PURPOSE: The purpose of this study was to determine whether or not hypoxia develops in rat lung tissue after radiation. METHODS AND MATERIALS: Fisher-344 rats were irradiated to the right hemithorax using a single dose of 28 Gy. Pulmonary function was assessed by measuring the changes in respiratory rate every 2 weeks, for 6 months after irradiation. The hypoxia marker was administered 3 h before euthanasia. The tissues were harvested at 6 weeks and 6 months after irradiation and processed for immunohistochemistry. RESULTS: A moderate hypoxia was detected in the rat lungs at 6 weeks after irradiation, before the onset of functional or histopathologic changes. The more severe hypoxia, that developed at the later time points (6 months) after irradiation, was associated with a significant increase in macrophage activity, collagen deposition, lung fibrosis, and elevation in the respiratory rate. Immunohistochemistry studies revealed an increase in TGF-beta, VEGF, and CD-31 endothelial cell marker, suggesting a hypoxia-mediated activation of the profibrinogenic and proangiogenic pathways. CONCLUSION: A new paradigm of radiation-induced lung injury should consider postradiation hypoxia to be an important contributing factor mediating a continuous production of a number of inflammatory and fibrogenic cytokines.
PURPOSE: The purpose of this study was to determine whether or not hypoxia develops in rat lung tissue after radiation. METHODS AND MATERIALS: Fisher-344 rats were irradiated to the right hemithorax using a single dose of 28 Gy. Pulmonary function was assessed by measuring the changes in respiratory rate every 2 weeks, for 6 months after irradiation. The hypoxia marker was administered 3 h before euthanasia. The tissues were harvested at 6 weeks and 6 months after irradiation and processed for immunohistochemistry. RESULTS: A moderate hypoxia was detected in the rat lungs at 6 weeks after irradiation, before the onset of functional or histopathologic changes. The more severe hypoxia, that developed at the later time points (6 months) after irradiation, was associated with a significant increase in macrophage activity, collagen deposition, lung fibrosis, and elevation in the respiratory rate. Immunohistochemistry studies revealed an increase in TGF-beta, VEGF, and CD-31 endothelial cell marker, suggesting a hypoxia-mediated activation of the profibrinogenic and proangiogenic pathways. CONCLUSION: A new paradigm of radiation-induced lung injury should consider postradiation hypoxia to be an important contributing factor mediating a continuous production of a number of inflammatory and fibrogenic cytokines.
Authors: R Yahyapour; E Motevaseli; A Rezaeyan; H Abdollahi; B Farhood; M Cheki; S Rezapoor; D Shabeeb; A E Musa; M Najafi; V Villa Journal: Clin Transl Oncol Date: 2018-01-09 Impact factor: 3.405
Authors: Sara Szabo; Swarajit N Ghosh; Brian L Fish; Sreedhar Bodiga; Rade Tomic; Gagan Kumar; Natalya V Morrow; John E Moulder; Elizabeth R Jacobs; Meetha Medhora Journal: Radiat Res Date: 2010-04 Impact factor: 2.841
Authors: Vijayalakshmi Sridharan; Sunil K Sharma; Eduardo G Moros; Peter M Corry; Preeti Tripathi; Benjamin J Lieblong; Chandan Guha; Martin Hauer-Jensen; Marjan Boerma Journal: Int J Radiat Biol Date: 2013-04-16 Impact factor: 2.694