Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activities of the copper-zinc- and manganese-containing superoxide dismutase enzymes (CuSOD and MnSOD) were studied in tissues of the sheep to determine the dependence of these activities on sheep age, and their relationship to tissue and dietary mineral concentrations. Tissue samples were obtained from day-old through 16-week-old lambs from flocks grazing pastures normal or high in copper and manganese, and from adult sheep. In liver, lung, heart, kidney and skeletal muscle, activities of CuSOD and MnSOD in day-old and week-old lambs were only half those measured in 16-week-old and adult sheep. Activities in 4-week-old lambs were intermediate between these two groups except for heart tissue, in which activities were not increased until lambs were 16 weeks old. For all age groups, heart and skeletal muscle had low activities of CuSOD. Minimal age-related changes were observed for CuSOD activities in erythrocyte and brain tissues. The low enzyme activities evident in most tissues of day-old lambs, occurred in the presence of apparently adequate tissue copper and manganese concentrations. Concentrations of these minerals in lamb tissues were equal to or greater than those observed in older sheep and although these concentrations increased considerably with increased pasture mineral concentrations, enzyme activities were unchanged. Age-related increases in tissue CuSOD and MnSOD activities, occurring as normal developmental processes, may be important factors in diseases attributed to uncontrolled tissue peroxidation in sheep.
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PMID:Age-related changes in activities of the superoxide dismutase enzymes in tissues of the sheep and the effect of dietary copper and manganese on these changes. 648 83

Extracellular-superoxide dismutase is a tetrameric copper-containing glycoprotein that previously has been demonstrated to be the major superoxide dismutase of human extracellular fluids. The occurrence of this enzyme in various human tissues that were removed from two accidental death victims and in 19 different human cultured cell lines was determined. All investigated tissues were found to contain extracellular-superoxide dismutase. There was a larger variation between tissues in the concentration of this enzyme than in CuZn superoxide dismutase and Mn superoxide dismutase. No relation could be demonstrated between the content of extracellular-superoxide dismutase and the content of the other superoxide dismutase isoenzymes in the various tissues. In uterus there was more extracellular-superoxide dismutase than Mn superoxide dismutase, but in all other tissues the content of extracellular-superoxide dismutase was lower than the content of the other isoenzymes. The concentration of extracellular-superoxide dismutase was higher in all investigated human tissues than in human plasma. 19 human cultured cell lines were found to be devoid of or to contain very little extracellular-superoxide dismutase. Most tissues contained more extracellular-superoxide dismutase than did the investigated cell lines.
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PMID:Extracellular superoxide dismutase in human tissues and human cell lines. 654 Dec 29

1. The activity of manganese-superoxide dismutase (EC 1.15.1.1; SOD) was increased in the livers and kidneys of adult rats after exposure to aqueous ethanol (200 ml/1) for 32 weeks. 2. The concentration of Mn in the livers and kidneys was significantly higher after 24 weeks, and by 32 weeks liver copper and zinc levels were lower. 3. The activity of foetal (day 19) liver superoxide dismutase was appreciably higher in offspring from dams receiving ethanol during pregnancy. Quantitatively the response appeared to be almost entirely due to the Mn-SOD form of the enzyme. 4. Maternal alcoholism during pregnancy had no effect on the levels of Cu, Mn or Zn in foetal (day 19) livers.
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PMID:Superoxide dismutase (EC 1.15.1.1), manganese and the effect of ethanol in adult and foetal rats. 688 37

Insulin stimulates the production of superoxide and hydrogen peroxide in various tissues. Hydrogen peroxide has been proposed to be an intracellular second messenger for insulin and a moderator of cellular proliferation and differentiation. We previously found that cell proliferation is increased in small intestinal mucosa of streptozotocin-diabetic rats. The current study was undertaken to determine if superoxide dismutase (SOD), the enzyme that converts superoxide to hydrogen peroxide, is altered in the mucosa of the alimentary tract and renal cortex of the diabetic rat, and if so, whether SOD responds to insulin treatment. Total SOD and cyanide-insensitive [manganese-containing SOD (Mn SOD)] SOD were measured by the nitroblue tetrazolium inhibition assay. We studied ad libitum fed animals, where diabetics are hyperphagic and pair-fed animals, where hyperphagia is not present. Since cyclic nucleotides appear to control cell proliferation in some tissues, we also measured cAMP and cGMP in mucosa of the small intestine. In ad libitum fed animals, total SOD was depressed in the mucosa of duodenum, jejunum, and ileum, but not in the cecum or colon of the streptozotocin-diabetic rats. The level of Mn-SOD was not affected by diabetes or insulin treatment, but the cyanide-sensitive [copper- and zinc containing SOD (Cu-Zn SOD] SOD was depressed in the small intestine and colon of diabetic rats. Insulin treatment restored total and Cu-Zn SOD activity in the small intestine to normal and increased Cu-Zn SOD activity in the colon to normal. Pair-fed animals showed the same changes in the SOD activity of jejunal mucosa that were found in ad libitum fed animals. In renal cortex, diabetes did not alter total SOD, but increased Mn SOD and decreased Cu-Zn SOD. Both responses were reversed by insulin treatment. Cyclic nucleotide concentrations were not affected by diabetes. We conclude that SOD enzymes re altered in diabetes, at least in proliferating tissues. Responses are tissue specific. The mucosa of the small intestine and colon show decreased Cu-Zn SOD, the SOD of the cecum is unaffected, and the kidney shows increased Mn SOD and decreased Cu-Zn SOD. The SOD responses of diabetics are reversed by insulin treatment.
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PMID:Superoxide dismutase activity in the intestine of the streptozotocin-diabetic rat. 704 72

The effect of superoxide dismutase (SOD) activity and isoenzyme pattern of detergents, incubation time, and sonication in the preparation of rat liver samples was investigated. The activity of the manganese form of the enzyme (Mn-SOD) was found to decrease significantly after 4 hr of incubation at room temperature, and activity of the copper, zinc form of the enzyme (Cu, Zn-SOD) was not changed significantly even after 24 hr, although levels were somewhat decreased. Sonication of the sample did not affect Cu, Zn-SOD activity, but total Mn-SOD activity was increased. Addition of detergents did not increase Mn-SOD activity when homogenates were sonicated, indicating that Mn-SOD is not membrane bound. Detergents also had no effect on Cu, Zn-SOD activity. None of the treatments investigated altered the isoenzyme patterns, providing evidence that these isoenzymes are not degradation products.
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PMID:Effect of sample preparation on analysis of superoxide dismutase activity and isoenzymes. 708 4

Superoxide dismutases might conceivably protect against both ionizing radiation and free radical-producing antibiotic antitumor drugs. Copper- and zinc-containing superoxide dismutase (CuZn superoxide dismutase) and manganese-containing superoxide dismutase (Mn superoxide dismutase) were specifically assayed in human malignant tumors and for comparison in human tissues. The tumors possessed less CuZn superoxide dismutase than did the more metabolically active tissues, but there was a large overlap between the tissue and the tumor levels. Mn superoxide dismutase was found in all tumors, and the ratio between the activities of CuZn superoxide dismutase and Mn superoxide dismutase was not different from that of the normal tissues. Human tumors are thus different from tumors from other species which have been reported to be deficient or very low in Mn superoxide dismutase. There was no obvious relation between sensitivity to ionizing radiation and content of the enzymes among the tumors and the tissues, nor did tumor types known to be responsive to radical-producing drugs possess less CuZn superoxide dismutase or Mn superoxide dismutase than other tumors.
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PMID:Copper- and zinc-containing superoxide dismutase and manganese-containing superoxide dismutase in human tissues and human malignant tumors. 724 54

1. Rainbow trout (Salmo gairdneri) of mean initial weight 15 g were given either a low-manganese or control diet containing 1.3 and 33 mg Mn/kg dry diet respectively. 2. Weight gains over a 24-week feeding period were the same for both groups of trout. 3. Hepatosomatic index, blood packed cell volume and haemoglobin concentration, plasma protein and the activities of aspartic aminotransferase (EC 2.6.1.1) and alanine aminotransferase (EC 2.6.1.2) were unaffected by dietary Mn intake. 4. Plasma potassium and iron levels were increased in the trout given the low-Mn diet. 5. The hepatic levels of magnesium, sodium, K, zinc, copper, Mn and phosphorus were significantly reduced in the fish given the low-Mn diet. 6. In those trout given the low-Mn diet the levels of Mn and calcium in the vertebral ash were significantly reduced. 7. The hepatic activity of Cu-Zu superoxide dismutase (EC 1.15.1.1; Cu-ZnSOD) and of Mn superoxide dismutase (EC1.15.1.1; MnSOD) in cardiac muscle and liver was reduced in the group of trout given the low-Mn diet. The fall in Cu-ZnSOD and MnSOD activities coincided with reduced tissue levels of their respective metal components.
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PMID:The effect of low dietary manganese intake on rainbow trout (Salmo gairdneri). 731 45

Reactive oxygen species (ROS) are involved in the mechanism of photoaging and carcinogenesis. Skin is endowed with antioxidant enzymes including superoxide dismutases (SOD): cytosolic copper zinc SOD and mitochondrial manganese SOD. The aim of our study was to estimate the protective effect of manganese against oxidative injury on cultured human skin fibroblasts. Dithranol, hydrogen peroxide and UV-A radiation (375 nm) were employed as oxidative stressors. The supply of manganese chloride produced an increase in cellular content of this element up to 24 fold without concomitant elevation of MnSOD activity. Nevertheless, manganese protects cells against two of the three ROS generating systems assessed, namely hydrogen peroxyde and UV-A. This protective effect depends on the concentration of manganese in the medium, 0.1 mM and 0.2 mM protect against UVA cytotoxicity, only 0.2 mM protects against H2O2 cytotoxicity.
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PMID:Does manganese protect cultured human skin fibroblasts against oxidative injury by UVA, dithranol and hydrogen peroxide? 749 40

The intracellular localization of Cu/Zn- and Mn-superoxide dismutase (SOD), which catalyze the dismutation of superoxide radicals (O2-) to O2 and H2O2, was studied in the thyroid tissue of various thyroid disorders by an immunohistochemical technique. The concentrations of both SODs in those tissues were measured also by a sandwich enzyme immunoassay technique. Copper/zinc-SOD in thyroid tissues were identified by immunocytochemical staining in most cases of papillary carcinoma and in some cases of other thyroid disorders. In normal follicular cells this enzyme is localized in the perinuclear cytoplasm, whereas in thyroid tumor or hyperplastic follicular cells it exists homogeneously in cytoplasm. Manganese-SOD stained strongly in papillary carcinoma and papillary-growing cells in the thyroid tissue of adenoma and Graves' disease. The concentrations of Cu/Zn-and Mn-SOD in thyroid tumor tissues and hyperplastic follicular disorders were significantly higher than those in normal thyroid tissue when they were compared as a function of protein or deoxyribonucleic acid contents. The ratio of Mn-SOD to Cu/Zn-SOD was significantly higher only in papillary carcinoma, except for other thyroid disorders as compared with that in the normal thyroid. In conclusion, SOD seems to be related to cell proliferation and differentiation in the thyroid follicular cell because Cu/Zn-SOD changes its localization in tumor and hyperplastic follicular cells and because the Mn-SOD concentration is increased in papillary carcinoma or papillary-growing cells.
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PMID:Localization of Cu/Zn and Mn superoxide dismutase in various thyroid disorders. 750 2

Studies have implicated active oxygen species (AOS) in the pathogenesis of various lung diseases. Many chemical and physical agents in the environment are potent generators of AOS, including ozone, hyperoxia, mineral dusts, paraquat, etc. These agents produce AOS by different mechanisms, but frequently the lung is the primary target of toxicity, and exposure results in damage to lung tissue to varying degrees. The lung has developed defenses to AOS-mediated damage, which include antioxidant enzymes, the superoxide dismutases [copper-zinc (CuZnSOD) and manganese-containing (MnSOD)], catalase, and glutathione peroxidase (GPX). In this review, antioxidant defenses to environmental stresses in the lung as well as in isolated pulmonary cells following exposure to a number of different oxidants, are summarized. Each oxidant appears to induce a different pattern of antioxidant enzyme response in the lung, although some common trends, i.e., induction of MnSOD following oxidants inducing inflammation or pulmonary fibrosis, in responses to oxidants occur. Responses may vary between the different cell types in the lung as a function of cell-cycle or other factors. Increases in MnSOD mRNA or immunoreactive protein in response to certain oxidants may serve as a biomarker of AOS-mediated damage in the lung.
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PMID:Regulation of antioxidant enzymes in lung after oxidant injury. 752 4


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