Showing papers on "Radiation-induced lung injury published in 2010"
TL;DR: The three-dimensional dose, volume, and outcome data for lung are reviewed in detail and it is confirmed that there is no evident threshold "tolerance dose-volume" levels and there are strong volume and fractionation effects.
Abstract: The three-dimensional dose, volume, and outcome data for lung are reviewed in detail. The rate of symptomatic pneumonitis is related to many dosimetric parameters, and there are no evident threshold "tolerance dose-volume" levels. There are strong volume and fractionation effects.
892 citations
TL;DR: The current knowledge of the molecular and cellular events that occur after radiation therapy, the clinical manifestations of radiation-induced lung injury, current strategies to minimize lung injury and recent experimental methods to reduce lung injury are discussed and their potential for translation into the clinic are discussed.
240 citations
TL;DR: For three cases of radiation pneumonitis, hyperpolarized helium-3 magnetic resonance imaging changes between pre- and post-treatment imaging were consistent with CT evidence of radiation-induced lung injury.
40 citations
TL;DR: Treatment with MnTE-2-PyP(5+), which has been demonstrated to reduce lung injury from radiation, reduced apparent protein degradation and apoptosis indicators, suggesting that preservation of lung structural integrity and prevention of cell loss may underlie the radioprotective effect of this compound.
Abstract: Purpose To identify temporal changes in protein expression in the irradiated rat lung and generate putative mechanisms underlying the radioprotective effect of the manganese superoxide dismutase mimetic MnTE-2-PyP 5+ . Methods and Materials Female Fischer 344 rats were irradiated to the right hemithorax with a single dose of 28 Gy and killed from day 1 to 20 weeks after irradiation. Proteomic profiling was performed to identify proteins that underwent significant changes in abundance. Some irradiated rats were administered MnTE-2-PyP 5+ and changes in protein expression and phosphorylation determined at 6 weeks after irradiation. Results Radiation induced a biphasic stress response in the lung, as shown by the induction of heme oxygenase 1 at 1–3 days and at 6–8 weeks after irradiation. At 6–8 weeks after irradiation, the down-regulation of proteins involved in cytoskeletal architecture (filamin A and talin), antioxidant defense (biliverdin reductase and peroxiredoxin II), and cell signaling (β-catenin, annexin II, and Rho-guanosine diphosphate dissociation inhibitor) was observed. Treatment with MnTE-2-PyP 5+ partially prevented the apparent degradation of filamin and talin, reduced the level of cleaved caspases 3 and 9, and promoted Akt phosphorylation as well as β-catenin expression. Conclusion A significant down-regulation of proteins and an increase in protein markers of apoptosis were observed at the onset of lung injury in the irradiated rat lung. Treatment with MnTE-2-PyP 5+ , which has been demonstrated to reduce lung injury from radiation, reduced apparent protein degradation and apoptosis indicators, suggesting that preservation of lung structural integrity and prevention of cell loss may underlie the radioprotective effect of this compound.
15 citations
TL;DR: The findings suggest that early treatment with IL-6RA after irradiation alone does not protect against radiation-induced lung injury, and anti-IL-6 monoclonal receptor antibody could ameliorate radiation- induced lung injury in mice.
Abstract: Radiation pneumonia and subsequent radiation lung fibrosis are major dose-limiting complications for patients undergoing thoracic radiotherapy. Interleukin-6 (IL-6) is a pleiotropic cytokine and plays important roles in the regulation of immune response and inflammation. The purpose of this study was to investigate whether anti-IL-6 monoclonal receptor antibody (IL-6RA) could ameliorate radiation-induced lung injury in mice. BALB/cAnNCrj mice having received thoracic irradiation of 21 Gy were injected intraperitoneally with IL-6RA (MR16-1) or control rat IgG twice, immediately and seven days after irradiation. Enzyme-linked immunosorbent assay was used to examine the plasma level of IL-6 and serum amyloid A (SAA). Lung injury was assessed by histological staining with haematoxylin and eosin or Azan, measuring lung weight, and hydroxyproline. The mice treated with IL-6RA did not survive significantly longer than the rat IgG control. We observed marked up-regulation of IL-6 in mice treated with IL-6RA 150 days after irradiation, whereas IL-6RA temporarily suppressed early radiation-induced increase in the IL-6 release level. Histopathologic assessment showed no differences in lung section or lung weight between mice treated with IL-6RA and control. Our findings suggest that early treatment with IL-6RA after irradiation alone does not protect against radiation-induced lung injury.
13 citations
2 citations
Journal Article•
TL;DR: The progress of research on radiation-induced lung injury is reviewed and more effective methods are expected to be explored to reduce radiation injury.
Abstract: OBJECTIVE:To review the progress of research on radiation-induced lung injury.METHODS:With "radiation-induced lung injury" and "chest tumor" as key words ,the literature was searched in Pubmed and CNKI data-bases between 01-1998 and 01-2009.Choice criteria: 1) molecular biology machanism;2) clinical factors,prevention and treatment of radiation-induced lung injury.A total of 34 literatures were selected.RESULTS:Radiation pneumonitis and pulmonary fibrosis are dose-limiting side effects of radiotherapy for lung cancer.Cytokines such as TGF-β,PDGF and TNF-α are associated with radiation-induced lung injury.Dose-volumetric parameters V20,V30,MLD and foundation lung function are predictors of developing radiation injury.AMF,GSH and traditional Chinese medicine have certain ability to treat radiation injury.CONCLUSION:More effective methods are expected to be explored to reduce radiation injury.
1 citations