OBJECTIVE In mice that are heterozygous for mitochondrial superoxide dismutase (SOD2(+/-)) with apoE deficiency (apoE(-/-)), mitochondrial DNA damage increases formation of atherosclerotic lesions. The purpose of this study was to determine whether SOD2 provides protection against increased vascular superoxide and endothelial dysfunction in apoE-deficient mice. METHODS AND RESULTS Four groups...

Pulmonary hypertension (PH) complicates bronchopulmonary dysplasia (BPD) in 25% of infants. Superoxide dismutase 2 (SOD2) is an endogenous mitochondrial antioxidant, and overexpression protects against acute lung injury in adult mice. Little is known about SOD2 in neonatal lung disease and PH. C57Bl/6 mice and isogenic SOD2+/+ and SOD2-/+ mice were placed in room air (control) or 75% O2 (chroni...

Mitochondria manganese superoxide dismutase (SOD2) is an important antioxidant enzyme, deficiency of which is associated with various human diseases. The known primary regulation of SOD2 is through transcriptional activation. Here, we report that SOD2 is acetylated at Lys 68 and that this acetylation decreases SOD2 activity. Mitochondrial deacetylase SIRT3 binds to, deacetylates and activates S...

Elevated reactive oxygen species (ROS) are linked to insulin resistance and islet dysfunction. Manganese superoxide dismutase (SOD2) is a primary defense against mitochondrial oxidative stress. To test the hypothesis that heterozygous SOD2 deletion impairs glucose-stimulated insulin secretion (GSIS) and insulin action, wild-type (sod2(+/+)) and heterozygous knockout mice (sod2(+/-)) were fed a ...

diabetes mellitus (dm) is a chronic heterogeneous disorder and oxidative stress is a key participant in the development and progression of it and its complications. anti-oxidant status can affect vulnerability to oxidative damage, onset and progression of diabetes and diabetes complications. superoxide dismutase 2 (sod2) is one of the major antioxidant defense systems against free radicals. sod...

Mitochondrial superoxide dismutase 2 (SOD2) converts superoxide anions to hydrogen peroxide and oxygen. Human data on SOD2 protein content in chronic kidney disease (CKD) are sparse and mortality data are lacking. We investigated SOD2 protein content in monocytes from patients with hemodialysis therapy (n = 81), CKD stage 1-5 (n = 120), and healthy controls (n = 13) using in-cell Western assays...

Mitochondria are the major source of superoxide (O(2)(-)) in the aerobic organisms. O(2)(-) produced by the mitochondria is converted to hydrogen peroxide by mitochondrial superoxide dismutase (SOD2). Mice with complete SOD2 deficiency (SOD2(-/-)) exhibit dilated cardiomyopathy and fatty liver leading to neonatal mortality, whereas mice with partial SOD2 deficiency (SOD2(+/-)) show evidence of ...

Recent studies have shown that homozygous Mn superoxide dismutase (Sod2) gene-knockout mice (Sod2(-/-)) die shortly after birth with extensive myocardial injury, whereas heterozygous mutants (Sod2(+/-)) are phenotypically normal in room air. In the current study, we showed that Sod2(+/-) mice with approximately 50% of normal pulmonary MnSOD activity and normal levels of lung CuZnSOD, catalase, ...

Mice heterozygous for the Sod2 gene (Sod2+/- mice) have been used to study the phenotype of life-long reduced Mn-superoxide dismutase (MnSOD) activity. The Sod2+/- mice have reduced MnSOD activity (50%) in all tissues throughout life. The Sod2+/- mice have increased oxidative damage as demonstrated by significantly elevated levels of 8-oxo-2-deoxyguanosine (8oxodG) in nuclear DNA in all tissues...

Failure to control nasopharyngeal carcinomas (NPC) is mainly due to a portion of radioresistant phenotype. Identifying gene targets for radiosensitization is an important strategy in improving anticancer treatments. Exposure of cells to ionizing radiation leads to the formation of reactive oxygen species that are associated with radiation-induced cellular apoptosis and necrosis. The antioxidant...