Figure 5

Effects of the NADPH oxidase and mitochondrial inhibitors, as well as of phagocytic NADPH oxidase gene deletion on the ESR signal intensity in isolated perfused lungs after addition of phorbol-12-myristate-13-acetate (PMA) during normoxic ventilation. (A) Effect of the NADPH oxidase inhibitor apocynin (500 μM) and the inhibitor of mitochondrial complex I, rotenone (350 nM) on the increase rate in ESR signal intensity after addition of PMA. Each inhibitor was added to the buffer fluid 30 min before addition of PMA. In the +SOD group, SOD was present throughout the experiments. * significant difference as compared to control. (B) Comparison of the increase rate in ESR signal intensity after addition of PMA in wildtype (WT) and gp91phox-deficient (gp91phox^-/-) mice. Lungs were perfused for 120 min prior to PMA addition (10 μM) either in the presence or absence of 150 U/ml SOD. * significant difference as compared to WT. Data are given as changes in the increase rate of the ESR signal intensity after PMA addition, as compared to the values before PMA addition (set as 100%). Data are from n = 4–5 experiments for each group.