Fig. 3.

Increases mitochondrial damage is attributed to reactive oxygen species (ROS) accumulation by peroxiredoxin (Prdx3) deficiency.

(A and B) Representative low- and high-magnification images of the boxed areas of Prdx3 wild-type (Prdx3 WT) and Prdx3-deficient (Prdx3 KO) mouse embryonic fibroblasts (MEFs). MEFs were infected with mito-catalase adenovirus for 24 h and immunostained with an antibody against Tom20 (green) plus 100 nM MitoTracker (red) (A) or 150 nM MitoTracker (green) plus 5 μM MitoSOX (red) (B) for 25 min. Scale bar, 2 (boxed areas) or 10 μm. (C and D) Quantification of depolarized (damaged) mitochondria (C) or mitochondrial ROS levels (D) in Prdx3 WT and Prdx3 KO MEFs (n = 25–33 cells). (E) Immunoblotting of whole-cell lysates of Prdx3 WT and Prdx3 KO MEFs infected with mito-catalase adenovirus for 24 h using catalase, Prdx3, and Tom20 antibodies. **P < 0.01. Data (A–E) are representative of three independent experiments. . (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)