415-47572006000300027
Abstract: the tk6 lymphoblastoid cell line is known to be mismatch repair (mmr) and p53 proficient. deficiency in mmr results in a mutator phenotype characterized by microsatellite instability (msi) and increased hprt mutant frequency (mf). increased hprt mf is also a biomarker of effect for exposure to ionizing radiation. in order to test if a mutator phenotype could be induced by low doses of gamma ionizing radiation, an hprt cloning assay and a msi investigation were performed after radiation exposure. the spontaneous mf was 1.6 x 10-6. the groups exposed to 0.2, 0.5 and 1.0 gy had hprt mfs of 2.3, 3.3 and 2.2 x 10-6, respectively. the spontaneous msi frequency per allele in non-selected cells was 5.4 x 10-3, as evidenced at the loci d11s35, nm23-h1, d8s135 and p53. msi frequencies in the groups exposed to 0.2, 0.5 and 1.0 gy were found to be < 4.7, < 7.7 and < 12 x 10-3, respectively. the frequencies of hprt mutants and msi found in this study suggest that low doses of ionizing radiation increase hprt mutant frequency without triggering the mutator phenotype pathway.
Lymphoma and Myeloma Cell Resistance to Cytotoxic Agents and Ionizing Radiations Is Not Affected by Exposure to Anti–IL-6 Antibody  [PDF]
Angélique Gougelet,Adeline Mansuy,Jean-Yves Blay,Laurent Alberti,Claudine Vermot-Desroches
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008026
Abstract: Production of high levels of IL-6 is often correlated with resistance to cytotoxics or ionizing radiations, in cancer cell lines as in various cancer patients. We investigated whether monoclonal antibodies directed against IL-6 may enable to reverse resistance of cancer cell lines.
Phosphoproteomics: new insights into cellular signaling
Marc Mumby, Deirdre Brekken
Genome Biology , 2005, DOI: 10.1186/gb-2005-6-9-230
Abstract: Although many biochemical mechanisms are involved in cellular signaling, reversible phosphorylation of serine, threonine, and tyrosine residues is the one most commonly used in mammalian cells. Protein kinases are one of the largest gene families in humans and mice, accounting for 1.7% of the human genome [1,2], and up to 30% of all proteins may be phosphorylated [3]. Traditional biochemical and genetic analyses of phosphoproteins, and of the kinases and phosphatases that modify them, have provided a wealth of information about signaling pathways. These approaches, which typically focus on one protein at a time, are, however, not readily amenable to understanding the complexity of protein phosphorylation or how individual phosphoproteins function in the context of signaling networks. The availability of genome databases and advancements in analytical technology, especially mass spectrometry, has made it possible to study many phosphoproteins and phosphorylation sites at once. The term 'phosphoproteomics' describes a sub-discipline of proteomics that is focused on deriving a comprehensive view of the extent and dynamics of protein phosphorylation. While phosphoproteomics will greatly expand knowledge about the numbers and types of phosphoproteins, its greatest promise is the rapid analysis of entire phosphorylation-based signaling networks.Current methods for analysis of the phosphoproteome rely heavily on mass spectrometry and 'phosphospecific' enrichment techniques. Emerging technologies that are likely to have important impacts on phosphoproteomics include protein [4] and antibody [5] microarrays, and fluorescence-based single-cell analysis [6]. While these methods have the potential for high sensitivity and high throughput, they require prior knowledge of particular phosphoprotein targets. In contrast, mass-spectrometry-based approaches both allow large-scale analysis and provide the ability to discover new phosphoproteins. The speed, selectivity, and sensitivity
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