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)

Male Wistar rats received an aqueous solution of ammonium metavanadate (AMV) of 0.15 mg/V/ml concentration instead of water for 14 days. The erythrocyte count and haemoglobin level in blood were not changed; the haematocrit index was slightly increased. The spontaneous lipid peroxidation in kidney and liver homogenates was increased. The Fe(II)- or ascorbate-induced lipid peroxidation was more pronounced in the kidney than in the liver. No changes in lipid peroxidation were observed in erythrocytes after AMV treatment. The AMV treatment resulted in a decrease in the activity of the antioxidant enzymes, catalase and glutathione peroxidase in the kidney and liver; the cytosolic Cu,Zn-SOD and mitochondrial Mn-SOD were unchanged. The activity of the enzymes in blood was not changed. The results are discussed with a view to the participation of lipid peroxidation in vanadium toxicity.
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PMID:Lipid peroxidation and antioxidant enzymes in vanadate-treated rats. 806 48

The effect of sodium metavanadate (NaVO3) consumption on trace element metabolism, components of the antioxidant defense system and lipid oxidative damage were studied in control (CON) and streptozotocin-induced diabetic (DIAB) rats. Ten days after injection, CON and DIAB rats received either 0 mM NaVO3/80 mM NaCl (0 group) or 1.2 mM NaVO3/80 mM NaCl (1.2V group) in their drinking water. DIAB groups had higher food and fluid intakes than the CON groups; vanadium (V) groups had lower food and fluid intakes than the saline groups. Vanadium therapy lowered plasma glucose concentrations of DIAB rats. The following parameters were similar among the groups: plasma Zn, Cu and Fe concentrations, plasma ceruloplasmin activity, liver Zn, Cu, Mn and Fe concentrations, kidney Mn and Fe concentrations, liver non-Se-dependent glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Red) and Mn-SOD activities, liver reduced glutathione (GSH) and oxidized glutathione (GSSG) concentrations and kidney non-Se-dependent GSH-Px activity. Kidney Zn and Cu concentrations were higher in DIAB rats than in CON rats. The CON-1.2V and DIAB-1.2V groups had V accumulation in the liver and kidney. Liver CuZn-SOD and Se-dependent GSH-Px and kidney CuZn-SOD and GSH-Red activities were lower in DIAB rats compared to CON rats; kidney Mn-SOD and kidney Se-dependent GSH-Px activities were higher in DIAB rats than CON rats. Vanadium treatment did not cause significant alterations in the antioxidant defense system; however, tissue vanadium concentrations were positively correlated to TBARS production. These results show that diabetes caused significant alterations in the antioxidant defense system and that V therapy was associated with a marked deterioration in health of both control and diabetic rats.
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PMID:Vanadium treatment of diabetic Sprague-Dawley rats results in tissue vanadium accumulation and pro-oxidant effects. 824 40

We examined the effects of inhibition of Cu,Zn superoxide dismutase (Cu,Zn SOD) and catalase (Cat) activities on the steady-state mRNA levels of the three major antioxidant enzymes [Cu,Zn SOD, Cat, and glutathione peroxidase (GP)] in human umbilical vein endothelial cells under normoxia and hyperoxia. Inhibition of Cat activity by aminotriazole was not associated with alteration of the other antioxidant enzymes or with potentiation of cell injury. On the other hand, inhibition of Cu,Zn SOD activity by N-N'-diethyl-dithiocarbamate (DDC) was associated with an increase in Cu,Zn SOD mRNA level and a decrease in Cat and GP mRNA level. The combination of DDC and hyperoxia treatments was associated with an additive effect on Cu,Zn SOD message. We propose that these coordinate mRNA changes might be an adaptation to the oxidative environment. This proposal supports the concept that the intracellular O2 metabolites themselves could be the signals that trigger the antioxidant enzymes gene expression.
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PMID:Effects of inhibition of catalase and superoxide dismutase activity on antioxidant enzyme mRNA levels. 827 80

Lipid peroxidation has been hypotesized as one of possible factors involved in the pathogenesis of neuronal damage and delayed vasospasm after subarachnoid hemorrhage. In the brain there are anti-oxidant enzymatic systems which act as scavengers of superoxides and free radicals. In the present study the pattern of enzymatic anti-oxidant activities (Cu-Zn and Mn superoxide dismutase, and glutathione peroxidase) was investigated in an experimental model of subarachnoid hemorrhage in the rat in order to verify whether the hemorrhagic insult may be responsible for an impairment of such anti-oxidant systems. Enzymatic activities were assayed in three different rat brain areas (cerebral cortex, hippocampus and brain stem) of sham-operated and at 30 min, 1, 6 and 48 h after subarachnoid hemorrhage induction. After the hemorrhage induction the Cu-Zn superoxide dismutase activity in cerebral cortex was significantly reduced at all the set times (p < .05), while Mn-superoxide dismutase activity was significantly decreased since 1 h (p < .05) until 48 h (p < .05). Glutathione peroxidase activity was significantly reduced only in the late phase (48 h) of subarachnoid hemorrhage (p < .01). In the hippocampus, all enzymatic activities were significantly reduced in the late phase. In the brain stem Cu-Zn superoxide dismutase was significantly impaired at 1 and 6 h (p < .05) after subarachnoid hemorrhage induction, while in the late phase (48 h) reached the control value. The mitochondrial Mn-superoxide dismutase was significantly reduced since 1 h (p < .05) until 48 h (p < .02) after subarachnoid hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antioxidant enzymatic activities after experimental subarachnoid hemorrhage in rats. 842 14

We examined antioxidant activity in the pre-conditioned canine myocardium with four 5-min episodes of regional ischemia and reperfusion. Immediately after repetitive brief ischemia, mitochondrial Mn-superoxide dismutase (SOD) activity in the ischemic myocardium significantly increased compared with that in the nonischemic myocardium (18.7 +/- 2.1 vs. 14.9 +/- 1.0 U/mg protein, P < 0.05). Although no difference was seen in the activity between these regions after 3 h of the sublethal ischemia, a significant increase in the activity of the ischemic myocardium reappeared after 24 h compared with that of the nonischemic myocardium (26.7 +/- 0.9 vs. 20.8 +/- 0.9 U/mg protein, P < 0.05). Mn-SOD content increased gradually in the ischemic myocardium after sublethal ischemia, with a peak after 24 h (2.8 +/- 0.1 vs. 2.1 +/- 0.1 microgram/mg protein, P < 0.05). There were no differences in the activity and content of Cu, Zn-SOD between these regions after sublethal ischemia. Activities of glutathione peroxidase and reductase were significantly higher and lower, respectively, in the ischemic myocardium than those of the nonischemic myocardium immediately after repetitive brief ischemia, but no differences between these regions were seen in activities after 3 or 24 h. These results indicate that a brief ischemic insult alters myocardial antioxidant activity not only immediately after but also 24 h after sublethal ischemia.
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PMID:Sublethal ischemia alters myocardial antioxidant activity in canine heart. 843 Aug 58

In the kidney, ischaemia-reperfusion results in both hypoxic and oxidant cellular injury which is most marked in the tubules of cortex and outer medulla. These contrasting conditions may have opposite effects on the expression of enzymes that reduce or repair oxidant damage. To investigate this, the activities of CuZn and Mn superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST) were measured after 4 h and 3, 6, and 10 days of reperfusion following sham surgery or 45- or 90-min left renal artery occlusion. The right kidney served as internal control. Sham surgery had no effect on Mn SOD or GPx, but caused small (p < 0.05) reductions in CuZn SOD and GST activities. Forty-five minutes of ischaemia had no net effect on Mn SOD, increased GPx activity (maximum at 6 days, p < 0.01), and reduced CuZn SOD (nadir 3 days, p < 0.02) and GST (nadir 6 days, p < 0.02) activities. Ninety minutes of ischaemia again had no net effect on Mn SOD, prevented the induction of GPx, and further suppressed the activities of CuZn SOD and GST. The activity of the non-anti-oxidant enzyme lactate dehydrogenase was equal in left and right kidneys after 45 min of ischaemia, but different (p < 0.01) 10 days following 90-min injury, due to a combination of reduced activity in the ischaemic kidney and an increase of activity in the internal control. The immediate effect of ischaemia-reperfusion injury on the kidney is to reduce the activity of intracellular anti-oxidant enzymes in proportion to the severity of the ischaemic insult. Recovery or net induction of enzyme activity paralleled tubular regeneration. Protection resulting in acquired resistance to a second ischaemic event is unlikely to be due to induction of anti-oxidant enzymes if it occurs within 6 days.
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PMID:Differential effect of ischaemia-reperfusion injury on anti-oxidant enzyme activity in the rat kidney. 852 79

Free radical production and lipid peroxidation are potentially important mediators in testicular physiology and toxicology. The cytochrome P450 enzymes of the steroidogenic pathway are known to produce free radicals. The present study was conducted to elucidate in vivo the gonadotropin regulation of free radical-mediated lipid peroxidation and the antioxidative defense system in the rat testis. GnRH antagonist (Org 30276; 1 mg/kg BW) and testosterone [40-mm SILASTIC brand (Dow-Corning) capsules] treatments were used to suppress serum gonadotropin levels. As expected, serum LH decreased to a very low level, whereas serum FSH decreased only slightly. Testosterone treatment for 8 days decreased the levels of the peroxide-metabolizing enzymes, catalase, glutathione peroxidase (GSH-Px), and glutathione transferase (-44%, -24%, and -31%, respectively; P < 0.01 for all). These changes predominately reflect the interstitial tissue, in which catalase and GSH-Px activities were much higher than in the seminiferous tubules. Testicular CuZn or Mn superoxide dismutase activities, which were high in the seminiferous tubules, were not affected by gonadotropin suppression. The total peroxyl radical-trapping capacity of the testis, or its components, vitamin E and ubiquinol 9, were not affected either. Lipid peroxidation was decreased after 8-day treatment, as detected by diminished formation of conjugated dienes and fluorescent chromolipids (-30% and -19%, respectively; P < 0.05 for both). Similar results of decreasing catalase and GSH-Px activities were found after gonadotropin suppression with GnRH antagonist treatment for 2 days or testosterone treatment for 5 days. Substitution with hCG, alone or in combination with recombinant human FSH, reversed the changes in enzyme activities, whereas FSH alone had no effect. After 5-day testosterone treatment, catalase messenger RNA expression was studied by Northern hybridization, and it was observed to parallel the changes in enzyme activity. The site of free radical production was studied by separating interstitial tissue and seminiferous tubules 5 h after hCG injection. GSH-Px was induced by hCG only in the interstitial tissue (+28%; P< 0.01), supporting the hypothesis of free radical production during steroidogenesis. Aminoglutethimide, an inhibitor of the P450 cholesterol side-chain cleavage enzyme, induced extensive lipid peroxidation in the testis. Presumably, aminoglutethimide leads to leakage of free radicals from the P450 enzyme when substrate oxygenation is prevented. In conclusion, the present study suggests that physiological LH action in the rat testis causes lipid peroxidation and maintains high activities of peroxide-metabolizing enzymes in the interstitial tissue.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Induction of lipid peroxidation during steroidogenesis in the rat testis. 853

cDNA clones for guinea pig antioxidant enzymes, copper-zinc (Cu-Zn) and manganese (Mn-) superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were isolated by reverse transcription (RT)-polymerase chain reaction (PCR) cloning, to explore the mechanism regulating the differential expression of antioxidant enzymes (AOEs) in guinea pig lung and liver, during development. Increases in MnSOD, CAT and GPx mRNA expression in lung and, MnSOD mRNA in liver, were seen during the final period of gestation, whereas CuZnSOD and CAT mRNA expression in liver, which was constant during gestation, increased in the postnatal period. In lung, CuZnSOD mRNA level decreased just prior to birth while in liver, GPx mRNA expression declined markedly over the last third of gestation. In lung, while the mRNA levels of MnSOD, CAT, and GPx increased pre-natally, they declined following birth. In contrast, the postnatal increase in mRNA for CuZnSOD and CAT and the prenatal increase in MnSOD mRNA expression in liver remained at least to adolescence. In adolescent guinea pigs, CuZnSOD and CAT mRNA were most abundantly expressed in liver, while MnSOD and GPx mRNA were most abundant in heart and spleen, respectively. These results demonstrate markedly different developmental patterns of AOEs expression in guinea pig lung and liver during both the pre- and post-natal period. The short-lasting, late-gestational increases of MnSOD, CAT, and GPx mRNA expression in lung, may be responsible for the temporary increases in the activity of these antioxidants in the late gestational period, whereas the steady increases of CuZnSOD, CAT mRNA following birth, and also the prenatal increases in MnSOD mRNA expression, are probably responsible for the higher postnatal activity of these antioxidants in liver.
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PMID:Differential patterns of antioxidant enzyme mRNA expression in guinea pig lung and liver during development. 859 2

Rat lung extract contains protein that binds to a cis element in the 3' untranslated region of glutathione peroxidase (GPx) mRNA; this region is located 200 bases downstream of the stop codon and 77 bases downstream of the selenocysteine insertion sequence. GPx mRNA-binding protein (GPx-BP) has the following characteristics in common with Mn superoxide dismutase mRNA-binding protein (MnSOD-BP): 1. RNA-binding activity is redox-sensitive; free sulfhydryl groups on the protein are required for binding. 2. RNA-binding activity is enriched in a 130,000 x g supernatant fraction and is inhibited by RNA in the polysomal fraction. 3. The MnSOD and GPx cis elements compete with each other for protein binding. 4. UV crosslinking studies with each probe reveal a [32P]-labeled protein of the same apparent molecular mass, 56 kDa. These observations provide evidence that MnSOD and GPx RNAs bind the same protein.
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PMID:Evidence that glutathione peroxidase RNA and manganese superoxide dismutase RNA bind the same protein. 867 Feb 49

In this study, the activities of major enzymes participating in free radical metabolism (xanthine oxidase, XO; Cu,Zn and Mn superoxide dismutases, SOD; glutathione peroxidase, GSH-Px; catalase, CAT) were measured in kidney tissues from guinea pigs treated with gentamicin alone (200 mg/kg/day), gentamicin plus vitamin C (600 mg/kg/day), gentamicin plus vitamin E (400 mg/kg/day), and gentamicin plus vitamins C and E together for 10 days, and from animals treated with physiological saline solution alone during this period. We found no significant differences between control and gentamicin groups with respect to XO and Cu,Zn-SOD activities. However, the activities of Mn-SOD, GSH-Px, and CAT were found to be significantly depressed in the gentamicin-treated group relative to controls. In the gentamicin plus vitamin C group, the renal tissue Mn-SOD activity was found to be higher as compared with control and gentamicin groups. In this group, XO, GSH-Px and CAT activities were also higher than in the gentamicin-treated group, but no statistically significant differences existed between the values of this group and controls. Similar results were also observed in the gentamicin plus vitamin E group for Mn-SOD, GSH-Px, CAT, and XO. In this group, the Cu,Zn-SOD activity was found to be decreased as compared with control and gentamicin groups. In the gentamicin plus vitamins C and E group, the Cu,Zn-SOD activity was found to be decreased, the XO activity to be unchanged, and Mn-SOD, GSH-Px, and CAT activities to be increased as compared with the gentamicin and control groups. The results suggest that the enzymatic antioxidant defense system was significantly disturbed because of the suppressed activities of Mn-SOD, GSH-Px, and CAT in the kidney tissues from animals treated with gentamicin. However, vitamins C and E given concurrently with gentamicin completely abrogated this enzymatic suppression.
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PMID:Reduced enzymatic antioxidant defense mechanism in kidney tissues from gentamicin-treated guinea pigs: effects of vitamins E and C. 868 38


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