UNIPROT:P04179 - FACTA Search

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Query: UNIPROT:P04179 (MnSOD)
2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In evaluating the relative expression of copper-zinc and manganese superoxide dismutase (CuZnSOD and MnSOD) in vivo in states like Down syndrome in which one dismutase is present at increased levels, we measured activities of both enzymes, in tissues of control and transgenic mice constitutively expressing increased levels of CuZnSOD, during exposure to normal and elevated oxygen tensions. Using SOD gel electrophoresis assay, CuZnSOD and MnSOD activities of brain, lung, heart, kidney, and liver from mice exposed to either normal (21%) or elevated (> 99% oxygen, 630 torr) oxygen tensions for 120 h were compared. Whereas CuZnSOD activity was elevated in tissues of transgenic relative to control mice under both normoxic or hyperoxic conditions, MnSOD activities in organs of transgenic mice were remarkably similar to those of controls under both conditions. To confirm the accuracy of this method in quantitating MnSOD relative to CuZnSOD expression, two other methods were utilized. In lung, which is the organ exposed to the highest oxygen tension during ambient hyperoxia, a sensitive, specific ELISA for MnSOD was used. Again, MnSOD protein was not different in transgenic relative to control mice during exposure to air or hyperoxia. In addition, lung MnSOD protein was not changed significantly by exposure to hyperoxia in either group. In kidney, a mitochondrion-rich organ, SOD assay, before and after inactivation of CuZnSOD with diethyldithiocarbamate, was used. MnSOD activity was not different in organs from air-exposed transgenic relative to control mice. The data indicated that expression of MnSOD in vivo was not affected by overexpression of the CuZnSOD and, therefore, the two enzymes are probably regulated independently.
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PMID:Expression of manganese superoxide dismutase is not altered in transgenic mice with elevated level of copper-zinc superoxide dismutase. 813 89

Previous studies using an in vivo rabbit model in which lung tissue hypoxia/hypoperfusion was created by unilateral lung collapse for 7 days demonstrated a decrease in MnSOD activity in previously hypoxic/hypoperfused lungs. In the present study, we determined whether tissue hypoxia/hypoperfusion decreased MnSOD protein concentration or mRNA expression in the lung as well, changes that would suggest pretranslational regulation of enzyme activity. Expression of MnSOD may be critical in determining the degree of tissue injury during re-oxygenation because the mitochondrial electron transport system produces reactive oxygen species (ROS) both during hypoxia and re-oxygenation. We purified MnSOD protein from rabbit livers to a specific activity of approximately 3,500 U/mg protein and found the amino terminal sequence nearly identical to those of the rat and human MnSOD proteins. Lung MnSOD protein content was quantitated by immunoassay, and MnSOD mRNA content was determined by slot blotting. Results from five control and six experimental rabbits, the right lungs of which had been hypoxic/hypoperfused because of collapse for 7 days, demonstrated a 32% decrease (P < 0.03) in MnSOD protein content (42 +/- 8 micrograms/mg DNA in hypoxic lungs compared with 61 +/- 3 micrograms/mg DNA in contralateral lungs) that was not due to decreased numbers of mitochondria. Lung succinate dehydrogenase activity, a mitochondrial marker, did not change in hypoxic/hypoperfused lungs. The mRNA for MnSOD did not change relative to B-actin mRNA in lungs that had been hypoxic and hypoperfused for 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:MnSOD protein content changes in hypoxic/hypoperfused lung tissue. 825 93

Activated oxygen or oxygen free radicals have been implicated in a number of physiological disorders in plants including freezing injury. Superoxide dismutase (SOD) catalyzes the dismutation of superoxide into O2 and H2O2 and thereby reduces the titer of activated oxygen molecules in the cell. To further examine the relationship between oxidative and freezing stresses, the expression of SOD was modified in transgenic alfalfa (Medicago sativa L.). The Mn-SOD cDNA from Nicotiana plumbaginifolia under the control of the cauliflower mosaic virus 35S promoter was introduced into alfalfa using Agrobacterium tumefaciens-mediated transformation. Two plasmid vectors, pMitSOD and pChlSOD, contained a chimeric Mn-SOD construct with a transit peptide for targeting to the mitochondria or one for targeting to the chloroplast, respectively. The putatively transgenic plants were selected for resistance to kanamycin and screened for neomycin phosphotransferase activity and the presence of an additional Mn-SOD isozyme. Detailed analysis of a set of four selected transformants indicated that some had enhanced SOD activity, increased tolerance to the diphenyl ether herbicide, acifluorfen, and increased regrowth after freezing stress. The F1 progeny of one line, RA3-ChlSOD-30, were analyzed by SOD isozyme activity, by polymerase chain reaction for the Mn-SOD gene, and by polymerase chain reaction for the neo gene. RA3-ChlSOD-30 had three sites of insertion of pChlSOD, but only one gave a functional Mn-SOD isozyme; the other two were apparently partial insertions. The progeny with a functional Mn-SOD transgene had more rapid regrowth following freezing stress than those progeny lacking the functional Mn-SOD transgene, suggesting that Mn-SOD serves a protective role by minimizing oxygen free radical production after freezing stress.
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PMID:Superoxide dismutase enhances tolerance of freezing stress in transgenic alfalfa (Medicago sativa L.). 829 Jun 27

Reactive oxygen species are highly toxic agents that appear to have an important role in male infertility. In order to understand the potential for the testis to be protected from reactive oxygen, the mRNA levels of the natural reactive oxygen scavenger, copper-zinc superoxide dismutase (SOD), were determined in testes and other organs in rats using northern analysis and in situ hybridization. Northern analysis of total RNA from organs of 60-day-old rats demonstrated an SOD mRNA with a transcript length of 0.77 kb; its concentration was highest in the kidney, liver, testis, and epididymis. In testis, northern analysis of total RNA demonstrated two mRNA transcripts of 0.77 kb and 0.94 kb. The concentrations of the 0.77-kb transcript varied only slightly between 10 and 100 days of age. In contrast, the 0.94-kb transcript became detectable by northern analysis between 30 and 40 days of age, then its concentration rose progressively to peak at 60 days. In situ hybridization studies demonstrated a uniform distribution of SOD mRNA within seminiferous tubules of prepubertal rats at 10 days of age and a heterogeneous, stage-specific pattern in older animals. In mature rats, the highest level of SOD mRNA was detected in tubules just prior to spermiation (stages VI-VIII). In conclusion, two SOD mRNA transcripts were identified in the rat testes that followed significantly different patterns of expression during development. In situ hybridization studies revealed that accumulation of the SOD mRNA in the seminiferous tubule was stage specific. These data suggest that SOD may play an important role during testicular development and spermatogenesis in rats.
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PMID:Identification and localization of copper-zinc superoxide dismutase gene expression in rat testicular development. 829 28

Reactive oxygen species such as superoxide anion (O2-), hydrogen peroxide (H2O2) and hydroxy radical (OH) possess potent oxygen toxicity to cells. Superoxide dismutases (SODs) are metalloenzymes that are essential for dismutation of O2- to H2O2 and O2. SODs are important initial components in the cellular defense against oxygen toxicity since O2- can react with H2O2 to generate single oxygen and hydroxy radicals, which are even more reactive and cytotoxic than O2- or H2O2. In mammalian tissues three superoxide dismutases (SODs) designated Cu,Zn-SOD, Mn-SOD and extracellular SOD exist. These enzymes play an important role in the antioxidant defense system against superoxide anion (O2-) generated in vivo and may be involved in various pathophysiological processes including inflammation, cancer diabetes, aging and ischemia. (1) The role of superoxide anion in ovulation and luteal function was investigated the localization of Cu, Zn-SOD and Mn-SOD in rat and human ovary by immunohistochemical methods. Cu,Zn-SOD was present in granulosa cells of mature Graafian follicles and growing follicles and Mn-SOD was present in luteal cells of the corpus luteum in rat. (2) To investigate the relationship between active oxygen radical-scavenge system and ovulatory mechanism in human. Mn-SOD was found in granulosa cells and theca cells of mature follicles, luteal cells of corpus luteum and epithelial cells of fallopian tubes. Cu,Zn-SOD was localized in theca cells of mature follicles, margin of corpus luteum and epithelial cells of tubal isthmus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Oxygen radicals-superoxide dismutase system and reproduction medicine]. 837 Oct 13

A canine model with cyclic flow variations (CFVs) in stenosed and endothelium-injured coronary arteries was used to examine the role of active oxygen species in platelet aggregation in vivo. We studied 90 anesthetized dogs in which the pericardial cavity was opened and the heart was exposed. The velocity of blood flow in the left anterior descending coronary artery (LAD) was monitored by a pulsed Doppler flow probe. In 67 dogs, the LADs were stenosed by applying external constrictors at the site where the endothelium was mechanically injured. CFVs developed in all 67 dogs. Treatment with the antioxidants recombinant human copper-zinc superoxide dismutase (r-h-CuZnSOD), recombinant human manganese superoxide dismutase (r-h-MnSOD), and catalase eliminated platelet aggregation-associated coronary CFVs in 63%, 62%, and 64% of animals, respectively. Intravenous infusion of epinephrine restored CFVs in most dogs. Ketanserin, a serotonin (5-hydroxytryptamine2) receptor antagonist, abolished epinephrine-restored CFVs and eliminated CFVs in dogs in which CFVs had not been eliminated by free radical scavengers. In an additional 23 dogs, the LADs were stenosed but not mechanically injured. For control studies, saline was infused into the LADs of 5 dogs. Xanthine/xanthine oxidase was infused into the LADs of 8 dogs and induced CFVs in 4. Hydrogen peroxide was infused into the other 10 dogs and induced CFVs in 9. Histological analysis of the coronary artery revealed that the intima was significantly injured by the infusion. In ex vivo platelet aggregation studies, the in vivo treatment with r-h-CuZnSOD, r-h-MnSOD, and catalase significantly inhibited platelet aggregation induced by platelet-activating factor. Thus, active oxygen species are involved in mediating platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries in vivo.
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PMID:Active oxygen species play a role in mediating platelet aggregation and cyclic flow variations in severely stenosed and endothelium-injured coronary arteries. 840 65

The regulation of Cu,Zn- and Mn-superoxide dismutases (SOD) was investigated by Northern blotting and gene fusions of SOD1 and SOD2 promoters with the beta-galactosidase reporter gene. Cu,ZnSOD expression was increased 3-fold under glucose derepressing conditions, and decreased 4- to 6-fold by oxygen or heme deficiency. MnSOD expression was increased 5-fold by glucose derepression, and decreased 8- to 10-fold by anaerobiosis and 4- to 5-fold by heme deficiency. Induction by paraquat was modest, about 50% for SOD1 and 100% for SOD2; it was apparently independent of the respiratory chain function.
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PMID:Regulation of Cu,Zn- and Mn-superoxide dismutase transcription in Saccharomyces cerevisiae. 841 79

The 27-day-old rat exposed to 100% oxygen (O2) for 8 days will have predictable lung vascular and parenchymal changes at 60 days of age. Using this model, the goals of this study are (1) to measure the lung antioxidant enzyme activities serially following intratracheal PEG antioxidant therapy during the 8-day O2 exposure; and (2) to assess chronic cardiopulmonary changes in the O2-exposed rats treated with PEG-CAT and/or PEG-CuZn SOD given intraperitoneally (IP) and/or intratracheally (IT). The study encompassed 202 male rats exposed to room air or oxygen. CuZn SOD doses were 300 U IT and 2000 U IP. The CAT dose was 500 or 4000 U IT and 10,000 U IP. At 60 days of age, the right ventricular systolic pressure (RVP), RV weight, % acinar wall arterial thickness, and parenchymal air space were significantly increased in O2-exposed rats compared to RA rats. The RVP, RV weight, and parenchymal changes were prevented by daily IT PEG-CAT 4000 U + CuZn SOD 300 U but the increased small artery muscularization was not. Three hours after the initial dose of IT PEG-CAT 4000 U, lung CAT activity was more than doubled and remained constant throughout the 8-day daily treatment course. This dose of CAT depressed the induction response to O2 of CuZn and MnSOD. It is concluded that daily intratracheal administration of PEG-CAT 4000 U + CuZn SOD 300 U can significantly ameliorate some of the chronic parenchymal and vascular lung O2 toxic changes. However, it appears that high-dose exogenous PEG-CAT suppresses the endogenous enzyme induction to hyperoxia of both CuZn and Mn-SOD.
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PMID:Lung antioxidant enzymes and cardiopulmonary responses in young rats exposed to hyperoxia and treated intratracheally with PEG catalase and superoxide dismutase. 846 59

Conditions that generate reactive oxygen species elevate Cu,Zn superoxidase dismutase (SOD) in endothelial cells (EC) concomitant with decreased cellular proliferation. The current studies were undertaken with both vascular EC and smooth muscle cells (SMC) to compare the influences of cellular proliferation with those of hyperoxia on induction of Cu,Zn SOD. To assess cell cycling alone, EC and SMC were growth arrested, then released from arrest. Cell cycling was monitored by [3H]thymidine incorporation, counts, and flow cytometry. SOD catalytic activity was measured spectrophotometrically and SOD protein by enzyme-linked immunosorbent assay. A digoxigenin-labeled probe was used to quantify SOD mRNA by Northern analysis. EC reached the S phase of the cell cycle in 18 h and completed one cycle in 24-30 h, whereas SMC took 24-30 h to reach the S phase and 48 h to complete one cycle. Cu,Zn SOD mRNA for both EC and SMC was very low during the Go/G1 phase, peaked during the S phase, and then reverted to lower values as cells progressed through their cycles. Cu,Zn SOD activity and immunoprotein content showed corresponding changes to those of mRNA. Exposure to hyperoxia (95% O2) delayed the entry of released cells into the S phase of the cell cycle and blocked the cells in the S or G2 phase, but induced Cu,Zn SOD mRNA before the S phase and caused persistence of elevation of Cu,Zn SOD mRNA as cells progressed through their cycles. Exposure to hyperoxia also induced Cu,Zn SOD mRNA in growth-arrested cells within 24-48 h. Thus our studies support roles for both cells cycle dependency and reactive oxygen species in the induction of Cu,Zn SOD.
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PMID:Cu,Zn superoxide dismutase in vascular cells: changes during cell cycling and exposure to hyperoxia. 847 66

Three forms of superoxide dismutase (SOD) exist in the lung: CuZnSOD, MnSOD and extracellular SOD. Evidence suggests that both CuZnSOD and MnSOD are important in pulmonary defense against oxygen toxicity. Enhancement of pulmonary levels of CuZnSOD by transgenic overexpression of CuZnSOD, or tracheal insufflation of liposome-encapsulated or polyethylene glycol-conjugated CuZnSOD, protects animals against oxygen toxicity. Likewise, transgenic overexpression of MnSOD, or induction of endogenous MnSOD by endotoxin, tumor necrosis factor, or interleukin 1, also protects animals against oxygen toxicity. The role of extracellular SOD in the pulmonary defense against oxygen toxicity is not clear.
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PMID:Superoxide dismutase and pulmonary oxygen toxicity. 851 41

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