Radiation Induced Bystander Effect: From &amp;lt;i&amp;gt;in Vitro&amp;lt;/i&amp;gt; Studies to Clinical Application

Wideł, Maria

doi:10.4236/ijmpcero.2016.51001

Cited by 31 publications

(17 citation statements)

References 90 publications

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“…The terms commonly refer to distant tumor regression after localized irradiation [97]. Abscopal effects were observed in different tumor types after conventional radiotherapy, as well after stereotactic ablative radiotherapy almost always combined with immunotherapy which act synergistically (reviewed by [13]). The mechanism of this synergy is based on reduction by radiation of immunosuppression and tolerance of tumor by microenvironment of the body, followed by induction of immune response [98,99].…”

Section: Clinical Look At Bystander Effect Induced By Radionuclidesmentioning

confidence: 99%

“…RIBE is communicated through cell-to-cell gap junctions or by extracellular environment, and typically refers to the damaging events such as reduced clonogenic survival [5,6], increased sister chromatid exchange [7,8], formation of micronuclei and cell death via apoptosis and necrosis [9][10][11][12], all presented in vitro, although similar events appear also in vivo. Many preclinical studies revealed the appearance of bystander effect and abscopal (out of field effect) in vivo (reviewed by [13]. The abscopal effect is an immune-mediated phenomenon.…”

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confidence: 99%

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Radionuclides in radiation-induced bystander effect; may it share in radionuclide therapy?

Wideł¹

2017

neo

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For many years in radiobiology and radiotherapy predominated the conviction that cellular DNA is the main target for ionizing radiation, however, the view has changed in the past 20 years. Nowadays, it is assumed that not only directed (targeted) radiation effect, but also an indirect (non-targeted) effect may contribute to the result of radiation treatment. Non-targeted effect is relatively well recognized after external beam irradiation in vitro and in vivo, and comprises such phenomena like radiation-induced bystander effect (RIBE), genomic instability, adaptive response and abscopal (out of field) effect. These stress-induced and molecular signaling mediated phenomena appear in non-targeted cells as variety responses resembling that observed in directly hit cells. Bystander effects can be both detrimental and beneficial in dependence on dose, dose-rate, cell type, genetic status and experimental condition. Less is known about radionuclide-induced non-targeted effects in radionuclide therapy, although, based on characteristics of the radionuclide radiation, on experiments in vitro utilizing classical and 3-D cell cultures, and preclinical study on animals it seems obvious that exposure to radionuclide is accompanied by various bystander effects, mostly damaging, less often protective. This review summarizes existing data on radionuclide induced bystander effects comprising radionuclides emitting beta- and alpha-particles and Auger electrons used in tumor radiotherapy and diagnostics. So far, separation of the direct effect of radionuclide decay from crossfire and bystander effects in clinical targeted radionuclide therapy is impossible because of the lack of methods to assess whether, and to what extent bystander effect is involved in human organism. Considerations on this topic are also included.

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Section: Clinical Look At Bystander Effect Induced By Radionuclidesmentioning

confidence: 99%

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confidence: 99%

Radionuclides in radiation-induced bystander effect; may it share in radionuclide therapy?

Wideł¹

2017

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“…8,9 IR causes not only targeted effects but also non-targeted effects several cell generations after initial exposure. [1][2][3][4][5][6] Therefore, we asked whether radiation effects somatic cell reprogramming with respect to the two different radiation responses. To assess the effect of targeted radiation on the reprogramming of somatic cells to pluripotency, as shown in Fig.…”

Section: Direct Exposure To Radiation Attenuates Pluripotency Inductimentioning

confidence: 99%

“…These responses can be observed in either cells exposed to signaling molecules released by irradiated cells, which activate non-irradiated cells or in subsequent generations of irradiated cells. 2,3 Among radiation-induced non-targeted response, the delayed effect such as delayed reproductive death and chromosomal instability have been described in the descendants of irradiated cells. Its persistence over many generations after irradiation has been considered relevant for the human health risk associated with radiation-induced carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Post-irradiation promotes susceptibility to reprogramming to pluripotent state in human fibroblasts

et al. 2017

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Ionizing radiation causes not only targeted effects in cells that have been directly irradiated but also non-targeted effects in several cell generations after initial exposure. Recent studies suggest that radiation can enrich for a population of stem cells, derived from differentiated cells, through cellular reprogramming. Here, we elucidate the effect of irradiation on reprogramming, subjected to two different responses, using an induced pluripotent stem cell (iPSC) model. iPSCs were generated from non-irradiated cells, directly-irradiated cells, or cells subsequently generated after initial radiation exposure. We found that direct irradiation negatively affected iPSC induction in a dose-dependent manner. However, in the post-irradiated group, after five subsequent generations, cells became increasingly sensitive to the induction of reprogramming compared to that in non-irradiated cells as observed by an increased number of Tra1-81-stained colonies as well as enhanced alkaline phosphatase and Oct4 promoter activity. Comparative analysis, based on reducing the number of defined factors utilized for reprogramming, also revealed enhanced efficiency of iPSC generation in post-irradiated cells. Furthermore, the phenotypic acquisition of characteristics of pluripotent stem cells was observed in all resulting iPSC lines, as shown by morphology, the expression of pluripotent markers, DNA methylation patterns of pluripotency genes, a normal diploid karyotype, and teratoma formation. Overall, these results suggested that reprogramming capability might be differentially modulated by altered radiation-induced responses. Our findings provide that susceptibility to reprogramming in somatic cells might be improved by the delayed effects of non-targeted response, and contribute to a better understanding of the biological effects of radiation exposure.

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“…It disrupts the redox balance, resulting in irreversible changes in the cell, and causing severe disturbances within the entire metabolic pathways (Widel et al, 2014). Such UVinduced oxidative stress and imbalance may lead to diseases such as diabetes, atherosclerosis, or cancer (Valko et al, 2005;Karpińska & Gromadzka, 2013;Kasperczyk et al, 2013;Buttke & Sandstrom, 2016;Widel, 2016).…”

Section: Introductionmentioning

confidence: 99%

UV radiation in HCT 116 cells influences intracellular H2O2 and glutathione levels, antioxidant expression, and protein glutathionylation

Adamiec

Skonieczna

2019

Acta Biochim Pol

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UV radiation influences cellular levels of hydrogen peroxide (H2O2) and glutathione (GSH) and alters the expression of antioxidant genes in the human colorectal cancer cell line HCT116. In this study, cells were irradiated with UV light of different wavelength (A, B, or C). A surge in H2O2 concentration and total glutathione (level occurred 6 hours later. Consequently, protein glutathionylation increased above control levels. Expression of the antioxidant enzymes: glutathione peroxidase (GPX) and glutathione reductase (GSR), assessed by real-time quantitative PCR, increased by 1.5–2 times after 24 hours post-irradiation, in comparison to the untreated controls. Glutathionylation of proteins was enhanced after UV radiation and the set of biotinylated glutathione ethyl ester (BioGEE) tagged proteins was detected by Western Blot procedure. This specific glutathione analogue is conjugated with antioxidant proteins during glutathionylation especially under oxidized conditions in cells. A pool of glutathionylated proteins in the treated cells showed peculiar characteristics. These proteins exhibited varying molecular weights. For UVA-irradiated cells, 24 hours after the treatment we observed two additional ~60 and ~72 kDa bands of glutathionylated proteins from NADPH oxidases (NOX family). Total glutathione level in the UV-irradiated HCT116 cells was higher than in the control. This correlates with the detection of glutathionylation in UV-irradiated cells in the first and twelfth hour of post-irradiation, and can be defined as a specific antioxidant element activation for cellular protection.

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Radiation Induced Bystander Effect: From <i>in Vitro</i> Studies to Clinical Application

Cited by 31 publications

References 90 publications

Radionuclides in radiation-induced bystander effect; may it share in radionuclide therapy?

Radionuclides in radiation-induced bystander effect; may it share in radionuclide therapy?

Post-irradiation promotes susceptibility to reprogramming to pluripotent state in human fibroblasts

UV radiation in HCT 116 cells influences intracellular H2O2 and glutathione levels, antioxidant expression, and protein glutathionylation

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