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)

The activities of superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione S-transferases, GSSG reductase, thiol transferases, gamma glutamylcysteine synthetase, and glucose-6-phosphate dehydrogenase, and the concentrations of H2O2 and reduced and oxidized glutathione were determined in the various developmental stages of houseflies. Housefly development was correlated with a progressive increase of cellular oxidizing equivalents and a loss of cellular reducing capacity. The loss of reducing equivalents appeared to result from a decrease in the activity of enzymes involved in glutathione and NADPH synthesis and a concomitant increase in glutathione-oxidizing enzymes. Relatively little change was observed in SOD activity during housefly development; however, the electrophoretic pattern of MnSOD varied in a manner specific to developmental stage. A striking increase in H2O2 concentration occurred prior to pupation possibly due to changes in substrate catabolism. These results support the hypothesis that the cellular environment becomes progressively more oxidizing during development.
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PMID:Developmental patterns in the antioxidant defenses of the housefly, Musca domestica. 199 75

Previous studies in conscious pigs have demonstrated that a sequence of ten 2-min coronary occlusion/2-min reperfusion cycles renders the heart relatively resistant to myocardial stunning 24 h later [late preconditioning (PC) against stunning] by an unknown mechanism. Since oxygen radicals contribute importantly to myocardial stunning and since antioxidant enzymes have been reported to be upregulated 24 h after PC in dogs and rabbits, we tested the hypothesis that late PC against stunning is related to an increase in endogenous antioxidant defenses. Chronically instrumented conscious pigs underwent a sequence of ten 2-min coronary occlusion/2-min reperfusion cycles (preconditioned group, n = 11) or received no intervention (control group, n = 5). Twenty-four hours later, pigs were killed and the myocardial levels of Mn superoxide dismutase (SOD), Cu-Zn SOD, catalase, glutathione (GSH) peroxidase, GSH reductase, GSH, GSH disulfide, alpha-tocopherol, and ascorbate were measured. There were no differences in any of the enzymatic or nonenzymatic antioxidants between the ischemic and nonischemic regions in the preconditioned group or between the control and the preconditioned group. Thus, when a marked protection against stunning was present (24 h after PC), no alteration in antioxidant defenses was observed. These results indicate that, in conscious pigs, late PC against myocardial stunning is not mediated by increased endogenous antioxidant defenses, thereby refuting one of the major current hypotheses regarding this phenomenon.
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PMID:Late preconditioning against stunning is not mediated by increased antioxidant defenses in conscious pigs. 936 27

Liver antioxidant enzyme activities, mRNA abundance, and glutathione (GSH) status were investigated in male Sprague-Dawley rats placed in an enclosure module aboard Space Shuttle STS-63 for 8 d (F, n = 6). F animals were compared to rats housed in an enclosure module on the ground (G, n = 9), which simulated the vibration and temperature conditions associated with launch and flight, and rats kept under conventional ground vivarium conditions in individual cages (V, n = 6). Spaceflight significantly decreased catalase, GSH reductase, and GSH sulfur-transferase activities in the liver (p < .05). Neither enzyme activity nor enzyme protein content of Cu-Zn and Mn superoxide dismutase (SOD) was affected by flight. The relative abundance of mRNA for Cu-Zn SOD and catalase was significantly decreased comparing F with G rats (p < .05). Spaceflight resulted in a dramatic decrease of liver GSH, glutathione disulfide, and total GSH contents (p < .01), which were accompanied by a lower gamma-glutamyl transpeptidase activity (p < .05). F rats showed a 47% (p < .05) increase in liver malondialdehyde concentration compared to G and V rats. Liver protein content was not affected by flight. These results indicate that spaceflight can downregulate antioxidant defense capacity and elicit an oxidative stress in the liver.
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PMID:Spaceflight downregulates antioxidant defense systems in rat liver. 943 15

The erythroid differentiation of K562 cells could be achieved by exposure to several pharmacologic agents, including hemin, butyric acid (BA), and anthracycline antitumor drugs such as aclarubicin (ACLA) and doxorubicin (DOX). When used at subtoxic concentrations, these drugs induce the overexpression of erythroid genes, leading to hemoglobinization of cells. Because anthracyclines are known to generate oxidative damage, we intended to demonstrate the involvement of an oxidative stress in the chemically induced differentiation process. The addition of antioxidants to anthracycline- and BA-induced cells decreased their growth and dramatically reduced the percentage of differentiated cells at day 3. Northern blot analysis showed that antioxidants also decrease the expression of erythroid genes and related transcription factors in induced cells. Moreover, analyses of oxidative stress markers showed that treatment with BA, ACLA, and DOX lead to a decrease in reduced glutathione and antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GRase], CuZn superoxide dismutase [SOD], and catalase [CAT]). In addition, DOX increased thiobarbituric acid reactants (TBARs), and MnSOD activity was decreased by BA and DOX. Finally, the production of reactive oxygen species (ROS) by differentiating agents was demonstrated using the dihydroethidium probe in a microspectrofluorometric assay. Altogether, these results strongly suggest the involvement of an oxidative stress generated by BA or anthracyclines as the first step in the irreversible differentiation process. Additionally, these results underline the differences between BA, ACLA, and DOX molecular mechanisms.
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PMID:Oxidative stress involvement in chemically induced differentiation of K562 cells. 1065 87

The role of pro/antioxidative processes during a low, subtoxic dose schedule of diazepam (3 mg/kg/day i.p.) for 7 days and its withdrawal in subcellular preparations of rat brain regions was studied in detail. The results indicated heterogeneity in the regional responses as well as in subcellular compartments. After 7 days of exposure to the drug, a decrease in the Mn-SOD activity was observed in the 3 regions studied while a significant increase in Cu/Zn-SOD activity was seen in cerebellum (CBL) and brain stem (BS) along with that of mitochondrial glutathione reductase. The post-mitochondrial fraction (PMF) showed a significant increase in GR activity in cerebrum. Enhancement of total and free thiol levels was observed in cerebrum and cerebellum whereas in BS free thiols were not enhanced. It was interesting to note that in the animals withdrawn from the drug and sacrificed after an interval of 7 days, the level of TBARS showed a highly significant increase in mitochondria of CB and CBL and 89% increase in BS. Similar trend was observed in the post-mitochondrial fractions of all the 3 regions whereas the activity of isozymes of SOD decreased (p < 0.001) in CBL and BS and to a lesser extent in CB. The GR activity was significantly decreased only in the mitochondria of cerebrum with a 34% rise in cerebellum and no change in BS. The PMFs showed a decrease in CB and CBL but a 20% rise in BS. Thus, the data show modulation of antioxidant responses during short-term administration of diazepam, and a lowering of peroxidative decomposition of polyunsaturated fatty acids of membranes. However, after withdrawal of the drug, PUFAs were found to be more vulnerable to peroxidative decomposition and changes in the antioxidant defenses were also observed, which did not come back to normal level during the study.
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PMID:Pro and antioxidant responses to repeated administration of diazepam in rat brain. 1083 99

The influence of a short-time isobaric hypoxia as well as reoxygenation on markers of oxidative stress (MDA, total SOD, GSH) and on the mRNA expression of the antioxidative enzymes (Cu/Zn-and Mn-SOD, catalase, GSH reductase and GSH peroxidase) has been studied in liver and kidneys of young (6 months) and old (22-25 months) Wistar rats. In livers of old animals, the concentration of GSH, the activity of SOD, and the mRNA expression of the antioxidative enzymes (except Mn-SOD) points to a restricted protection against oxidative stress or a lower production of ROS compared to young animals. Hypoxia resulted in a significant decrease of enzyme gene expression in both age groups. Reoxygenation caused an increase in mRNA of Cu/Zn-SOD and GPX in livers of young and of Mn-SOD in livers of old animals. In kidneys, gene expression of Cu/Zn-SOD, GSH reductase, and GPX was significantly higher in old animals compared to young animals. Whereas hypoxia caused a decrease of gene expression in the livers, it lead to a significant increase of Cu/Zn-SOD, catalase, and GSH reductase mRNA in kidneys of young rats. A reduced gene expression was observed after reoxygenation. In old kidneys, the expression of all enzymes except for catalase progressively declined in the hypoxic and reoxygenation groups. These data show that gene expression of antioxidative enzymes is affected by age and significantly differs between liver and kidney.
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PMID:Effect of age and hypoxia/reoxygenation on mRNA expression of antioxidative enzymes in rat liver and kidneys. 1255 17

Despite extensive interest in the rodent nasal cavity as a target organ for toxicity, there is very limited information regarding nasal defenses against oxidative stress and xenobiotic-derived oxidants. Using immunohistochemistry, we have examined the distribution of Cu,Zn and Mn superoxide dismutase (SOD), catalase, glutathione (GSH) peroxidase, and DT-diaphorase in rat nasal tissues. In addition, we have determined the concentrations of ascorbate and alpha-tocopherol and the activities of SOD (combined Cu,Zn and Mn forms), catalase, GSH peroxidase, GSH reductase, and DT-diaphorase in nasal respiratory epithelium (RE), olfactory epithelium (OE), and in lung. Immunohistochemistry demonstrated that all four enzymes were similarly distributed, with the greatest staining intensity in dorsal-medial regions of the nasal cavity. In respiratory epithelium, ciliated columnar cells and subepithelial glands stained positively, while in olfactory tissue the enzymes were detected in the sustentacular cells and Bowman's glands. With the exception of SOD, enzyme activities were higher in RE than OE, while concentrations of ascorbate and alpha-tocopherol were higher in OE than RE. With the exception of catalase, nasal activities were either higher than or comparable to those of the lung. Thus, the rat nasal cavity appears to be well protected against oxidative damage.
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PMID:Antioxidant status of the rat nasal cavity. 1261 49

Exploratory studies were undertaken to ascertain the role of pro/antioxidative processes during a 3 weeks administration of low sub-toxic dose of diazepam and its withdrawal. Rats were administered 3 mg/kg diazepam for 21 consecutive days and the changes observed in different regions of rat brain at the sub-cellular level. Mitochondria from cerebrum showed a 27% lowering of TBARS whereas those from cerebellum and brain stem showed 48 and 24% enhanced MDA levels respectively. No significant alteration in the SOD isozymes was observed after the dose schedule. The mitochondrial glutathione reductase (GR) activity showed a decrease in all the regions with maximum decrease (36%) recorded in brain stem while post mitochondrial fraction showed significant lowering in cerebrum (37%). Total -SH content increased in all the three regions with maximum enhancement recorded in cerebellum while the free thiol content also showed significant changes (p < 0.001) in cerebellum and brain stem. One week after the withdrawal of the drug MDA levels decreased by 38% in cerebrum and 53% each in mitochondrial fractions of cerebellum and brain stem. Regional heterogeneity in response was also observed in the post mitochondrial fractions. Mn-SOD showed lowered activity in cerebellum (22%) and in brain stem (15%). The mitochondrial GR activity decreased in all the regions being highest in cerebrum with no significant change in post mitochondrial fractions. The total and free -SH content in the withdrawn animals increased by 46% in cerebellum with no change in the other two regions. The results indicate towards lower oxidative phenomenon during 3 weeks treatment with diazepam while abrupt withdrawal causes lowering of antioxidant defenses which showed regional heterogeneity. A decrease in peroxidative decomposition of polyunsaturated fatty acids of membranes was observed on withdrawal, which could be due to stabilisation of membranes after long-term binding of diazepam.
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PMID:Effect of diazepam treatment and its withdrawal on pro/antioxidative processes in rat brain. 1270 44

In this study, we evaluated the oxidant status and antioxidant defense capabilities of the heart during the course of Trypanosoma cruzi infection and disease development in a murine model system. Our data show that the extent of protein carbonylation and lipid peroxidation is increased in the heart, but not the skeletal muscle, of infected mice. The level of oxidative injury biomarkers in the myocardium consistently increased with chronic disease severity. The antioxidant defense constituted by catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GSR), and reduced glutathione was increased in murine heart and skeletal tissue in response to the stress of T. cruzi infection. After the initial burst, CAT, GPx, and GSR remained unresponsive to the severity of chronic tissue damage in chagasic hearts. The cardiac level of Mn(2+) superoxide dismutase (MnSOD) was diminished in chagasic mice. Our data suggest that the host responds to acute injuries by activating antioxidant defenses that are of sufficient magnitude to scavenge the reactive oxidants in skeletal tissue. The myocardia of infected mice, however, sustain increased oxidative injuries with disease progression. We surmise that MnSOD deficiencies, resulting in the increased release of mitochondrial free radicals, lead to sustained oxidative stress that exceeds the cardiac antioxidant defense capacity and contribute to persistent oxidative damage in chagasic myocardium.
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PMID:Oxidative damage during chagasic cardiomyopathy development: role of mitochondrial oxidant release and inefficient antioxidant defense. 1552 41

Growth of pea (Pisum sativum L.) plants with 50 microM CdCl2 for 15 d produced a reduction in the number and length of lateral roots, and changes in structure of the principal roots affecting the xylem vessels. Cadmium induced a reduction in glutathione (GSH) and ascorbate (ASC) contents, and catalase (CAT), GSH reductase (GR) and guaiacol peroxidase (GPX) activities. CuZn-superoxide dismutase (SOD) activity was also diminished by the Cd treatment, although Mn-SOD was slightly increased. CAT and CuZn-SOD were down-regulated at transcriptional level, while Mn-SOD, Fe-SOD and GR were up-regulated. Analysis of reactive oxygen species (ROS) and nitric oxide (NO) levels by fluorescence and confocal laser microscopy (CLM) showed an over-accumulation of O2*- and H2O2, and a reduction in the NO content in lateral and principal roots. ROS overproduction was dependent on changes in intracellular Ca+2 content, and peroxidases and NADPH oxidases were involved. Cadmium also produced an increase in salicylic acid (SA), jasmonic acid (JA) and ethylene (ET) contents. The rise of ET and ROS, and the NO decrease are in accordance with senescence processes induced by Cd, and the increase of JA and SA could regulate the cellular response to cope with damages imposed by cadmium.
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PMID:Cadmium effect on oxidative metabolism of pea (Pisum sativum L.) roots. Imaging of reactive oxygen species and nitric oxide accumulation in vivo. 1689 16


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