scholarly journals Mitochondrial Complex II Dysfunction Can Contribute Significantly to Genomic Instability after Exposure to Ionizing Radiation

2009 ◽  
Vol 172 (6) ◽  
pp. 737-745 ◽  
Author(s):  
Disha Dayal ◽  
Sean M. Martin ◽  
Kjerstin M. Owens ◽  
Nukhet Aykin-Burns ◽  
Yueming Zhu ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Genomic Instability ◽  
Mitochondrial Complex ◽  
Complex Ii

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.

scholarly journals Exome sequencing identifies NFS 1 deficiency in a novel Fe‐S cluster disease, infantile mitochondrial complex II / III deficiency

2013 ◽  
Vol 2 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Sali M. K. Farhan ◽  
Jian Wang ◽  
John F. Robinson ◽  
Piya Lahiry ◽  
Victoria M. Siu ◽  
...  
Keyword(s):  
Exome Sequencing ◽  
Mitochondrial Complex ◽  
Complex Ii

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

Discovery of 1,2,4-triazole-1,3-disulfonamides as dual inhibitors of mitochondrial complex II and complex III

2015 ◽  
Vol 39 (9) ◽  
pp. 7281-7292 ◽  
Author(s):  
Hua Cheng ◽  
Yan-Qing Shen ◽  
Xia-Yan Pan ◽  
Yi-Ping Hou ◽  
Qiong-You Wu ◽  
...  
Keyword(s):  
Complex Iii ◽  
Dual Function ◽  
Mitochondrial Complex ◽  
Complex Ii ◽  
Dual Inhibitors

1,2,4-Triazole-1,3-disulfonamide derivatives as dual function inhibitors of mitochondrial complex II (SQR) and complex III (cyt bc1) were discovered.

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