Oxidative stress and complement activation associated with the RPE of 18–20-mo-old Klc1^−/− mice. (A and B) MDA immunoreactivity in WT (A) and Klc1^−/− (B) retinal sections. Transmitted light images are on the right of each panel. (C and D) C3 immunoreactivity in WT (C) and Klc1^−/− (D) retinal sections. (E and F) Amplified areas of C and D, respectively. Note the increase in the width of C3 immunoreactivity in the mutant (F), invading most of the cytoplasm of RPE cells. (G and H) Quantification of C3 immunofluorescence in terms of fluorescence intensity (G; *, P = 0.02) and width of the band of fluorescence (H; **, P = 0.005). At least five images, spanning the central/midcentral retina from at least three animals of each group, were analyzed. Student’s t test (*, P < 0.05; **, P < 0.01). (I and J) C3 immunoreactivity in the central, middle, and peripheral retina of WT (I) and Klc1^−/− (J) mice. (K) Quantification of C3 immunofluorescence in the central (*, P = 0.02), middle (**, P = 0.002), and peripheral (NS, P = 0.4) retina of WT and Klc1^−/− mice; n = 3 animals. (L and M) Retinal sections of WT (L) and Klc1^−/− (M) mice immunolabeled with antibodies against C3d. Note the higher immunolabeling in BM and the basal side of RPE cells in the mutant retina. (N and O) Retinal sections of WT (N) and Klc1^−/− (O) mice immunolabeled for the C5b-9 complex, showing deposition of the membrane attack complex in some areas of the innermost side of the choroid, adjacent to the RPE, in Klc1^−/− mice. Ch, choroid; RPE, retinal pigment epithelium. Bars, 10 µm. Error bars are means ± SEM.