| First Author | Homma T | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 463 |
| Issue | 4 | Pages | 1040-6 |
| PubMed ID | 26079888 | Mgi Jnum | J:228682 |
| Mgi Id | MGI:5708458 | Doi | 10.1016/j.bbrc.2015.06.055 |
| Citation | Homma T, et al. (2015) SOD1 deficiency induces the systemic hyperoxidation of peroxiredoxin in the mouse. Biochem Biophys Res Commun 463(4):1040-6 |
| abstractText | A deficiency of superoxide dismutase 1 (SOD1) or peroxiredoxin (Prx) 2 causes anemia in mice due to elevated oxidative stress. In the current study, we investigated whether intrinsic oxidative stress caused by a SOD1 deficiency affected the redox status of Prx2 and other isoforms in red blood cells (RBCs) and several organs of mice. We observed a marked elevation in hyperoxidized Prx2 levels in RBCs from SOD1-deficient mice. Hyperoxidized Prx2 reportedly undergoes a rhythmic change in isolated RBCs under culture conditions. We confirmed such changes in RBCs from wild-type mice but observed no evident changes in SOD1-deficient RBCs. In addition, an elevation in hyperoxidized Prxs, notably Prx2 and Prx3, was observed in several organs from SOD1-deficient mice. However, a SOD1 deficiency had no impact on the wheel-running activity of the mice. Thus, although the redox status of some Prxs is systemically shifted to a more oxidized state as the result of a SOD1 deficiency, which is associated with anemia and some diseases, a redox imbalance appears to have no detectable effect on the circadian activity of mice. |
