Topical Collection "Radiation Toxicity in Cells"

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A topical collection in International Journal of Molecular Sciences (ISSN 1422-0067). This collection belongs to the section "Molecular Toxicology".

Editor

Collection Editor
Dr. Terrence Piva
School of Medical Sciences, RMIT University, PO Box 71 Bundoora, Victoria 3083, Australia
Website: http://www.rmit.edu.au/staff/terry-piva
E-Mail: terry.piva@rmit.edu.au
Phone: +61-3-99256503
Fax: +61 3 9925 7063
Interests: cell death; photobiology; photoimmunology; skin cancer; enzymology; cell metabolism; oxidative stress; cancer metabolism; cell signalling; cytokines; inflammation; enzyme kinetics; metal oxide nanoparticles; sunscreens

Topical Collection Information

Dear Colleagues,

Life forms on the planet are exposed to different forms of radiation. Such radiation may be emitted from the sun, such as X-rays, radio waves, and visible, ultraviolet or infrared light. Radiation may also come from other natural sources, such as α-, β- or γ-radiation.  Concern has also been raised about the effects of exposure to microwaves, naturally occurring radioactivity, and heat (thermal radiation).  The mechanisms by which these forms of radiation affect cell function differ considerably, but high levels of exposure can result in cell death, and long-term exposure is known to cause a range of cancers.

This issue will look at the cytotoxic effects of radiation on living systems; studies will range from those concerning cultured cells to those discussing population and epidemiology.   While emphasis will be placed on radiation-induced cytotoxicity, studies discussing radiation’s connections with DNA damage, intracellular signaling pathways, caspase activation, membrane damage, ROS/RNS production, gene activation, organelle dysfunction, and animal and epidemiological studies are also encouraged.  Reviews of the mechanisms involved in the cytotoxic effects of electromagnetic radiation are welcomed, as well as studies discussing the effects of long-term human exposure to these forms of radiation.  I encourage you to submit a manuscript to this issue so as to help shed further “light” on the lethal effects that radiation has on cells and individuals.

Prof. Dr. Terrence Piva
Collection Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1600 CHF (Swiss Francs).

Keywords

  • radiation
  • ultraviolet light
  • X-rays
  • γ radiation
  • microwaves
  • cell death pathways
  • DNA damage
  • cell membrane
  • ROS
  • signaling pathways
  • epidemiology studies
  • animal studies

Published Papers (33 papers)

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2015  ( 3 papers )


2014  ( 7 papers )


2013  ( 23 papers )


2015
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Int. J. Mol. Sci. 2015, 16(4), 7753-7775; doi:10.3390/ijms16047753
Received: 2 February 2015 / Revised: 27 March 2015 / Accepted: 31 March 2015 / Published: 8 April 2015
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Int. J. Mol. Sci. 2015, 16(4), 7776-7795; doi:10.3390/ijms16047776
Received: 11 February 2015 / Revised: 27 March 2015 / Accepted: 31 March 2015 / Published: 8 April 2015
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Int. J. Mol. Sci. 2015, 16(3), 5789-5802; doi:10.3390/ijms16035789
Received: 15 January 2015 / Revised: 25 February 2015 / Accepted: 4 March 2015 / Published: 12 March 2015
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2014
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Int. J. Mol. Sci. 2015, 16(1), 68-90; doi:10.3390/ijms16010068
Received: 20 November 2014 / Accepted: 17 December 2014 / Published: 23 December 2014
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Int. J. Mol. Sci. 2014, 15(11), 21419-21432; doi:10.3390/ijms151121419
Received: 10 September 2014 / Revised: 31 October 2014 / Accepted: 4 November 2014 / Published: 19 November 2014
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Int. J. Mol. Sci. 2014, 15(11), 19777-19790; doi:10.3390/ijms151119777
Received: 27 May 2014 / Revised: 24 October 2014 / Accepted: 27 October 2014 / Published: 30 October 2014
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Int. J. Mol. Sci. 2014, 15(10), 18919-18940; doi:10.3390/ijms151018919
Received: 21 August 2014 / Revised: 1 October 2014 / Accepted: 8 October 2014 / Published: 20 October 2014
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Int. J. Mol. Sci. 2014, 15(7), 11555-11565; doi:10.3390/ijms150711555
Received: 7 May 2014 / Revised: 20 June 2014 / Accepted: 24 June 2014 / Published: 27 June 2014
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Int. J. Mol. Sci. 2014, 15(2), 2157-2171; doi:10.3390/ijms15022157
Received: 18 November 2013 / Revised: 30 December 2013 / Accepted: 16 January 2014 / Published: 29 January 2014
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Int. J. Mol. Sci. 2014, 15(1), 927-943; doi:10.3390/ijms15010927
Received: 21 October 2013 / Revised: 26 December 2013 / Accepted: 31 December 2013 / Published: 10 January 2014
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2013
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Int. J. Mol. Sci. 2013, 14(12), 23791-23800; doi:10.3390/ijms141223791
Received: 8 October 2013 / Revised: 20 November 2013 / Accepted: 25 November 2013 / Published: 5 December 2013
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Int. J. Mol. Sci. 2013, 14(11), 22678-22696; doi:10.3390/ijms141122678
Received: 9 October 2013 / Revised: 1 November 2013 / Accepted: 6 November 2013 / Published: 18 November 2013
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Int. J. Mol. Sci. 2013, 14(11), 22449-22461; doi:10.3390/ijms141122449
Received: 4 September 2013 / Revised: 25 October 2013 / Accepted: 30 October 2013 / Published: 14 November 2013
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Int. J. Mol. Sci. 2013, 14(10), 19618-19635; doi:10.3390/ijms141019618
Received: 26 June 2013 / Revised: 9 September 2013 / Accepted: 13 September 2013 / Published: 27 September 2013
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Int. J. Mol. Sci. 2013, 14(9), 18078-18092; doi:10.3390/ijms140918078
Received: 24 June 2013 / Revised: 21 August 2013 / Accepted: 26 August 2013 / Published: 4 September 2013
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Int. J. Mol. Sci. 2013, 14(9), 17881-17896; doi:10.3390/ijms140917881
Received: 17 June 2013 / Revised: 2 August 2013 / Accepted: 7 August 2013 / Published: 2 September 2013
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Int. J. Mol. Sci. 2013, 14(9), 17525-17535; doi:10.3390/ijms140917525
Received: 24 June 2013 / Revised: 14 August 2013 / Accepted: 21 August 2013 / Published: 27 August 2013
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Int. J. Mol. Sci. 2013, 14(8), 17029-17054; doi:10.3390/ijms140817029
Received: 9 July 2013 / Revised: 5 August 2013 / Accepted: 9 August 2013 / Published: 19 August 2013
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Int. J. Mol. Sci. 2013, 14(8), 16943-16957; doi:10.3390/ijms140816943
Received: 24 June 2013 / Revised: 1 August 2013 / Accepted: 5 August 2013 / Published: 16 August 2013
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Int. J. Mol. Sci. 2013, 14(8), 15931-15958; doi:10.3390/ijms140815931
Received: 17 June 2013 / Revised: 19 July 2013 / Accepted: 22 July 2013 / Published: 31 July 2013
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Int. J. Mol. Sci. 2013, 14(8), 15810-15826; doi:10.3390/ijms140815810
Received: 6 June 2013 / Revised: 15 July 2013 / Accepted: 22 July 2013 / Published: 30 July 2013
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Int. J. Mol. Sci. 2013, 14(8), 15695-15723; doi:10.3390/ijms140815695
Received: 30 May 2013 / Revised: 15 July 2013 / Accepted: 17 July 2013 / Published: 29 July 2013
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Int. J. Mol. Sci. 2013, 14(8), 15260-15285; doi:10.3390/ijms140815260
Received: 17 June 2013 / Revised: 27 June 2013 / Accepted: 1 July 2013 / Published: 24 July 2013
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Int. J. Mol. Sci. 2013, 14(7), 15017-15028; doi:10.3390/ijms140715017
Received: 13 June 2013 / Revised: 8 July 2013 / Accepted: 11 July 2013 / Published: 18 July 2013
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Int. J. Mol. Sci. 2013, 14(7), 14974-14995; doi:10.3390/ijms140714974
Received: 5 March 2013 / Revised: 25 June 2013 / Accepted: 1 July 2013 / Published: 17 July 2013
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Int. J. Mol. Sci. 2013, 14(7), 14105-14118; doi:10.3390/ijms140714105
Received: 3 May 2013 / Revised: 3 June 2013 / Accepted: 21 June 2013 / Published: 8 July 2013
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Int. J. Mol. Sci. 2013, 14(7), 14119-14135; doi:10.3390/ijms140714119
Received: 25 May 2013 / Revised: 18 June 2013 / Accepted: 25 June 2013 / Published: 8 July 2013
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Int. J. Mol. Sci. 2013, 14(7), 14024-14063; doi:10.3390/ijms140714024
Received: 8 May 2013 / Revised: 14 June 2013 / Accepted: 17 June 2013 / Published: 5 July 2013
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Int. J. Mol. Sci. 2013, 14(7), 13719-13726; doi:10.3390/ijms140713719
Received: 5 June 2013 / Revised: 15 June 2013 / Accepted: 19 June 2013 / Published: 1 July 2013
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Int. J. Mol. Sci. 2013, 14(6), 12222-12248; doi:10.3390/ijms140612222
Received: 25 April 2013 / Revised: 18 May 2013 / Accepted: 24 May 2013 / Published: 7 June 2013
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Int. J. Mol. Sci. 2013, 14(6), 11795-11815; doi:10.3390/ijms140611795
Received: 13 March 2013 / Revised: 17 May 2013 / Accepted: 24 May 2013 / Published: 3 June 2013
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Int. J. Mol. Sci. 2013, 14(5), 9099-9110; doi:10.3390/ijms14059099
Received: 5 March 2013 / Revised: 19 April 2013 / Accepted: 22 April 2013 / Published: 25 April 2013
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Int. J. Mol. Sci. 2013, 14(2), 3773-3785; doi:10.3390/ijms14023773
Received: 9 January 2013 / Revised: 29 January 2013 / Accepted: 6 February 2013 / Published: 8 February 2013
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: TP53INP1 Gene is Implicated in Radiation-Induced Senescence
Authors:
Nikolett Sándor, Boglárka Schilling Tóth, Enikő Kis, Géza Sáfrány, Hargita Hegyesi
Affiliation:
Division of Molecular Radiobiology and Biodosimetry, F. Joliot-Curie National Research Institute for Radiobiology and Radiohygiene, Anna 5, Budapest, 1221 Hungary
Abstract:
Background and Purpose: Tumor protein 53-induced nuclear protein-1 (TP53INP1) encodes two nuclear protein isoforms (TP53INP1α and TP53INP1β) and transcription is activated by p53. Overexpression of TP53INP1 promotes apoptosis and cell cycle arrest in different tumor cell lines. Therefore, TP53INP1 appears as a key element in p53-mediated cell death and cell cycle arrest, induced by cellular stress. Moreover, it was shown that TP53INP1 interacted with p53 and these interactions modified the transcriptional activity of p53 on several target genes such as CDKN1A, PIG-3 and MDM2. The objective of this study was to assess whether TP53INP1 plays a functional role in regulating cellular responses to IR. Methods: F11hTERT (telomerase immortalized) human fibroblast cells were used in the study. To investigate the role of TP53INP1 in radiation response the gene was silenced by the stable transfection of shRNAs using lentiviral vectors. Radiation induced direct and bystander effects were assessed by following survival using colony-forming assay and by investigating mitochondrial DNA deletions by real-time PCR. Alterations in cell cycle distribution were analyzed by flow cytometry, while radiation-induced senescence was studied with SA-β-Gal staining. Autophagy changes were measured by Acridine Orange staining and the expression of TP53INP1, GDF-15, GADD45A and CDKN1A was measured by real-time PCR. Results: We demonstrate here radiation induced dose dependent expressional changes of TP53INP1 in both irradiated and bystander fibroblast cells. We established stable fibroblast cell lines where the expression of TP53INP1 was constitutively knocked-down by RNA interference. TP53INP1 was required for IR induced maximal elevation of CDKN1A and GDF-15 expressions. Likewise, autophagy and senescence was deregulated following irradiation in the absence of TP53INP1. TP53INP1 deficient cells showed resistance of the G2-delay, and the proliferation rate was higher compared with wild type F11hTERTcells. Finally, we showed that TP53INP1 proficiency is important for clonogenic survival after radiation. Conclusions: These data reveal novel functional roles for TP53INP1 in cell cycle, survival and responses to IR. Taken together, we concluded that autophagy impairment induces premature senescence through a TP53INP1-dependent manner in primary human fibroblasts.

Type of Paper: Review
Title:
Cellular pathways involved in radiation toxicity and protection
Authors:
Patrick Maier
Abstract:
During the last decades improvements in planning and application of radiotherapy in combination with surgery and chemotherapy resulted in increased survival rates of tumour patients. However, the success of radiotherapy is impaired by two reasons: firstly radioresistance of tumour cells and secondly radiation-induced damage of normal tissue cells located in the field of ionizing radiation. These limitations demand the development of drugs for either radiosensitisation of tumour cells or radioprotection of normal tissue cells. For this reason, in order to identify targets the detailed understanding of the cellular pathways involved in radiation response is an absolute requirement. The most important pathways of radioresponse and several proteins as targets for radiosensitisation or radioprotection will be described in this review.

Type of Paper: Review
Title:
Molecular, cellular and functional effects of radiation-induced brain injury: a review
Authors:
M. Adamkov, S. Balentova
Abstract:
Radiation therapy is the most effective non-surgical treatment of primary brain tumors and metastases. Preclinical studies have provided valuable insights into pathogenesis of radiation-induced injury to the central nervous system. Radiation-induced brain injury can damage the neuronal, glial and vascular compartments of the brain and may lead to molecular, cellular and functional changes. Given its central role in memory and adult neurogenesis, the majority of studies have focused on the hippocampus. These findings have been interpreted to suggest that the hippocampal avoidance in cranial radiotherapy will prevent radiation-induced cognitive impairment of patients. Multiple rodent studies have shown that this problem is more complex that was previously thought. Regarding the fact, that radiation-induced cognitive impairment reflects both hippocampal and non-hippocampal compartments, there is a critical importance to investigate the molecular, cellular and functional modifications in various brain regions as well as their integration at clinically relevant doses and schedules. Our purpose is to provide a literature overview and our published results in order to help a translation of preclinical findings to the clinical practice, with aim to improve the quality of life in patients with brain tumors.

Type of Paper: Review
Title: Alpha-1-microglobulin (A1M) in protection of kidneys during PRRT
Author: Bo Åkerström
Abstract: Alpha-1-microglobulin (A1M) is a reductase and radical scavenging protein ubiqutously present in plasma and extravascular tissue. Human A1M has antioxidation properties and was shown to prevent radiation-induced in vitro cell damage and protect non-irradiated surrounding cells. Peptide-receptor radionuclide therapy (PRRT) is in clinical use for treatment of patients with neuroendocrine tumours. A major side-effect of PRRT is renal toxicity due to glomerular filtration of the radionuclide-conjugated peptides. This review will summarize the physiology of A1M, clinical and experimental aspects of PRRT and its side-effects, and finally discuss the possible use of A1M to protect the kidneys during PRRT.

Title: Effector Function of CTLs is Increased By Irradiated Colorectal and Breast Tumor Cells That Modulate OX-40L and 4-1BBL and Is Reversed Following Dual Blockade
Author: Charlie Garnett Benson
Abstract: Background: Sub-lethal doses of ionizing radiation (IR) can alter the phenotype of target tissue by modulating genes that influence effector T-cell activity. Previous studies indicate that cancer cells responded to radiation by up-regulating surface expression of death receptors, cell adhesion molecules and tumor-associated antigens (TAA). However, there is limited information available regarding how T cells themselves are altered following these interactions with irradiated tumor cells. Methods: Here, several human colorectal and breast tumor cell lines were exposed to radiation (0-10Gy) in vitro and changes in the expression of molecules costimulatory to effector T cells (4-1BBL, OX-40L, CD70, ICOSL) were examined by flow cytometry. T cell effector function was assessed to determine if changes in these proteins were directly related to the changes in T cell function. Results: We found OX-40L and 4-1BBL to be the most consistently upregulated proteins on the surface of colorectal tumor cells post-IR while ICOSL and CD70 remained largely unaltered. Expression of both OX-40L and 4-1BBL was also altered following irradiation of breast carcinoma cells supporting the ability of radiation to modulate these genes across diverse cancer types. Co-stimulatory molecule expression was also altered in irradiated murine tumor cells both in vitro and in vivo. Expression of these gene products correlated with enhanced killing of both irradiated human colorectal and breast tumor cells by TAA-specific T-cells. Importantly, blocking of both OX-40L and 4-1BBL reversed radiation-enhanced T-cell killing of human tumor targets as well as T-cell survival and activation. Conclusions: Overall, results of this study suggest that, beyond simply rendering tumor cells more sensitive to immune attack, radiation can be used to specifically modulate expression of genes that directly stimulate effector T cell activity

Last update: 15 April 2015

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