Protein Oxidation in the Lungs of C57BL/6J Mice Following X-Irradiation.

ABSTRACT: Damage to normal lung tissue is a limiting factor when ionizing radiation is used in clinical applications. In addition, radiation pneumonitis and fibrosis are a major cause of mortality following accidental radiation exposure in humans. Although clinical symptoms may not develop for months after radiation exposure, immediate events induced by radiation are believed to generate molecular and cellular cascades that proceed during a clinical latent period. Oxidative damage to DNA is considered a primary cause of radiation injury to cells. DNA can be repaired by highly efficient mechanisms while repair of oxidized proteins is limited. Oxidized proteins are often destined for degradation. We examined protein oxidation following 17 Gy (0.6 Gy/min) thoracic X-irradiation in C57BL/6J mice. Sevent

SUBMITTER: Barshishat-Kupper M 

PROVIDER: S-EPMC5217375 | biostudies-literature | 2015 Aug

REPOSITORIES: biostudies-literature