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. 2010 Oct 19;183(8):1043–1054. doi: 10.1164/rccm.201002-0181OC

Figure 3.

Figure 3.

Mitochondrial superoxide production results in the activation of BAX and cell death. (A) Primary rat alveolar epithelial type II cells were infected with an adenovirus expressing no transgene (Ad-Null) or SOD2 (Ad-SOD2) and the relative abundance of SOD2 was measured by immunoblotting 48 hours later. (B) Cells were cotransfected with an adenovirus encoding an oxidant-sensitive GFP targeted to the mitochondrial matrix (mito-Ro-GFP) and either Ad-Null or Ad-SOD2 48 hours before exposure to hyperoxia or normoxia for 4 hours. The oxidation of mito-Ro-GFP was then assessed using flow cytometry. (C) Sham transfected cells or cells transfected with Ad-Null or Ad-SOD2 were exposed to hyperoxia for 16 hours after which the cells were immunostained with an antibody that recognizes an activated form of Bax (green, left column) and the mitochondrial marker MitoTracker Red (red, middle column). The right column is a merged image. Each column is a representative image sampled from three separate isolations. (D) Identically infected cells were exposed to hyperoxia for 48 hours and cell death was measured (LDH release). *P < 0.05 compared with normoxic controls. †P < 0.05 for comparison of difference between Ad-SOD2 and Ad-SOD null transfected cells.