Special Issue "Radiation Toxicity in Cells"

Guest Editor
Prof. Dr. Terrence Piva
RMIT University, PO Box 71, Bundoora, Victoria 3083, Australia
Website: http://www.rmit.edu.au/browse;ID=kn6c15nk6ilu
E-Mail: terry.piva@rmit.edu.au
Phone: Office +61 3 9925 6503; Lab 9925 7278
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

Dear Colleagues,

Life forms on the planet are exposed to different forms of radiation be it emitted from the sun as X-rays, radio waves, visible, ultraviolet or infrared light, or from 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) has on individuals.  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 cancers in people.  This issue will look at the cytotoxic effects of radiation.   While emphasis will be placed on modes of cell death, studies on DNA damage, intracellular signalling pathways, caspase activation, membrane damage, production of ROS, gene activation, organelle dysfunction are also encouraged.  Reviews of the mechanisms involved in the cytotoxic effects of electromagnetic radiation are welcomed, as well as studies on the effect of long-term exposure to these forms of radiation on humans.  I encourage you to submit a manuscript to this issue and help shed further “light” on the lethal effects that radiation has on cells and individuals.

Prof. Dr. Terrence Piva
Guest Editor

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed Open Access monthly journal published by MDPI.

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.

• radiation
• ultraviolet light
• X-rays
• γ radiation
• microwaves
• cell death
• DNA damage
• cell membrane
• caspases
• signalling pathways

Type of Paper: Article
Title: DNA Damage in Human Cells Under Intermittent and Continuous Exposure to a GMS-1800 Mobile Phone Signal
Author: Isabelle Lagroye
Affiliation : Laboratoire de bioélectromagnétisme EPHE, Laboratoire IMS UMR 5218, site ENSCBP, 16 avenue Pey Berland, 33607 Pessac ; E-Mail : isabelle.lagroye@ims-bordeaux.fr
Abstract: There is still some debate about potential DNA damages caused by radiofrequency fields (RF) emitted by mobile phones, particularly with intermittent exposure. The present work investigated /in vitro /the potential genotoxic effects of continuous or intermittent (5 minutes ON – 10 minutes OFF) GSM-1800 exposure at 2 W/kg during 1 to 48 hours. The skin and brain are the organs mostly exposed when using a mobile phone. Human primary dermal fibroblasts and human brain cell lines, CHME-5 and SH-SY5Y, were therefore exposed and DNA single-strand breaks were detected using the alkaline comet assay. Human cells were exposed to GSM-1800 under blind conditions using the SXC-1800 system built at IT’IS, and to ultraviolet radiation or Tert-butyl hydroxyperoxide used as positive controls. Immediately after exposure, the cells were treated for detection via the comet assay. At least a hundred comets per exposure condition were analyzed, using the CometScore™ software. Two parameters, i.e. the percentage of DNA in the tail of comets and the Olive moment were considered in the analysis. Our results show that continuous or intermittent exposures to GSM-1800 did not result in induction of DNA damage whatever the exposure duration and the human cell type were, suggesting that the GSM-1800 signal is not a genotoxic agent.

Type of Paper: Article
Title: Inhibition of poly(ADP-ribose) polymerase enhances radiochemosensitivity in cancers proficient in DNA double-strand break repair.
Author: Charles Kunos
Affiliation: Director of Gynecologic Radiation Oncology, Department of Radiation Oncology, University Hospitals Seidman Cancer Center, Case Comprehensive Cancer Center and Case Western Reserve University, 11100 Euclid Avenue/MAILSTOP: LTR 6068, Cleveland, Ohio 44106; E-Mail: charles.kunos@uhhospitals.org
Abstract: Pharmacologic inhibitors of poly(ADP-ribose) polymerase (PARP) putatively enhance radiation toxicity in cancer cells. Although there is considerable information on the molecular interactions of PARP and BRCA1- and BRCA2-deficient cancers, very little is known of the PARP inhibition effect upon DNA double-strand break repair after ionizing radiation or after stalled replication forks. In this work, we investigated whether PARP inhibition by ABT-888 (veliparib) would augment the death-provoking effects of ionizing radiation or the topoisomerase I poison topotecan in cervical and ovarian cancer cells. Radiation toxicity in cells was ABT-888 dose dependent. Also, synergistic topotecan-ABT-888 lethality was observed and is explained by increased unrepaired DNA double-strand breaks at 24 hours. Our findings support enhanced radiochemotherapy toxicity by ABT-888 inhibition of PARP in cancers proficient in DNA double-strand break repair.