Quantitative proteomic analysis of mitochondrial proteins reveals prosurvival mechanisms in the perpetuation of radiation-induced genomic instability.

Free Radical Biology & Medicine
Stefani N ThomasJanet E Baulch

Abstract

Radiation-induced genomic instability is a well-studied phenomenon that is measured as mitotically heritable genetic alterations observed in the progeny of an irradiated cell. The mechanisms that perpetuate this instability are unclear; however, a role for chronic oxidative stress has consistently been demonstrated. In the chromosomally unstable LS12 cell line, oxidative stress and genomic instability were correlated with mitochondrial dysfunction. To clarify this mitochondrial dysfunction and gain insight into the mechanisms underlying radiation-induced genomic instability we have evaluated the mitochondrial subproteome and performed quantitative mass spectrometry analysis of LS12 cells. Of 98 quantified mitochondrial proteins, 17 met criteria for fold changes and reproducibility; and 11 were statistically significant in comparison with the stable parental GM10115 cell line. Previous observations implicated defects in the electron transport chain (ETC) in the LS12 cell mitochondrial dysfunction. Proteomic analysis supports these observations, demonstrating significantly reduced levels of mitochondrial cytochrome c, the intermediary between complexes III and IV of the ETC. Results also suggest that LS12 cells compensate for ETC...Continue Reading

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Citations

Oct 10, 2013·Radiation and Environmental Biophysics·Omid AzimzadehSoile Tapio
Oct 15, 2013·Proteomics·Robert WildgruberJohann Bauer
Nov 26, 2015·Environmental and Molecular Mutagenesis·Janet E BaulchCharles L Limoli
Feb 26, 2015·Mutagenesis·Deborah J KeszenmanJanet E Baulch
Jul 31, 2013·Free Radical Biology & Medicine·Winnie Wai-Ying Kam, Richard B Banati
Dec 17, 2016·International Journal of Molecular Sciences·Eva Yi KongKwan Ngok Yu
Jan 6, 2017·International Journal of Radiation Biology·Charles L Limoli

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