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Published: 10 December 2022
Last updated: 29 January 2023

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1

Rugo, Rebecca E., Michael W. Epperly, Darcy Franicola, Benjamin Greenberger, Paavani Komanduri, Hong Wang, Dominika M. Wiktor-Brown, Joel S. Greenberger, and Bevin P. Engelward. "DNA Methyltransferases Modulate the Bystander Effect in Mouse Embryonic Stem Cells." Blood 110, no. 11 (November 16, 2007): 4154. http://dx.doi.org/10.1182/blood.v110.11.4154.4154.

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Abstract Cells exposed to radiation or other genotoxic agents can induce DNA damage and other stress responses in non-irradiated cells that are either cultured with the irradiated cells or have been exposed to culture medium from irradiated cells. This is called the bystander effect. In a previous study we found that the descendents of bystander cells exposed to Mitomycin C (MMC) are themselves capable of inducing homologous recombination in un-exposed cells. This suggests that MMC induces persistent and transmissible changes in expression in bystander cells. Bystander effects are likely caused by epigenetic mechanisms rather than “classic” mutations, i.e. changes in DNA sequence. One of the epigenetic mechanisms cells employ for changing expression is DNA methylation in which DNA methyltransferases (DNMTs) add a methyl group to the 5 carbon of cytosine. In this study we asked if ionizing radiation can induce transmissible DNA damage in bystander cells by examining if bystander cells exposed to irradiated cells were themselves able to induce damage in naive cells. Furthermore, we asked if this was dependent on DNMT activity in the irradiated cells. We irradiated wild-type (WT) and DNMT triple knockout (DNMT TKO) mouse embryonic stem cells (ESCs) and after two weeks of continuous culture, we collected conditioned medium (CM). CM was then added to cultures of naive WT ESCs (primary bystanders). Three weeks later, CM was collected from the primary bystanders and added to naïve WT cells (secondary bystanders). We assessed DNA damage by evaluating strand breaks using the alkaline Comet assay and sister chromatid exchange (SCE) analysis. As expected, we found that medium from cells irradiated with 5 Gy induced modest damage in bystander cells. The median Olive tail moment was 2.8 in bystander cells exposed to conditioned medium from irradiated cells compared to 1.0 in control bystander cells (p < 0.0001). Homologous recombination was 0.15 chromatid exchanges per chromosome compared to 0.092 in control bystanders (p < 0.0001). We also observed an increase in strand breaks in secondary bystanders of a similar magnitude to that found in primary bystanders, indicating that radiation-induced bystanders are themselves able to induce damage. In contrast to WT cells, the irradiated DNMT TKO cells did not induce strand breaks in bystander cells, as measured by the Comet assay, but did induce HR. Surprisingly, we also observed that un-irradiated DNMT TKO cells induce DNA damage in bystanders, and furthermore that the magnitude of the effect is similar to that induced by irradiated WT cells. These data suggest that methyltransferases have a complex role in bystander effects. Bystander effects may be mediated by free radicals. To see if the DNMT TKO cells had changes in antioxidant levels, glutathione (GSH) and glutathione peroxidase (GPX) activity were determined. There was no significant change in GSH levels between WT and DNMT TKO cells. However, DNMT TKO cells had significantly higher levels of GPX activity (275.4 + 19.8 mU/mg protein) compared to control cells (122.0 + 16.4 mU/mg, p= 0.0001). Taken together, these results show that radiation-induced bystander cells can themselves induce damage in un-irradiated cells and suggest that cells lacking DNA methylation activity can induce bystander effects.
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2

Shemetun, O. V., and M. A. Pilins’ka. "Radiation-induced “bystander” effect." Cytology and Genetics 41, no. 4 (August 2007): 251–55. http://dx.doi.org/10.3103/s0095452707040111.

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3

Elbakrawy, Eman, Savneet Kaur Bains, Scott Bright, Raheem AL-Abedi, Ammar Mayah, Edwin Goodwin, and Munira Kadhim. "Radiation-Induced Senescence Bystander Effect: The Role of Exosomes." Biology 9, no. 8 (July 27, 2020): 191. http://dx.doi.org/10.3390/biology9080191.

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Ionizing Radiation (IR), especially at high doses, induces cellular senescence in exposed cultures. IR also induces “bystander effects” through signals released from irradiated cells, and these effects include many of the same outcomes observed following direct exposure. Here, we investigate if radiation can cause senescence through a bystander mechanism. Control cultures were exposed directly to 0, 0.1, 2, and 10 Gy. Unirradiated cells were treated with medium from irradiated cultures or with exosomes extracted from irradiated medium. The level of senescence was determined post-treatment (24 h, 15 days, 30 days, and 45 days) by β-galactosidase staining. Media from cultures exposed to all four doses, and exosomes from these cultures, induced significant senescence in recipient cultures. Senescence levels were initially low at the earliest timepoint, and peaked at 15 days, and then decreased with further passaging. These results demonstrate that senescence is inducible through a bystander mechanism. As with other bystander effects, bystander senescence was induced by a low radiation dose. However, unlike other bystander effects, cultures recovered from bystander senescence after repeated passaging. Bystander senescence may be a potentially significant effect of exposure to IR, and may have both beneficial and harmful effects in the context of radiotherapy.
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4

Yu, Kwan Ngok. "Radiation-Induced Rescue Effect: Insights from Microbeam Experiments." Biology 11, no. 11 (October 23, 2022): 1548. http://dx.doi.org/10.3390/biology11111548.

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The present paper reviews a non-targeted effect in radiobiology known as the Radiation-Induced Rescue Effect (RIRE) and insights gained from previous microbeam experiments on RIRE. RIRE describes the mitigation of radiobiological effects in targeted irradiated cells after they receive feedback signals from co-cultured non-irradiated bystander cells, or from the medium previously conditioning those co-cultured non-irradiated bystander cells. RIRE has established or has the potential of establishing relationships with other non-traditional new developments in the fields of radiobiology, including Radiation-Induced Bystander Effect (RIBE), Radiation-Induced Field Size Effect (RIFSE) and ultra-high dose rate (FLASH) effect, which are explained. The paper first introduces RIRE, summarizes previous findings, and surveys the mechanisms proposed for observations. Unique opportunities offered by microbeam irradiations for RIRE research and some previous microbeam studies on RIRE are then described. Some thoughts on future priorities and directions of research on RIRE exploiting unique features of microbeam radiations are presented in the last section.
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5

Azzam, Edouard I., and John B. Little. "The radiation-induced bystander effect: evidence and significance." Human & Experimental Toxicology 23, no. 2 (February 2004): 61–65. http://dx.doi.org/10.1191/0960327104ht418oa.

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A multitude of biological effects observed over the past two decades in various in vivo and in vitro cell culture experiments have indicated that low dose/low fluence ionizing radiation has significantly different biological responses than high dose radiation. Exposure of cell populations to very low fluences of particles or incorporated radionuclides results in significant biological effects occurring in both the irradiated and nonirradiated cells in the population. Cells recipient of growth medium from irradiated cultures can also respond to the radiation exposure. This phenomenon, termed the ‘bystander response’, has been postulated to impact both the estimation of risks of exposure to ionizing radiation and radiotherapy. Amplification of radiation-induced cyto-toxic and genotoxic effects by the bystander effect is in contrast to the observations of adaptive responses, which are generally induced following exposure to low dose, low linear energy transfer radiation and which tend to attenuate radiation-induced damage. In this article, the evidence for existence of radiation-induced bystander effects and our current knowledge of the biochemical and molecular events involved in mediating these effects are described. Potential similarities between factors that mediate the radiation-induced bystander and adaptive responses are highlighted.
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6

Stenerlöw, Bo. "Radiation-induced bystander effects." Acta Oncologica 45, no. 4 (January 2006): 373–74. http://dx.doi.org/10.1080/02841860600768960.

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7

Östreicher, Jan, Kevin M. Prise, Barry D. Michael, Jürgen Vogt, Tilman Butz, and Judith M. Tanner. "Radiation-Induced Bystander Effects." Strahlentherapie und Onkologie 179, no. 2 (February 2003): 69–77. http://dx.doi.org/10.1007/s00066-003-1000-9.

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8

Pilinska, M., O. Shemetun, O. Talan, O. Dibska, S. Kravchenko, and V. Sholoiko. "STUDY THE EFFECTS OF IONIZING RADIATION ON THE LEVEL OF CHROMOSOME INSTABILITY IN HUMAN SOMATIC CELLS DURING THE DEVELOPMENT OF TUMOR-INDUCED BYSTANDER EFFECT." Проблеми радіаційної медицини та радіобіології = Problems of Radiation Medicine and Radiobiology 25 (2020): 353–61. http://dx.doi.org/10.33145/2304-8336-2020-25-353-361.

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Objective. to determine the impact of the irradiated in vitro blood cells from patients with B-cell chronic lymphocytic leukemia (CLL) on the level of chromosomal instability in peripheral blood lymphocytes (PBL) from healthy persons during the development of tumor-induced bystander effect. Materials and methods. Separate and joint cultivation of PBL from healthy persons (cells-bystanders) together with blood cells from CLL patients irradiated in vitro at the G0 stage of the mitotic cycle by γ-quanta 137Cs in a dose of 0.5 Gy 137Cs (cells-inductors) was used. For joint cultivation our own model system for co-cultivation of PBL from individuals of different sex, designed by us to investigate the bystander effects at the cytogenetic level was used. Traditional cytogenetic analysis of uniformly painted chromosomes with group karyotyping was performed. The frequency of chromosome aberrations in cells-inductors and cells-bystanders as the markers of chromosome instability were determined. Results. Found that at co-cultivation of PBL from healthy individuals with irradiated blood cells from CLL patients the middle group frequency of chromosome aberrations in the bystander cells (5.18 ± 0.51 per 100 metaphases, p < 0.001) was statistically significant higher than its background level determined at a separate cultivaton (1.52 ± 0.30 per 100 metaphases), and at co-cultivation with non-irradiated blood cells from CLL patients (3.31 ± 0.50 per 100 metaphases, p < 0.01). Conclusions. Co-cultivation of in vitro irradiated blood cells from CLL patients with PBL from healthy persons leads to an increase in the level of chromosome instability in the bystander cells due to synergism between tumor-induced and radiation-induced bystander effects. Key words: human peripheral blood lymphocytes, B-cell chronic lymphocytic leukemia, ionizing radiation, chromosomal instability, tumor-induced bystander effect.
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9

Snyder, Andrew R. "Review of radiation-induced bystander effects." Human & Experimental Toxicology 23, no. 2 (February 2004): 87–89. http://dx.doi.org/10.1191/0960327104ht423oa.

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It is now apparent that the target for the biological effects of ionizing radiation (IR) is not solely the irradiated cell(s), but also includes the surrounding cells/tissue as well. Radiation-induced bystander effects (BSEs) are defined by the presence of the biological effects of radiation in cells that were not themselves in the field of irradiation. Decreased plating efficiency, increased sister chromatid exchanges, oncogenic transformation, among other endpoints have been used to describe the BSE. Two primary means have been established for the transmission of the bystander signal; one is mediated by gap-junction intracellular communication, and the other is initiated through the secretion of factors from irradiated cells. While the basis for these phenomena have been established in cell culture systems, there is also evidence for their presence in vivo. This in vivo effect may contribute to increased tumor cell killing, and may also play a role in the abscopal effects of radiation, where radiation responses are seen in areas separated from the irradiated tissue. Although the precise molecular components and mechanisms remain unknown, their discovery will shed new light on the role of the BSEs in radiation risk assessment, and clinical radiotherapy in the clinic.
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10

Faria, Fernando P., Ronald Dickman, and Carlos H. C. Moreira. "Models of the radiation-induced bystander effect." International Journal of Radiation Biology 88, no. 8 (June 11, 2012): 592–99. http://dx.doi.org/10.3109/09553002.2012.692568.

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11

KASHINO, Genro, and Naoki MATSUDA. "Radiation-Induced Bystander Effect-Application of Microbeam." RADIOISOTOPES 54, no. 1 (2005): 23–25. http://dx.doi.org/10.3769/radioisotopes.54.23.

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12

Paluch-Ferszt, M., U. Kaźmierczak, and Z. Szefliński. "Radiation-Induced Bystander Effect Research: Literature Review." Acta Physica Polonica A 139, no. 3 (March 2021): 266–72. http://dx.doi.org/10.12693/aphyspola.139.266.

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13

Jalal, Nasir, Saba Haq, Namrah Anwar, Saadiya Nazeer, and Umar Saeed. "Radiation induced bystander effect and DNA damage." Journal of Cancer Research and Therapeutics 10, no. 4 (2014): 819. http://dx.doi.org/10.4103/0973-1482.144587.

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14

Khvostunov, Igor K., and Hooshang Nikjoo. "Computer modelling of radiation-induced bystander effect." Journal of Radiological Protection 22, no. 3A (September 1, 2002): A33—A37. http://dx.doi.org/10.1088/0952-4746/22/3a/306.

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15

Wright, Eric G. "Commentary on radiation-induced bystander effects." Human & Experimental Toxicology 23, no. 2 (February 2004): 91–94. http://dx.doi.org/10.1191/0960327104ht424oa.

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The paradigm of genetic alterations being restricted to direct DNA damage after exposure to ionizing radiation has been challenged by observations in which effects of ionizing radiation arise in cells that in themselves receive no radiation exposure. These effects are demonstrated in cells that are the descendants of irradiated cells (radiation-induced genomic instability) or in cells that are in contact with irradiated cells or receive certain signals from irradiated cells (radiation-induced bystander effects). Bystander signals may be transmitted either by direct intercellular communication through gap junctions, or by diffusible factors, such as cytokines released from irradiated cells. In both phenomena, the untargeted effects of ionizing radiation appear to be associated with free radical-mediated processes. There is evidence that radiation-induced genomic instability may be a consequence of, and in some cell systems may also produce, bystander interactions involving intercellular signalling, production of cytokines and free radical generation. These processes are also features of inflammatory responses that are known to have the potential for both bystander-mediated and persisting damage as well as for conferring a predisposition to malignancy. Thus, radiation-induced genomic instability and untargeted bystander effects may reflect interrelated aspects of inflammatory type responses to radiation-induced stress and injury and contribute to the variety of the pathological consequences of radiation exposures.
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16

Nikjoo, Hooshang, and Igor Khvostunov. "Biophysical model of the radiation-induced bystander effect." International Journal of Radiation Biology 79, no. 1 (January 2003): 43–52. http://dx.doi.org/10.1080/713864979.

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17

Ballarini, F., D. Alloni, A. Facoetti, A. Mairani, R. Nano, and A. Ottolenghi. "Modelling radiation-induced bystander effect and cellular communication." Radiation Protection Dosimetry 122, no. 1-4 (December 1, 2006): 244–51. http://dx.doi.org/10.1093/rpd/ncl446.

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18

Sawant, S. G., W. Zheng, K. M. Hopkins, G. Randers-Pehrson, H. B. Lieberman, and E. J. Hall. "The Radiation-Induced Bystander Effect for Clonogenic Survival." Radiation Research 157, no. 4 (April 2002): 361–64. http://dx.doi.org/10.1667/0033-7587(2002)157[0361:tribef]2.0.co;2.

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19

Nikjoo, Hooshang, and Igor K. Khvostunov. "Biophysical model of the radiation-induced bystander effect." International Journal of Radiation Biology 79, no. 1 (January 2003): 43–52. http://dx.doi.org/10.1080/0955300021000034701.

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20

Nikjoo, Hooshang, and Igor K. Khvostunov. "A theoretical approach to the role and critical issues associated with bystander effect in risk estimation." Human & Experimental Toxicology 23, no. 2 (February 2004): 81–86. http://dx.doi.org/10.1191/0960327104ht422oa.

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This paper presents a quantitative biophysical model of the radiation-induced bystander effect. The principle aim of the bystander model is to establish whether bystander signal can be associated with low molecular weight factors that are transmitted by diffusion type processes in the medium surrounding the recipient cells. Cell inactivation and induced oncogenic transformation by microbeam and broadbeam irradiation systems were considered. The biophysical model postulates that the oncogenic bystander response observed in non-hit cells originates from specific signals received from inactivated cells. The bystander signals are assumed to be protein like molecules spreading in the culture media by Brownian motion. The bystander signals are assumed to switch cells into a state of cell death (apoptotic/mitotic/necrosis) or induced oncogenic transformation modes. The bystander cell survival observed after treatment with the irradiated conditioned medium using broadbeam and the microbeam irradiation modalities were analysed and interpreted in the framework of the Bystander Diffusion Model (BSDM). The model predictions for cell inactivation and induced oncogenic transformation frequencies agree well with observed data from microbeam and broadbeam experiments. In the case of irradiation with constant fraction of cells, transformation frequency for the bystander effect increases with increasing radiation dose. The BSDM predicts that the bystander effect cannot be interpreted solely as a low-dose effect phenomenon. It is shown that the bystander component of radiation response can increase with dose and can be observed at high doses as well as low doses. The validity of this conclusion is supported by analysis of experimental results from high-LET microbeam experiments.
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21

Pilinska, M. A., G. M. Shemetun, O. V. Shemetun, S. S. Dybsky, O. B. Dybska, O. O. Talan, L. R. Pedan, and D. A. Кurinnyi. "CHROMOSOMAL MUTAGENESIS IN HUMAN SOMATIC CELLS: 30-YEAR CYTOGENETIC MONITORING AFTER CHORNOBYL ACCIDENT." Experimental Oncology 38, no. 4 (December 22, 2016): 276–79. http://dx.doi.org/10.31768/2312-8852.2016.38(4):276-279.

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In the lecture we have generalized and analyzed the data of cytogenetic laboratory of National Research Center for Radiation Medicine of the National Academy of Medical Sciences of Ukraine on 30-year selective cytogenetic monitoring among the priority contingents of different ages exposed to radiation after Chornobyl accident in Ukraine. It is highlighted that not only targeted but also untargeted radiation-induced cytogenetic effects should be explored, especially in delayed terms following radiation exposure. The new methodical approaches for studying “bystander effect”, individual radiosensitivity, and various forms of radiation-induced chromosomal instability (delayed, hidden, transmissible) have been proposed. These approaches proved to be advantageous for analyzing cytogenetic patterns of induction and persistence of chromosomal instability in human somatic cells because of “bystander effect” and “bystander type effect”. The phenomenon of positive “reverse” bystander effect has been found. The possibility of modifying the inherited individual human susceptibility to mutagenic exposure by ionizing radiation has been estimated. Finally, the association between hypersensitivity to radiation exposure and realization of oncopathology in exposed individuals has been revealed. The increased intensity of human somatic chromosomal mutagenesis was confirmed not only in the nearest but in the delayed terms following Chornobyl accident as a result of radiation-induced both targeted and untargeted cytogenetic effects. Such effects can be considered as risk factors for malignant transformation of cells, hereditary diseases, birth defects, and multifactorial somatic pathology. This article is a part of a Special Issue entitled “The Chornobyl Nuclear Accident: Thirty Years After”.
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22

Hargitai, Rita, Dávid Kis, Eszter Persa, Tünde Szatmári, Géza Sáfrány, and Katalin Lumniczky. "Oxidative Stress and Gene Expression Modifications Mediated by Extracellular Vesicles: An In Vivo Study of the Radiation-Induced Bystander Effect." Antioxidants 10, no. 2 (January 21, 2021): 156. http://dx.doi.org/10.3390/antiox10020156.

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Radiation-induced bystander effect is a biological response in nonirradiated cells receiving signals from cells exposed to ionising radiation. The aim of this in vivo study was to analyse whether extracellular vesicles (EVs) originating from irradiated mice could induce modifications in the redox status and expression of radiation-response genes in bystander mice. C57BL/6 mice were whole-body irradiated with 0.1-Gy and 2-Gy X-rays, and EVs originating from mice irradiated with the same doses were injected into naïve, bystander mice. Lipid peroxidation in the spleen and plasma reactive oxygen metabolite (ROM) levels increased 24 h after irradiation with 2 Gy. The expression of antioxidant enzyme genes and inducible nitric oxide synthase 2 (iNOS2) decreased, while cell cycle arrest-, senescence- and apoptosis-related genes were upregulated after irradiation with 2 Gy. In bystander mice, no significant alterations were observed in lipid peroxidation or in the expression of genes connected to cell cycle arrest, senescence and apoptosis. However, there was a systemic increase in the circulating ROM level after an intravenous EV injection, and EVs originating from 2-Gy-irradiated mice caused a reduced expression of antioxidant enzyme genes and iNOS2 in bystander mice. In conclusion, we showed that ionising radiation-induced alterations in the cellular antioxidant system can be transmitted in vivo in a bystander manner through EVs originating from directly irradiated animals.
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23

Tudor, Mihaela, Antoine Gilbert, Charlotte Lepleux, Mihaela Temelie, Sonia Hem, Jean Armengaud, Emilie Brotin, Siamak Haghdoost, Diana Savu, and François Chevalier. "A Proteomic Study Suggests Stress Granules as New Potential Actors in Radiation-Induced Bystander Effects." International Journal of Molecular Sciences 22, no. 15 (July 26, 2021): 7957. http://dx.doi.org/10.3390/ijms22157957.

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Besides the direct effects of radiations, indirect effects are observed within the surrounding non-irradiated area; irradiated cells relay stress signals in this close proximity, inducing the so-called radiation-induced bystander effect. These signals received by neighboring unirradiated cells induce specific responses similar with those of direct irradiated cells. To understand the cellular response of bystander cells, we performed a 2D gel-based proteomic study of the chondrocytes receiving the conditioned medium of low-dose irradiated chondrosarcoma cells. The conditioned medium was directly analyzed by mass spectrometry in order to identify candidate bystander factors involved in the signal transmission. The proteomic analysis of the bystander chondrocytes highlighted 20 proteins spots that were significantly modified at low dose, implicating several cellular mechanisms, such as oxidative stress responses, cellular motility, and exosomes pathways. In addition, the secretomic analysis revealed that the abundance of 40 proteins in the conditioned medium of 0.1 Gy irradiated chondrosarcoma cells was significantly modified, as compared with the conditioned medium of non-irradiated cells. A large cluster of proteins involved in stress granules and several proteins involved in the cellular response to DNA damage stimuli were increased in the 0.1 Gy condition. Several of these candidates and cellular mechanisms were confirmed by functional analysis, such as 8-oxodG quantification, western blot, and wound-healing migration tests. Taken together, these results shed new lights on the complexity of the radiation-induced bystander effects and the large variety of the cellular and molecular mechanisms involved, including the identification of a new potential actor, namely the stress granules.
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24

Zhang, Ziqi, Kui Li, and Mei Hong. "Radiation-Induced Bystander Effect and Cytoplasmic Irradiation Studies with Microbeams." Biology 11, no. 7 (June 21, 2022): 945. http://dx.doi.org/10.3390/biology11070945.

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Although direct damage to nuclear DNA is considered as the major contributing event that leads to radiation-induced effects, accumulating evidence in the past two decades has shown that non-target events, in which cells are not directly irradiated but receive signals from the irradiated cells, or cells irradiated at extranuclear targets, may also contribute to the biological consequences of exposure to ionizing radiation. With a beam diameter at the micrometer or sub-micrometer level, microbeams can precisely deliver radiation, without damaging the surrounding area, or deposit the radiation energy at specific sub-cellular locations within a cell. Such unique features cannot be achieved by other kinds of radiation settings, hence making a microbeam irradiator useful in studies of a radiation-induced bystander effect (RIBE) and cytoplasmic irradiation. Here, studies on RIBE and different responses to cytoplasmic irradiation using microbeams are summarized. Possible mechanisms related to the bystander effect, which include gap-junction intercellular communications and soluble signal molecules as well as factors involved in cytoplasmic irradiation-induced events, are also discussed.
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25

Jokar, Safura, Inês A. Marques, Saeedeh Khazaei, Tania Martins-Marques, Henrique Girao, Mafalda Laranjo, and Maria Filomena Botelho. "The Footprint of Exosomes in the Radiation-Induced Bystander Effects." Bioengineering 9, no. 6 (May 31, 2022): 243. http://dx.doi.org/10.3390/bioengineering9060243.

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Radiation therapy is widely used as the primary treatment option for several cancer types. However, radiation therapy is a nonspecific method and associated with significant challenges such as radioresistance and non-targeted effects. The radiation-induced non-targeted effects on nonirradiated cells nearby are known as bystander effects, while effects far from the ionising radiation-exposed cells are known as abscopal effects. These effects are presented as a consequence of intercellular communications. Therefore, a better understanding of the involved intercellular signals may bring promising new strategies for radiation risk assessment and potential targets for developing novel radiotherapy strategies. Recent studies indicate that radiation-derived extracellular vesicles, particularly exosomes, play a vital role in intercellular communications and may result in radioresistance and non-targeted effects. This review describes exosome biology, intercellular interactions, and response to different environmental stressors and diseases, and focuses on their role as functional mediators in inducing radiation-induced bystander effect (RIBE).
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26

Ward, John F. "The radiation-induced lesions which trigger the bystander effect." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 499, no. 2 (February 2002): 151–54. http://dx.doi.org/10.1016/s0027-5107(01)00286-x.

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27

Wang, Hongzhi, K. N. Yu, Jue Hou, Qian Liu, and Wei Han. "Radiation-induced bystander effect: Early process and rapid assessment." Cancer Letters 356, no. 1 (January 2015): 137–44. http://dx.doi.org/10.1016/j.canlet.2013.09.031.

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28

WADA, SEIICHI, MAUKO SUDO, SAKIKO TAMURA, TAKEHIKO KAKIZAKI, NOBUHIKO ITO, and KOICHIRO SERA. "ANALYSIS OF THE LETHAL EFFECTS OF LOW-DOSE RADIATION ON GLIOMA CELLS: RELATIONSHIP OF THE BYSTANDER EFFECT AND METAL ELEMENTS." International Journal of PIXE 21, no. 01n02 (January 2011): 47–54. http://dx.doi.org/10.1142/s012908351100215x.

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Investigation of the radiation-induced bystander effect plays an important role in the understanding of the mechanisms of radiation response after low-dose irradiation. Sphingomyelinase (SMase) was activated by radiation and required the metal element for its activation. For further elucidation of the bystander effect, we investigated the relationship between its induction by acid SMase and a factor secreted from the irradiated tumor cells. In the cell culture medium transfer experiment after irradiation at a dose of 0.1 Gy , cell death was induced in non-irradiated cells. However, when cells received prior treatment with SMase inhibitor, cell death was not induced. When fluctuations in the activation of SMase and metal elements were detected, both intracellularly and extracellularly after irradiation, an increase in SMase activity and Zn concentration occurred within the cells at 5 min and outside of the cells at 15 min after irradiation. This increase in zinc concentration at 15 min after irradiation was suppressed by treatment with SMase inhibitor. These results suggest that activation of SMase, which is related to the bystander effect, is dependent on zinc.
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29

Mothersill, C., G. Moran, F. McNeill, M. D. Gow, J. Denbeigh, W. Prestwich, and C. B. Seymour. "A Role for Bioelectric Effects in the Induction of Bystander Signals by Ionizing Radiation?" Dose-Response 5, no. 3 (July 1, 2007): dose—response.0. http://dx.doi.org/10.2203/dose-response.06-011.mothersill.

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The induction of “bystander effects” i.e. effects in cells which have not received an ionizing radiation track, is now accepted but the mechanisms are not completely clear. Bystander effects following high and low LET radiation exposure are accepted but mechanisms are still not understood. There is some evidence for a physical component to the signal. This paper tests the hypothesis that bioelectric or biomagnetic phenomena are involved. Human immortalized skin keratinocytes and primary explants of mouse bladder and fish skin, were exposed directly to ionizing radiation or treated in a variety of bystander protocols. Exposure of cells was conducted by shielding one group of flasks using lead, to reduce the dose below the threshold of 2mGy 60Cobalt gamma rays established for the bystander effect. The endpoint for the bystander effect in the reporter system used was reduction in cloning efficiency (RCE). The magnitude of the RCE was similar in shielded and unshielded flasks. When cells were placed in a Faraday cage the magnitude of the RCE was less but not eliminated. The results suggest that liquid media or cell-cell contact transmission of bystander factors may be only part of the bystander mechanism. Bioelectric or bio magnetic fields may have a role to play. To test this further, cells were placed in a Magnetic Resonance Imaging (MRI) machine for 10min using a typical head scan protocol. This treatment also induced a bystander response. Apart from the obvious clinical relevance, the MRI results further suggest that bystander effects may be produced by non-ionizing exposures. It is concluded that bioelectric or magnetic effects may be involved in producing bystander signaling cascades commonly seen following ionizing radiation exposure.
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Matsumoto, Hideki, Akihisa Takahashi, and Takeo Ohnishi. "Radiation-Induced Adaptive Responses and Bystander Effects." Biological Sciences in Space 18, no. 4 (2004): 247–54. http://dx.doi.org/10.2187/bss.18.247.

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Erkang, Jiang, and Wu Lijun. "Caffeine Markedly Enhanced Radiation-Induced Bystander Effects." Plasma Science and Technology 11, no. 2 (April 2009): 250–54. http://dx.doi.org/10.1088/1009-0630/11/2/23.

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32

Seymour, Colin B., and Carmel Mothersill. "Radiation-induced bystander effects — implications for cancer." Nature Reviews Cancer 4, no. 2 (February 2004): 158–64. http://dx.doi.org/10.1038/nrc1277.

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33

Morgan, William F., Andreas Hartmann, Charles L. Limoli, Shruti Nagar, and Brian Ponnaiya. "Bystander effects in radiation-induced genomic instability." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 504, no. 1-2 (July 2002): 91–100. http://dx.doi.org/10.1016/s0027-5107(02)00083-0.

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34

Mothersill, Carmel, and Colin Seymour. "Radiation-induced bystander effects, carcinogenesis and models." Oncogene 22, no. 45 (October 2003): 7028–33. http://dx.doi.org/10.1038/sj.onc.1206882.

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35

Sasaki, Kohei, Kosuke Wakui, Kaori Tsutsumi, Akio Itoh, and Hiroyuki Date. "A Simulation Study of the Radiation-Induced Bystander Effect: Modeling with Stochastically Defined Signal Reemission." Computational and Mathematical Methods in Medicine 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/389095.

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The radiation-induced bystander effect (RIBE) has been experimentally observed for different types of radiation, cell types, and cell culture conditions. However, the behavior of signal transmission between unirradiated and irradiated cells is not well known. In this study, we have developed a new model for RIBE based on the diffusion of soluble factors in cell cultures using a Monte Carlo technique. The model involves the signal emission probability from bystander cells following Poisson statistics. Simulations with this model show that the spatial configuration of the bystander cells agrees well with that of corresponding experiments, where the optimal emission probability is estimated through a large number of simulation runs. It was suggested that the most likely probability falls within 0.63–0.92 for mean number of the emission signals ranging from 1.0 to 2.5.
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36

Mairs, Robert J., Natasha E. Fullerton, Michael R. Zalutsky, and Marie Boyd. "Targeted Radiotherapy: Microgray Doses and the Bystander Effect." Dose-Response 5, no. 3 (July 1, 2007): dose—response.0. http://dx.doi.org/10.2203/dose-response.07-002.mairs.

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Indirect effects may contribute to the efficacy of radiotherapy by sterilizing malignant cells that are not directly irradiated. However, little is known of the influence of indirect effects in targeted radionuclide treatment. We compared γ-radiation-induced bystander effects with those resulting from exposure to three radiohaloanalogues of meta-iodobenzylguanidine (MIBG): [131I]MIBG (low linear energy transfer (LET) β-emitter), [123I]MIBG (high LET Auger electron emitter), and meta-[211At]astatobenzylguanidine ([211At]MABG) (high LET α-emitter). Cells exposed to media from γ-irradiated cells exhibited a dose-dependent reduction in survival fraction at low dosage and a plateau in cell kill at > 2 Gy. Cells treated with media from [131I]MIBG demonstrated a dose-response relationship with respect to clonogenic cell death and no annihilation of this effect at high radiopharmaceutical dosage. In contrast, cells receiving media from cultures treated with [211At]MABG or [123I]MIBG exhibited dose-dependent toxicity at low dose but elimination of cytotoxicity with increasing radiation dose (i.e. U-shaped survival curves). Therefore radionuclides emitting high LET radiation may elicit toxic or protective effects on neighboring untargeted cells at low and high dose respectively. We conclude that radiopharmaceutical-induced bystander effects may depend on LET and be distinct from those elicited by conventional radiotherapy.
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37

Yakovlev, Vasily A. "Role of nitric oxide in the radiation-induced bystander effect." Redox Biology 6 (December 2015): 396–400. http://dx.doi.org/10.1016/j.redox.2015.08.018.

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38

Xia, Junchao, Liteng Liu, Jianming Xue, Yugang Wang, and Lijun Wu. "Modeling of radiation-induced bystander effect using Monte Carlo methods." Nuclear Instruments and Methods in Physics Research Section B: Beam Interactions with Materials and Atoms 267, no. 6 (March 2009): 1015–18. http://dx.doi.org/10.1016/j.nimb.2009.02.010.

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39

Gow, M. D., C. B. Seymour, Soo-Hyun Byun, and C. E. Mothersill. "Effect of dose rate on the radiation-induced bystander response." Physics in Medicine and Biology 53, no. 1 (December 13, 2007): 119–32. http://dx.doi.org/10.1088/0031-9155/53/1/008.

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40

Faqihi, Fahime, Ali Neshastehriz, Shokouhozaman Soleymanifard, Robabeh Shabani, and Nazila Eivazzadeh. "Radiation-induced bystander effect in non-irradiated glioblastoma spheroid cells." Journal of Radiation Research 56, no. 5 (July 9, 2015): 777–83. http://dx.doi.org/10.1093/jrr/rrv039.

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41

Zhou, H., G. Randers-Pehrson, C. A. Waldren, and T. K. Hei. "Radiation-induced bystander effect and adaptive response in mammalian cells." Advances in Space Research 34, no. 6 (January 2004): 1368–72. http://dx.doi.org/10.1016/j.asr.2003.10.049.

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42

Mothersill, Carmel, and Colin Seymour. "Possible implications of radiation-induced ''bystander effects'' for radiation protection." International Journal of Low Radiation 1, no. 1 (2003): 34. http://dx.doi.org/10.1504/ijlr.2003.003479.

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43

Morgan, William F., and Marianne B. Sowa. "Non-targeted bystander effects induced by ionizing radiation." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 616, no. 1-2 (March 2007): 159–64. http://dx.doi.org/10.1016/j.mrfmmm.2006.11.009.

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44

Fakir, Hatim, Werner Hofmann, Wai Y. Tan, and Rainer K. Sachs. "Triggering-Response Model for Radiation-Induced Bystander Effects." Radiation Research 171, no. 3 (March 2009): 320–31. http://dx.doi.org/10.1667/rr1293.1.

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45

Kis, Dávid, Ilona Barbara Csordás, Eszter Persa, Bálint Jezsó, Rita Hargitai, Tünde Szatmári, Nikolett Sándor, et al. "Extracellular Vesicles Derived from Bone Marrow in an Early Stage of Ionizing Radiation Damage Are Able to Induce Bystander Responses in the Bone Marrow." Cells 11, no. 1 (January 4, 2022): 155. http://dx.doi.org/10.3390/cells11010155.

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Ionizing radiation (IR)-induced bystander effects contribute to biological responses to radiation, and extracellular vesicles (EVs) play important roles in mediating these effects. In this study we investigated the role of bone marrow (BM)-derived EVs in the bystander transfer of radiation damage. Mice were irradiated with 0.1Gy, 0.25Gy and 2Gy, EVs were extracted from the BM supernatant 24 h or 3 months after irradiation and injected into bystander mice. Acute effects on directly irradiated or EV-treated mice were investigated after 4 and 24 h, while late effects were investigated 3 months after treatment. The acute effects of EVs on the hematopoietic stem and progenitor cell pools were similar to direct irradiation effects and persisted for up to 3 months, with the hematopoietic stem cells showing the strongest bystander responses. EVs isolated 3 months after irradiation elicited no bystander responses. The level of seven microRNAs (miR-33a-3p, miR-140-3p, miR-152-3p, miR-199a-5p, miR-200c-5p, miR-375-3p and miR-669o-5p) was altered in the EVs isolated 24 hour but not 3 months after irradiation. They regulated pathways highly relevant for the cellular response to IR, indicating their role in EV-mediated bystander responses. In conclusion, we showed that only EVs from an early stage of radiation damage could transmit IR-induced bystander effects.
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Ahmad, S. B., F. E. McNeill, S. H. Byun, W. V. Prestwich, C. Seymour, and C. E. Mothersill. "Ion beam induced luminescence: Relevance to radiation induced bystander effects." Nuclear Instruments and Methods in Physics Research Section B: Beam Interactions with Materials and Atoms 288 (October 2012): 81–88. http://dx.doi.org/10.1016/j.nimb.2012.05.043.

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47

Wong, T. P. W., Y. L. Law, A. K. W. Tse, W. F. Fong, and K. N. Yu. "Influence of Magnolol on the bystander effect induced by alpha-particle irradiation." Applied Radiation and Isotopes 68, no. 4-5 (April 2010): 718–21. http://dx.doi.org/10.1016/j.apradiso.2009.09.034.

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48

Jasmer, Kimberly J., Kristy E. Gilman, Kevin Muñoz Forti, Gary A. Weisman, and Kirsten H. Limesand. "Radiation-Induced Salivary Gland Dysfunction: Mechanisms, Therapeutics and Future Directions." Journal of Clinical Medicine 9, no. 12 (December 18, 2020): 4095. http://dx.doi.org/10.3390/jcm9124095.

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Salivary glands sustain collateral damage following radiotherapy (RT) to treat cancers of the head and neck, leading to complications, including mucositis, xerostomia and hyposalivation. Despite salivary gland-sparing techniques and modified dosing strategies, long-term hypofunction remains a significant problem. Current therapeutic interventions provide temporary symptom relief, but do not address irreversible glandular damage. In this review, we summarize the current understanding of mechanisms involved in RT-induced hyposalivation and provide a framework for future mechanistic studies. One glaring gap in published studies investigating RT-induced mechanisms of salivary gland dysfunction concerns the effect of irradiation on adjacent non-irradiated tissue via paracrine, autocrine and direct cell–cell interactions, coined the bystander effect in other models of RT-induced damage. We hypothesize that purinergic receptor signaling involving P2 nucleotide receptors may play a key role in mediating the bystander effect. We also discuss promising new therapeutic approaches to prevent salivary gland damage due to RT.
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49

Кurinnyi, D., S. Rushkovsky, O. Demchenko, M. Romanenko, T. Liashchenko, and M. Pilinska. "MODIFICATION OF THE TUMOR/INDUCED BYSTANDER EFFECT BY IRRADIATION UNDER COCULTIVATION OF LYMPHOCYTES FROM PATIENTS WITH CHRONIC LYMPHOCYTIC LEUKEMIA AND LYMPHOCYTES FROM HEALTHY DONORS." Проблеми радіаційної медицини та радіобіології = Problems of Radiation Medicine and Radiobiology 26 (2021): 248–59. http://dx.doi.org/10.33145/2304-8336-2021-26-248-259.

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Objective: Study the tumor-induced bystander effect of blood cells from chronic lymphocytic leukemia (CLL) patients on non-transformed bystander cells (peripheral blood lymphocytes (PBL) of conditionally healthy individuals) and the possibility of its modification after the impact of ionizing radiation. Materials and methods. We carried out cocultivation and separate cultivation of blood samples from conditionally healthy volunteers and patients with CLL according to our technique. Using the Comet assay, the relative level of DNA damage was evaluated. Results. A statistically significant increase (р < 0.001) in the level of DNA damage in PBL culture of conditionally healthy individuals after co-cultivation with malignant cells of CLL patients was observed. After irradiation, a drop in the level of cells with a high degree of DNA damage was noted, which was connected with an increase in the frequency of cells that were delayed in division at the S stage of the cell cycle. An increase in apoptotic activity in cultures of bystander cells was observed in all variants of the experiment (р < 0.001). Conclusion. The influence of irradiated blood cells of patients with CLL results in an enhancement of the tumorinduced bystander effect manifestation in the PBL of conditionally healthy individuals. Key words: tumor-induced bystander effect, peripheral blood lymphocytes, Comet assay, ionizing radiation.
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50

Rastogi, Shubhra, Amini Hwang, Josolyn Chan, and Jean Y. J. Wang. "Extracellular vesicles transfer nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander effects." Molecular Biology of the Cell 29, no. 18 (September 2018): 2228–42. http://dx.doi.org/10.1091/mbc.e18-02-0130.

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Ionizing radiation (IR) not only activates DNA damage response (DDR) in irradiated cells but also induces bystander effects (BE) in cells not directly targeted by radiation. How DDR pathways activated in irradiated cells stimulate BE is not well understood. We show here that extracellular vesicles secreted by irradiated cells (EV-IR), but not those from unirradiated controls (EV-C), inhibit colony formation in unirradiated cells by inducing reactive oxygen species (ROS). We found that µEV-IR from Abl nuclear localization signal–mutated ( Abl-µNLS) cells could not induce ROS, but expression of wild-type Abl restored that activity. Because nuclear Abl stimulates miR-34c biogenesis, we measured miR-34c in EV and found that its levels correlated with the ROS-inducing activity of EV. We then showed that EV from miR-34c minigene–transfected, but unirradiated cells induced ROS; and transfection with miR-34c-mimic, without radiation or EV addition, also induced ROS. Furthermore, EV-IR from miR34-family triple-knockout cells could not induce ROS, whereas EV-IR from wild-type cells could cause miR-34c increase and ROS induction in the miR-34 triple-knockout cells. These results establish a novel role for extracellular vesicles in transferring nuclear Abl-dependent and radiation-induced miR-34c into unirradiated cells to cause bystander oxidative stress.
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