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)

1. The activity of antioxidant defense enzymes (SOD, CAT, GSH-Px and GST) was analysed during the autumn and winter in the ground squirrel adapted to 30 degrees C and subsequently exposed to cold for 6 and 24 hr. 2. The liver CAT activity as well as the IBAT CAT and GSH-Px activities differed between animals adapted to 30 degrees C, studied in autumn, and those studied in winter. 3. MnSOD activity in the liver was increased in autumn but decreased in winter after 6 hr cold exposure reaching the control level 24 hr later. Cold exposure induced a decrease in CAT activity (except after 24 hr cold exposure in winter) and an increase in GSH-Px activity. Lower GST activity was found after 24 hr exposure to cold in winter. 4. The IBAT SOD activity decreased under the influence of cold during both seasons with a tendency to return to the control level only in winter. Cold exposure produced a decrease in GST in both seasons and CAT activity in autumn. GSH-Px activity was increased in winter only. 5. The results indicate a seasonal dependence of the activity of antioxidant defence enzymes in the ground squirrel. Seasonal influence was evidenced in animals exposed to cold as well.
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PMID:Seasonal dependence of the activity of antioxidant defence enzymes in the ground squirrel (Citellus citellus): the effect of cold. 161 72

Free radical-induced gastric mucosal injury was caused by severe depletion of glutathione and alpha-tocopherol. Intravenous infusion of hypoxanthine (HX) via the jugular vein and local intra-arterial infusion of xanthine oxidase (XO) via the left gastric artery caused marked gastric mucosal injury in the antrum and the corpus. This study was performed to determine whether antioxidants in the gastric mucosa are mobilized during oxidative stress in the rat stomach. The level of thiobarbituric acid (TBA) reactive substance in the gastric mucosa was not significantly changed. The levels of total glutathione and alpha-tocopherol in the gastric mucosa significantly decreased. Total superoxide dismutase (Cu/Zn-and Mn-SOD) and glutathione peroxidase activities were not significantly changed. Administration of SOD reversed the glutathione level but not the alpha-tocopherol level in the gastric mucosa. To determine the role of glutathione and alpha-tocopherol in oxidative stress, the stomach was removed from a normal, alpha-tocopherol supplemented, and glutathione-depleted rat and used for experimentation. Frozen slices of the rat stomach were infused with HX-XO then examined histochemically using cold Schiff's reagent for signs of lipid peroxidation. It was found that the alpha-tocopherol supplemented stomach inhibited lipid peroxidation induced by HX-XO. Biochemical measurements and histochemical examination showed that the glutathione-depleted frozen tissue section and the homogenate had increased by lipid peroxidation induced by HX-XO. These findings suggested that alpha-tocopherol and glutathione may play a role in protecting the gastric mucosa against oxygen free radicals.
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PMID:Role of lipid peroxidation and antioxidants in gastric mucosal injury induced by the hypoxanthine-xanthine oxidase system in rats. 919 86

The aim of this study was to investigate the influence of acute cold exposure on the mRNA expression and immunoreactivity of superoxide dismutase (SOD) isoenzymes [Mn-SOD, Cu,Zn-SOD, and extracellular-SOD (EC-SOD)] in different tissues from lean and obese (ob/ob) mice at 10 months of age. The animals were kept at 10 degrees C for 3 h, with the colonic temperature in obese mice declining progressively during the cold stress, but not in lean mice, probably because of a strong tendency to atrophy of the brown adipose tissue (BAT) in obese mice. In the expression of mRNAs for lean mice, acute cold exposure led to a significant increase only in Mn-SOD in testes, but a significant decline in Cu,Zn-SOD in kidney and in Mn-SOD and EC-SOD in white adipose tissue (WAT), as well as in all SOD isoenzymes in lung and BAT. In obese mice, the mRNA level of Mn-SOD in heart and gastrocnemius muscle was significantly decreased following the cold exposure, whereas that of EC-SOD in testes was significantly increased. These changes, however, were not always accompanied by those in the corresponding protein levels; for example, the significant decreases in the expression of mRNAs for the three SOD isoenzymes in lung and BAT from lean mice did not result in any changes in the respective isoenzyme protein levels. These results suggest that, except for testes, a cold-exposure period of 3 h down-regulates SOD isoenzymes at the transcriptional process especially in lean mice, but is not long enough to induce their protein synthesis. It seems likely, thus, that, despite a marked decrease in colonic temperature, acute exposure to cold has less effect on SOD isoenzymes in obese mice as compared with those in normal lean siblings.
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PMID:Effects of acute cold stress on mrna expression and immunoreactivity of three superoxide dismutase isoenzymes in genetically obese mice. 1112 8

The response of aerobically grown Escherichia coli cells to the cold shock induced by the rapid lowering of growth temperature from 37 to 20 degrees C was found to be basically the same as the oxidative stress response. The enhanced sensitivity of cells deficient in two superoxide dismutases, Mn-SOD and Fe-SOD, and the increased expression of the Mn-SOD gene, sodA, in response to cold stress were interpreted as both oxidative and cold stresses are due to a rise in the intracellular level of superoxide anion. The long-term cultivation of E. coli at 20 degrees C was also accompanied by the typical oxidative stress response reactions--an enhanced expression of the Mn-SOD and catalase HPI genes and a decrease in the intracellular level of reduced glutathione (GSH) and in the GSH/GSSG ratio.
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PMID:[Role of the antioxidant system in response of Escherichia coli bacteria to cold stress]. 1133 38

Manganese superoxide dismutase (Mn-SOD, SOD2) is an inducible antioxidant localized to the mitochondria, which have been shown to be both the sites of superoxide anion (O(2)*-)) production and the target of free radical attacks. Knock-out mice with targeted disruption of Sod2 (SOD2-KO) are more susceptible to ischemic damage than their wild-type (WT) counterparts, showing increased loss of mitochondrial cytochrome c after trauma, but less apoptotic cell death in the first 24 h following controlled cortical injury. In this study, we sought to investigate whether oxidative stress plays a significant role in the development of secondary brain damage following cold injury-induced brain trauma (CIBT), a model of vasogenic edema. We first measured the levels of O(2)(*-) production 2 h after CIBT by means of in situ hydroethidine oxidation. We then examined lesion size, brain swelling, apoptosis by morphology and TUNEL-staining, neutrophil infiltration, and hemorrhage rates in both SOD2-KO and WT mice at 1, 3, and 7 days post-CIBT. We found no significant differences between SOD2-KO and WT littermates in any of the paradigms or endpoints studied. There was, however, a significant increase in hemorrhagic transformations in all animals that paralleled a robust inflammatory response at 3 days post insult compared with the 24-h endpoint. In the CIBT model used in this study, a 50% reduction in SOD2 activity did not appear to alter the injury response, suggesting that accumulation of free radicals does not play a significant role in secondary brain damage as previously thought with this particular model.
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PMID:Effects of cold injury-induced trauma in manganese superoxide dismutase-deficient mice. 1290 41

Interscapular brown adipose tissue (IBAT) hyperplasia involves a new metabolic and structural profile, resulting from acclimation of animals to a cold environment. Cold-induced changes of several antioxidative defense (AD) components in IBAT and their interrelationship with uncoupling protein 1 (UCP1), sympathetic innervation and apoptosis were studied using cold-acclimated adult rat males (4 +/- 1 degrees C, 45 days). Their age-matches were maintained at 22 +/- 1 degrees C serving as the controls. In cold-adapted rats, activities of CuZn- and Mn-superoxide dismutase (SOD) and apoptosis were reduced, while catalase (CAT), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST) activities and glutathione (GSH) content were increased compared to the control. IBAT mass, protein content, plasma free fatty acid (FFA) concentration, sympathetic innervation and UCP1 level were significantly increased in cold-acclimated group compared to the corresponding control. These results suggest that decreased CuZn and MnSOD activities in IBAT represent an adaptive response due to UCP1-induced mitochondrial uncoupling. Additionally, intensive fatty acid oxidation led to an increased H(2)O(2) production which resulted in increased CAT, GSH-Px and GST activities and GSH level. Generally speaking, cold-induced changes of AD in the IBAT are closely connected with newly established metabolic profile in this tissue, thus making an important part of the entire tissue homeostasis including cell survival.
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PMID:Free radical equilibrium in interscapular brown adipose tissue: relationship between metabolic profile and antioxidative defense. 1629 Jan 37

The analysis of differences in gene expression, responding to cryopreservation may explain some of the observed differences in further development of the preimplantation stage embryos. The aim of this study was to create a link, for the first time, between morphological/developmental observations and gene activity changes following cryopreservation of embryos. Efficiency of two vitrification methods, solid surface and in-straw vitrifications for pronuclear-stage mouse zygotes and 8-cell stage mouse embryos was compared based on morphological survival, blastocyst formation, and changes in embryonic gene expression. Both stages of embryos were vitrified by SSV using 35% ethylene glycol (EG) for vitrification solution (VS) and in-straw vitrification using 40% EG for VS. No significant differences were found between immediate survival rates of embryos vitrified by SSV and in-straw vitrification in both stages. Blastocyst rates were significantly higher with SSV and not significantly different from that of control. These results showed that SSV was more efficient than in-straw vitrification. Treatment with cytochalasin-b did not improve cryosurvival during SSV. The quantification of selected gene transcripts from single embryo (6 embryos/treatment group) were carried out by quantitative real-time RT-PCR. It was performed by adding 1/8 of each embryo cDNA to the PCR mix containing the specific primers to amplify housekeeping gene (beta-actin), heat shock protein gene (Hsp70), genes related to oxidative stress (MnSOD and CuSOD), cold stress (CirpB, Rbm3), and cell-cycle arrest (Trp53). We found upregulation of all six stress-related genes at 3 hr post-warming in pronuclear stage embryos. Expression of these genes showed much higher level (2-33-fold) in in-straw vitrification than in in vitro control embryos. In SSV-treated embryos we could detect only slight changes (0.3-2-fold). At 10 hr post-warming, all genes were downregulated in embryos vitrified by in-straw method. In SSV-treated group expression of Hsp70 showed slight increase and Trp53 showed decrease. In contrast to pronuclear stage, there was no clear pattern of gene expression changes after vitrification in 8-cell stage embryos. Several genes were upregulated both at 3 and 10 hr post-warming. Moreover, we found upregulation of beta-actin gene which we expected to use as a reference gene in in-straw treated embryos in both 3 and 10 hr post-warming, while in pronuclear stage embryos and in SSV treatment there was no effect on beta-actin expression level. There was no difference in gene expression between blastocysts developed from fresh or vitrified embryos. In conclusion, the real-time RT-PCR method from single embryo opened new opportunities for the understranding of molecular events following cryopreservation. The upregulation of stress-related genes at 3 hr post-warming in pronuclear stage embryos might have been an early indicator of reduced viability following in-straw vitrification in good correlation with the developmental data to blastocyst stage.
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PMID:Gene expression profiles and in vitro development following vitrification of pronuclear and 8-cell stage mouse embryos. 1654 60

A psychrophilic superoxide dismutase (SOD) has been characterized from the Antarctic eubacterium Pseudoalteromonas haloplanktis (Ph). PhSOD is a homodimeric iron-containing enzyme and displays a high specific activity, even at low temperature. The enzyme is inhibited by sodium azide and inactivated by hydrogen peroxide; it is also very sensitive to peroxynitrite, a physiological inactivator of the human mitochondrial Mn-SOD. Even though PhSOD is isolated from a cold-adapted micro-organism, its heat stability is well above the maximum growth temperature of P. haloplanktis, a feature common to other Fe- and Mn-SODs. The primary structure of PhSOD was determined by a combination of mass spectrometry and automated Edman degradation. The polypeptide chain is made of 192 amino acid residues, corresponding to a molecular mass of 21251 Da. The alignment with other Fe- and Mn-SODs showed a high amino acid identity with Fe-SOD from Vibrio cholerae (79%) and Escherichia coli (70%). A significant similarity is also shared with human mitochondrial Mn-SOD. PhSOD has the unique and highly reactive Cys57 residue, located in a variable region of the protein. The three-dimensional model of the PhSOD monomer indicates that Cys57 is included in a region, whose structural organization apparently discriminates between dimeric and tetrameric SODs. This residue forms a disulfide adduct with beta-mercaptoethanol, when this reducing agent is added in the purification procedure. The reactivity of Cys57 leads also to the formation of a disulfide bridge between two PhSOD subunits in specific denaturing conditions. The possible modification of Cys57 by physiological thiols, eventually regulating the PhSOD functioning, is discussed.
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PMID:Psychrophilic superoxide dismutase from Pseudoalteromonas haloplanktis: biochemical characterization and identification of a highly reactive cysteine residue. 1671 57

Alterations of pancreatic antioxidative defense (AD) and possible nitric oxide (NO) role in AD organization of adult rats receiving l-arginine.HCl (2.25%) or N(omega)-nitro-l-arginine methyl ester (L-NAME.HCl, 0.01%) as drinking liquids and maintained at room (22+/-1 degrees C) or low (4+/-1 degrees C) temperature for 45 days were studied. For that purpose, copper, zinc- and manganese superoxide dismutase (CuZnSOD, MnSOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione S-transferase (GST) and glutathione reductase (GR) activities were determined. Cold-induced decrease of CuZnSOD was inhibited with L-NAME, while l-arginine produced the same effect as cold in both supplemented groups. Cold acclimation elevated GSH-Px activity. l-Arginine and L-NAME expressed no effect on GSH-Px in rats kept at room temperature. L-NAME additionally elevated cold-induced GSH-Px activity, l-arginine expressing a similar trend. Cold-induced increase in GST activity was inhibited by L-NAME, while l-arginine inhibited this enzyme in both supplemented groups. Cold acclimation increased GR activity in control and L-NAME-treated group and l-arginine expressed a similar trend. Neither of the treatments affected MnSOD and CAT activities. Cold-induced changes of pancreatic AD were additionally affected by the alterations in l-arginine-NO-producing pathway. Some AD changes in the same direction with l-arginine or L-NAME point to the complexity of nitrogen compounds metabolism and function, accompanied by tissue-specific response.
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PMID:The effects of cold acclimation and nitric oxide on antioxidative enzymes in rat pancreas. 1739 42

Cold preservation has greatly facilitated the use of cadaveric kidneys for renal transplantation, but, clearly, damage occurs during both the preservation episode and the reperfusion phase (following transplantation). The aims of this study were twofold: to develop an in vivo model that was capable of evaluating renal function at early time points following cold preservation, and to evaluate the extent of renal mitochondrial damage that occurs following short periods of cold preservation in vivo. To accomplish these goals, we developed a novel rat model of in vivo renal cold ischemia followed by warm reperfusion (cold I/R) which avoided the complexity involved with transplantation. Briefly, after a right nephrectomy, cold I/R was initiated via pulsatile perfusion (40 minutes) of the left kidney with a cold University of Wisconsin solution followed by 18 hours of warm reperfusion. Cold I/R resulted in significant renal injury, nitrotyrosine production, and inactivation of the key mitochondrial antioxidant enzyme, manganese superoxide dismutase. Furthermore, the activities of the mitochondrial respiratory complexes were significantly reduced following cold I/R. In conclusion, short-term cold I/R results in inactivation of MnSOD, which may lead to the inhibition of mitochondrial complexes and subsequent renal injury. These data suggest that compounds designed to prevent early mitochondrial injury in kidneys that undergo cold preservation would significantly improve renal function and graft survival following transplantation.
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PMID:Cold preservation mediated renal injury: involvement of mitochondrial oxidative stress. 1830 Jan 10


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