Overexpression of extracellular superoxide dismutase reduces severity of radiation-induced lung toxicity through downregulation of the TGF-β signal transduction pathway

Abstract

Purpose/Objective: Superoxide dismutase is a naturally occurring enzyme, which scavenges free radicals produced during different pathophysiological processes. Ionizing radiation generates free radicals, which lead to activation and production of inflammatory and pro-fibrogenic cytokines. Activation of TGF-β is central to the development of radiation (RT)-induced pulmonary toxicity. The biological effects of TGF-β is mediated through its signal transduction pathway via phosphorylation of the protein Smad 3. The objective of this study is to determine whether overexpression of ECSOD, ameliorates acute radiation induced injury by inhibiting activation of TGF-β with a resulting downregulation of the phophorylation of smad3 (psmad3).