Abstract
Purpose/Objective: The risk of unacceptable radiation (RT)-induced lung injury remains a significant limiting factor in the current treatment of the tumors involving the thoracic region. Despite advances in normal tissue radiobiology, demonstrating that ionizing radiation triggers a cascade of genetic and molecular events that proceed during a latent period of pulmonary injury, the precise mechanisms underlying RT-induced lung injury remain unclear. An association between the presence of hypoxia in lung tissue and the development of RT-induced lung injury has been recently reported (Vujaskovic et al. 2001) suggesting hypoxia to be underlying process that perpetuates development of RT-induced lung injury. The objective of this study is to quantify the amount of hypoxia using the fully calibrated hypoxia marker EF5, and to determine whether hypoxia in the irradiated lungs occurs due to limitations in perfusion rather than due to macrophages associated increase in oxygen consumption.
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