Oxidative lung damage may be associated with the destruction of alveolar cells. Type II alveolar epithelial cells (AECs), as progenitors of type I cells, are indispensable for the renovation of alveolar structure after lung injury. Extensive damage to type II cells could be responsible for unfavorable outcome. However, the susceptibility of type II AECs to oxidative stress is unclear. Materials We investigated the susceptibility of freshly isolated and cultured rat type II AECs to and Methods: oxidative stress (H2O2 and Fe2+). Thiobarbituric acid reactive substances (TBARS) were measured as indices of lipid peroxidation and cytotoxicity was estimated by the MTT test. Aminotriazol (ATZ), an inhibitor of intracellular catalase, was used to estimate the protective role of catalase. Results: TBARS concentration increased significantly in freshly isolated, oxidant-exposed cells (4.0?1.3 vs. 8.3?2.2 nmol/g protein, p=0.0313) and insignificantly in cultured cells (1.7?0.4 vs. 4.4?1.7 nmol/g protein). ATZ was toxic even to cells not exposed to oxidants. Inhibition of catalase in cells exposed to oxidants resulted in an insignificant increase in TBARs: 4.5?1.5 vs. 16.2?3.9 nmol/g protein, p=0.0625, and 4.0?0.8 vs.7.6?4.0 for freshly isolated and cultured cells, respectively. Oxidative stress itself did not increase cytotoxicity. Conclusions: Type II AECs are not resistant to oxidative stress. We cannot, however, explain why cells with evidence of lipid peroxidation do not show increased cytotoxicity. The toxicity of ATZ is not related to oxidative cell damage. In cells exposed to oxidants, TBARS may further increase when catalase is inhibited, which suggests an important protective role for catalase.