In patients with non-small-cell lung carcinoma (NSCLC), the surgical resection remains the primary and preferred approach to the treatment of stage I-II NSCLC. Despite advances in surgical techniques, these patients have a risk of development a severe lung injury, because during lobectomy the operated lung is completely collapsed and hypoperfused. This hypoperfusion is due in part to a reactive hypoxic pulmonary vasoconstriction in response to alveolar hypoxia, which optimizes gas exchange. Hypoxic or ischemic tissues increase the reactive oxygen species (ROS) production in mitochondria respiratory chain, because the respiratory cytochromes become redox-reduced allowing them to directly transfer electrons to O2 producing large amount of superoxide anions, which contributes to more vasoconstriction. The primary site of ROS production during hypoxia appears to be complex III, and paradoxical increase of ROS production during hypoxia may be explained by an effect of O2 within mitochondria inner membrane on the ubisemiquinone radical in complex III. Thus, patients undergoing lobar resection suffer a relative lung ischemia-hypoxia during the collapse, followed by expansion-reperfusion injury attributed to the production of ROS. Acute lung injury (ALI) and postoperative adult respiratory distress syndrome (ARDS) after major thoracic surgery remains the leading cause of death from pulmonary surgery. Because to date few studies have assessed this subject in detail, we have showed recently also an increase of oxidative stress damage during lung lobectomy, associated to a direct correlation of lung collapse time with oxidative stress marker levels in exhaled breath condensate and blood.