Radiation-induced hypoxia may perpetuate late normal tissue injury.

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Vujaskovic, Z; Anscher, MS; Feng, QF; Rabbani, ZN; Amin, K; Samulski, TS; Dewhirst, MW; Haroon, ZA

Published Date

  • July 15, 2001

Published In

Volume / Issue

  • 50 / 4

Start / End Page

  • 851 - 855

PubMed ID

  • 11429211

International Standard Serial Number (ISSN)

  • 0360-3016

Language

  • eng

Conference Location

  • United States