Bone Marrow Protein Oxidation in Response to Ionizing Radiation in C57BL-6J MiceReport as inadecuate


Bone Marrow Protein Oxidation in Response to Ionizing Radiation in C57BL-6J Mice


Bone Marrow Protein Oxidation in Response to Ionizing Radiation in C57BL-6J Mice - Download this document for free, or read online. Document in PDF available to download.

1

Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA

2

Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA





*

Author to whom correspondence should be addressed.



Abstract The bone marrow is one of the most radio-sensitive tissues. Accidental ionizing radiation exposure can damage mature blood cells and hematopoietic progenitor-stem cells, and mortality can result from hematopoietic insufficiency and infection. Ionizing radiation induces alterations in gene and protein expression in hematopoietic tissue. Here we investigated radiation effects on protein carbonylation, a primary marker for protein oxidative damage. C57BL-6 mice were either sham irradiated or exposed to 7.5 Gy 60Co 0.6 Gy-min total body irradiation. Bone marrow was obtained 24 h post-irradiation. Two dimensional 2-D gel electrophoresis and Oxyblot immunodetection were used to discover carbonylated proteins, and peptide mass fingerprinting was performed for identification. 2D gels allowed the detection of 13 carbonylated proteins in the bone marrow; seven of these were identified, with two pairs of the same protein. Baseline levels of carbonylation were found in 78 kDa glucose-related protein, heat shock protein cognate 71 KDa, actin, chitinase-like protein 3 CHI3L1, and carbonic anhydrase 2 CAII. Radiation increased carbonylation in four proteins, including CHI3L1 and CAII, and induced carbonylation of one additional protein not identified. Our findings indicate that the profile of specific protein carbonylation in bone marrow is substantially altered by ionizing radiation. Accordingly, protein oxidation may be a mechanism for reduced cell viability. View Full-Text

Keywords: acute radiation syndrome; protein carbonylation; proteomic analysis acute radiation syndrome; protein carbonylation; proteomic analysis





Author: Yong-Chul Kim 1, Michal Barshishat-Kupper 1, Elizabeth A. McCart 1, Gregory P. Mueller 2 and Regina M. Day 1,*

Source: http://mdpi.com/



DOWNLOAD PDF




Related documents