| First Author | Son TG | Year | 2006 |
| Journal | Mech Ageing Dev | Volume | 127 |
| Issue | 5 | Pages | 451-7 |
| PubMed ID | 16500693 | Mgi Jnum | J:107922 |
| Mgi Id | MGI:3622522 | Doi | 10.1016/j.mad.2006.01.005 |
| Citation | Son TG, et al. (2006) SMP30 deficiency causes increased oxidative stress in brain. Mech Ageing Dev 127(5):451-7 |
| abstractText | Senescence marker protein 30 (SMP30), an important aging marker molecule, has been identified functionally as a calcium regulatory protein. Recent evidence showed its new assumed role as an effective anti-oxidative property. However, the role of SMP30 in the brain has not been explored. To delineate its role in the brain, we utilized SMP30 knock-out (SMP30 KO) mice in the current study. We focused on the oxidative status of the brain by examining selected oxidative markers in brains of SMP30 KO mice. Results showed that the generation of reactive species (RS) and NADPH oxidase activities were significantly elevated in SMP30 deficient brain. The increased oxidative status in these mice was further confirmed by increased oxidatively modified proteins such as dityrosine formation and carbonylation in the cortex of SMP30 KO mice. Moreover, SMP30 deficient brain showed the increased Mac-1 protein and myeloperoxidase (MPO) activity in the brain, supporting the putative anti-oxidative action of SMP30. Interestingly, the activities of major antioxidant enzymes, superoxide dismutase, catalase and reduced glutathione peroxidase in the brain were not affected by SMP30 depletion. Our results documented that brain SMP30 has a protective action against oxidative damage, without influencing antioxidant enzyme status. |
