FIGURE 1.

Cre‐Lox approach increases hPRDX3 expression in skeletal muscle mitochondria without upregulation of other antioxidant enzymes. (a) A schematic of peroxiredoxin3 human transgene construct (PRDX3) demonstrates a flanked STOP codon by LoxP sites. The PRDX3^fl/lf mice were bred to mice containing Cre recombinase driven by Human Skeletal Actin (HSA)‐Cre promotor to induce constitutive expression of PRDX3 in skeletal muscle. (b) The mRNA expression of human PRDX3. n = 6. Data were analyzed using ordinary two‐way ANOVA with Tukey post hoc tests. (c) Representative immunoblot images showing PRDX3 expression of mitochondrial and cytosolic fractions. Human PRDX3 antibody was used for the assay. (d) Representative immunoblots demonstrating human PRDX3 and mouse Prdx3 protein expression in WT, Sod1KO, WT‐PRDX3tg, and Sod1KO‐PRDX3tg from whole muscle homogenate. The antibody detects both human PRDX3 and mouse Prdx3 proteins. (e) Protein expression of key antioxidant enzymes using a targeted proteomics approach in muscle homogenates. n = 4. Student t‐tests were used comparing means between WT and mPRDX3 groups. Values are shown mean ± SEM. *p < 0.05. Prdx, peroxiredoxin; m Prdx3, mouse Prdx3; PRDX3, human PRDX3; txn, thioredoxin; txnrd, thioredoxin reductase; Sod, superoxide dismutase; Cat, catalase; Gpx, glutathione peroxidase; GSR, glutathione reductase