scholarly journals An update on the mechanisms and pathophysiological consequences of genomic instability with a focus on ionizing radiation

2015 ◽  
pp. 225 ◽  
Author(s):  
Christian Streffer
Keyword(s):  
Ionizing Radiation ◽  
Genomic Instability

scholarly journals Genomic instability induced by radiation-mimicking chemicals is not associated with persistent mitochondrial degeneration

2021 ◽  
Author(s):  
Luukkonen Jukka ◽  
Höytö Anne ◽  
Sokka Miiko ◽  
Syväoja Juhani ◽  
Juutilainen Jukka ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Neuroblastoma Cells ◽  
Superoxide Production ◽  
Mitochondrial Activity ◽  
Mitochondrial Superoxide

AbstractIonizing radiation has been shown to cause induced genomic instability (IGI), which is defined as a persistently increased rate of genomic damage in the progeny of the exposed cells. In this study, IGI was investigated by exposing human SH-SY5Y neuroblastoma cells to hydroxyurea and zeocin, two chemicals mimicking different DNA-damaging effects of ionizing radiation. The aim was to explore whether IGI was associated with persistent mitochondrial dysfunction. Changes to mitochondrial function were assessed by analyzing mitochondrial superoxide production, mitochondrial membrane potential, and mitochondrial activity. The formation of micronuclei was used to determine immediate genetic damage and IGI. Measurements were performed either immediately, 8 days, or 15 days following exposure. Both hydroxyurea and zeocin increased mitochondrial superoxide production and affected mitochondrial activity immediately after exposure, and mitochondrial membrane potential was affected by zeocin, but no persistent changes in mitochondrial function were observed. IGI became manifested 15 days after exposure in hydroxyurea-exposed cells. In conclusion, immediate responses in mitochondrial function did not cause persistent dysfunction of mitochondria, and this dysfunction was not required for IGI in human neuroblastoma cells.

Commentary on radiation-induced bystander effects

2004 ◽  
Vol 23 (2) ◽  
pp. 91-94 ◽  
Author(s):  
Eric G Wright
Keyword(s):  
Free Radical ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Inflammatory Responses ◽  
Genetic Alterations ◽  
Bystander Effects ◽  
Intercellular Signalling ◽  
Radiation Induced ◽  
Radical Generation ◽  
In Cells

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.

Genomic instability induced by high and low let ionizing radiation

2000 ◽  
Vol 25 (10) ◽  
pp. 2107-2117 ◽  
Author(s):  
C.L. Limoli ◽  
B. Ponnaiya ◽  
J.J. Corcoran ◽  
E. Giedzinski ◽  
M.I. Kaplan ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Genomic Instability

Genomic Instability Induced by Ionizing Radiation

1996 ◽  
Vol 146 (3) ◽  
pp. 247 ◽  
Author(s):  
William F. Morgan ◽  
Joseph P. Day ◽  
Mark I. Kaplan ◽  
Eva M. McGhee ◽  
Charles L. Limoli
Keyword(s):  
Ionizing Radiation ◽  
Genomic Instability

Ionizing Radiation-Induced Genomic Instability in CHO cells Is Followed by Selection of Radioresistant Cell Clones

2009 ◽  
Vol 147 (5) ◽  
pp. 596-598 ◽  
Author(s):  
D. V. Guryev ◽  
A. N. Osipov ◽  
E. Yu. Lizunova ◽  
N. Yu. Vorobyeva ◽  
O. V. Boeva
Keyword(s):  
Ionizing Radiation ◽  
Genomic Instability ◽  
Cho Cells ◽  
Cell Clones ◽  
Radiation Induced ◽  
Selection Of

scholarly journals Ionizing Radiation Induces Delayed Hyperrecombination in Mammalian Cells

2004 ◽  
Vol 24 (11) ◽  
pp. 5060-5068 ◽  
Author(s):  
Lei Huang ◽  
Suzanne Grim ◽  
Leslie E. Smith ◽  
Perry M. Kim ◽  
Jac A. Nickoloff ◽  
...  
Keyword(s):  
Cell Death ◽  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mammalian Cells ◽  
Chromosomal Instability ◽  
Radiation Risk ◽  
Green Fluorescence Protein ◽  
Initial Exposure ◽  
Reproductive Cell ◽  
Reproductive Cell Death

ABSTRACT Exposure to ionizing radiation can result in delayed effects that can be detected in the progeny of an irradiated cell multiple generations after the initial exposure. These effects are described under the rubric of radiation-induced genomic instability and encompass multiple genotoxic endpoints. We have developed a green fluorescence protein (GFP)-based assay and demonstrated that ionizing radiation induces genomic instability in human RKO-derived cells and in human hamster hybrid GM10115 cells, manifested as increased homologous recombination (HR). Up to 10% of cells cultured after irradiation produce mixed GFP+/− colonies indicative of delayed HR or, in the case of RKO-derived cells, mutation and deletion. Consistent with prior studies, delayed chromosomal instability correlated with delayed reproductive cell death. In contrast, cells displaying delayed HR showed no evidence of delayed reproductive cell death, and there was no correlation between delayed chromosomal instability and delayed HR, indicating that these forms of genome instability arise by distinct mechanisms. Because delayed hyperrecombination can be induced at doses of ionizing radiation that are not associated with significantly reduced cell viability, these data may have important implications for assessment of radiation risk and understanding the mechanisms of radiation carcinogenesis.

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