Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of endotoxin on antioxidant gene expression and antioxidant enzyme activity in homogenates of the heart, liver, and kidney from Sprague-Dawley rats was compared by quantitation of m-RNA and enzyme activities. Alterations in the message level for Cu-Zn superoxide dismutase (SOD), Mn SOD, and catalase varied with the tissue type, length of exposure to endotoxin, and dose of endotoxin. In general, endotoxin treatment reduced Cu-Zn SOD expression in the heart and liver, but had no noticeable effect in the kidney. Mn SOD message levels were increased in the heart and kidney but decreased in the liver. Catalase expression was reduced in the kidney and increased marginally in the heart and liver. With regard to enzyme activity, endotoxin treatment reduced Cu-Zn SOD activity in the heart, liver, and kidney. Mn SOD activity showed little change in the heart, but increased in the liver and, to a lesser extent, in the kidney. Catalase activity showed little change in the heart and kidney but was decreased at 12 h in the liver. The differing responses of tissues to the oxidant stress of endotoxin exposure should be considered when evaluating the effect of endotoxin on antioxidant enzymes.
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PMID:Tissue differences in antioxidant enzyme gene expression in response to endotoxin. 888 5

To elucidate the role of oxygen-derived free radicals and superoxide dismutase in traumatic brain injury (TBI), blood-brain barrier (BBB) permeability, brain edema, behavioral function, and necrotic cavity volume (CV) were evaluated after TBI using nontransgenic (nTg) mice and heterozygous and homozygous transgenic (Tg) mice with a 1.5- (Tg 1.5x), 3.1-(Tg3.1x) and five- (Tg5x) fold increase in human copper, zinc-superoxide dismutase (CuZn-SOD) activity. Traumatic brain injury was produced by the weight-drop method. Evans blue dye leakage 4 hours after injury was attenuated in a CuZn-SOD dose-dependent manner with decreases of 18.6%, 40.9%, and 48.8%, in the Tg1.5x, Tg3.1x, and Tg5x groups, respectively. The water content 6 hours after injury in the Tg3.1x (79.64%) and Tg5x (79.45%) groups was significantly lower than in nTg mice (81.37%). There was an initial decrease in body weight and in motor performance, as measured by beam walk and beam balance tasks undertaken 1 day after TBI. However, the average reduction in beam balance and beam walk performance deficits and changes in body weight postinjury were significantly ameliorated in Tg mice. The CV was significantly smaller in Tg mice than in nTg mice (p < 0.01). These results indicate that superoxide radicals play a deleterious role following TBI. Furthermore, Tg mice provide a useful model for demonstrating the beneficial role of an antioxidant enzyme in TBI without the confounding effect of pharmacokinetics, toxicity, and BBB permeability associated with exogenous agents.
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PMID:Attenuation of acute and chronic damage following traumatic brain injury in copper, zinc-superoxide dismutase transgenic mice. 889 28

The purpose of this study was to determine the antioxidant enzyme activities in renal tissues of early stage ddY mice, an animal model for primary IgA nephropathy. Eight- and 40-week-old ddY female mice and normal healthy Balb/c female mice were used in this study. The levels of Cu/Zn-SOD, Mn-SOD, and GSH-PX activities in the renal cortex were significantly higher in 40-week-old ddY mice than in Balb/c control mice of the same age; no change of catalase activity was observed. There were no significant differences in the levels of Cu/Zn-SOD, Mn-SOD, GSH-PX, and catalase activities between the ddY mice and Balb/c mice at 8 weeks of age. Urinary protein was slightly higher in 40-week-old ddY mice. IgA or C3 was deposited at low levels in the glomerular mesangial areas of 8-week-old ddY mice. Marked depositions of IgA and C3 extended from the glomerular mesangial areas to the capillary walls of 40-week-old ddY mice. Expansion of glomerular mesangial matrices and mild mesangial cell proliferation was observed in 40-week-old ddY mice. Antioxidant enzyme activities in the renal cortex were already increased in the early stage IgA nephropathy in 40-week-old ddY mice. These findings suggest that measurements of antioxidant enzyme activities in the renal cortex of 40-week-old ddY mice was useful for evaluation of the pathogenesis of renal involvement in the early stage of IgA nephropathy.
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PMID:Detection of antioxidant enzyme activities in renal tissues of early stage IgA nephropathy in ddY mice. 895 8

This study was conducted to observe the effects of endurance exercise training on antioxidant enzyme activity in the liver and gastrocnemius muscle of rats being fed dietary casein and soy protein. The respective influences of dietary casein and soy protein on the activity of antioxidant enzymes were also compared. Thirty-nine male Wistar rats, aged 3 weeks, were randomly assigned to six groups: a normal protein control group, a normal protein endurance training group, a casein protein control group, a casein protein endurance training group, a soy protein control group, and a soy protein endurance training group. The endurance exercise training groups were adapted to a treadmill for 2 weeks prior to the date the rats were forced to run for 60 min at 25 m/min, 5 days/week for 12 weeks. We found that antioxidant enzyme activity in the gastrocnemius muscle was neither effected by the dietary proteins (casein and soy protein) nor by the above endurance exercise training load. However, hepatic Cu,Zn-SOD activity increased significantly for the dietary casein and soy protein diet groups as compared with the normal protein diet group (P < 0.01). Furthermore, significant increases both in hepatic Cu,Zn-SOD activity in the normal protein group and hepatic GSHpx activity in the casein and soy protein groups were observed when rats were loaded with 25 m/min of endurance exercise training (P < 0.01). These results suggest that, under the above experimental conditions, a casein or soy protein diet increase hepatic Cu,Zn-SOD activity, while endurance exercise training is effective in increasing hepatic Cu;Zn-SOD activity on a normal protein diet and in increasing hepatic GSHpx activity for cysteine and methionine deficient diets.
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PMID:Antioxidant enzymes response to endurance exercise training and dietary proteins in rat skeletal muscle and liver. 897 3

Nitric oxide mediates esophageal peristalsis and lower esophageal sphincter (LES) relaxation. Superoxide produced with inflammation inactivates nitric oxide. Superoxide is cleared in biological systems by superoxide dismutase. We tested the hypothesis that superoxide and the superoxide scavenging system modulate LES function. Transverse strips of muscle from the opossum LES relaxed when stimulated by an electrical field. Diethyldithiocarbamite was used to inhibit copper/zinc superoxide dismutase. Xanthine and xanthine oxidase were used to generate superoxide. Xanthine with xanthine oxidase or diethyldithiocarbamite alone had no effect on the LES. However, xanthine/xanthine oxidase and diethyldithiocarbamite reduced LES relaxation 34.1% and increased its resting tone 71.2%. Superoxide dismutase did not affect LES function, but protected the tissue from the effects of diethyldithiocarbamite and xanthine/xanthine oxidase. These studies are consistent with the hypothesis that superoxide acts by inactivating nitric oxide and suggest that these antioxidant enzyme systems may play a role in the maintenance of LES function.
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PMID:Effects of oxygen radicals and radical scavenging on opossum lower esophageal sphincter. 907 44

An oxidant stress has been shown to prevail in experimental and clinical nephrotic syndrome. Such oxidant stress may be induced by a reduced activity of antioxidant systems. We examined the altered expression of manganese-superoxide dismutase (Mn-SOD), an antioxidant enzyme, in patients with idiopathic nephrotic syndrome, in whom an increased oxidant stress had been demonstrated. The Mn-SOD activities in peripheral blood mononuclear cells obtained from 12 patients with active nephrotic syndrome (6.0 +/- 1.1 years of age, mean +/- SE) and hypoproteinemia were 42% lower (p < 0.05) than in 12 control subjects (5.5 +/- 0.5 years of age) with normal serum total protein concentrations. Reverse-transcriptase polymerase chain reaction also demonstrated that Mn-SOD messenger RNA expression in the patients with nephrotic syndrome was, on average, 59% lower than in control subjects. Because expressions of some genes are sensitive to serum, the serum dependency of Mn-SOD gene transcription was studied in glomerular endothelial cells transfected with a luciferase reporter gene fused with a rat Mn-SOD DNA fragment of -806 to +22 bp of the transcription initiation site (-806:+22). When these cells were exposed to different concentrations of fetal bovine serum (0.5% to 15%), the transcriptional activities determined by luciferase activities were proportional to serum concentrations. This serum-dependent transcriptional activation was also demonstrated by the fragment (-220:+22) but not by the fragment (-220:-20). When glomerular endothelial cells transfected with the fragment (-220:+22) were treated with 5% serum from patients with active nephrotic syndrome, transcriptional activation was more than 80% less than that by 5% serum from control subjects without nephrosis. These results indicate that Mn-SOD gene transcription is regulated at least in part by serum, and that the serum-dependent transcription of the gene is diminished in patients with idiopathic nephrotic syndrome. The regulatory region of serum-dependent gene transcription resides within its early promoter region. Our findings suggest that down-regulation of antioxidant enzyme transcription may contribute increased oxidant stress in idiopathic nephrotic syndrome.
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PMID:Down-regulation of manganese-superoxide dismutase gene expression in idiopathic nephrotic syndrome. 915 91

This study investigated expression of the key antioxidant enzyme copper/zinc superoxide dismutase in the villous trophoblast of the human placenta at different gestational ages from 8 weeks (last menstrual period) to term. Immunostaining for the enzyme was observed in the cytotrophoblast cells at all stages. Staining was generally absent from the syncytiotrophoblast at 8 weeks, except for small isolated areas close to the basal surface. The size and location of these areas suggested they were the result of recent cytotrophoblastic fusion. By 10 weeks, examples were more frequent and diffuse staining throughout most of the syncytiotrophoblast was observed at 12 weeks. The intensity of the immunostaining within the syncytiotrophoblast continued to increase until 14 weeks, by which time it matched generally that within the cytotrophoblast cells. A similar pattern of staining was observed within term material. These results are entirely consistent with the hypothesis that the oxygen tension within the intervillous space is low throughout the first trimester of pregnancy. They support the idea that an effective maternal circulation to the human placenta is only established at the start of the second trimester.
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PMID:Variations in expression of copper/zinc superoxide dismutase in villous trophoblast of the human placenta with gestational age. 917 23

The major cause of death following transplantation is cardiovascular disease. Among the many processes involved in atherogenesis, oxidative stress and modification of low density lipoprotein has been assigned a major role. This in turn may be affected by the immunosuppressive regime used. We studied oxidative stress in 40 renal transplant patients receiving two different immunosuppressive regimens (20 on cyclosporin, 20 on azathioprine/prednisolone), and 19 normal controls. Changes in lipid peroxidation (assessed as thiobarbituric acid reacting substances, TBARS), antioxidant enzyme activities (glutathione reductase GSHPx, glutathione peroxidase GSHPx and superoxide dismutase SOD) vitamin E and antioxidant associated trace metals (selenium, copper, zinc) were studied. Alteration of erythrocyte membrane fluidity was examined using the fluorescent probe 1,6 diphenyl-1,3,5-hexatriene (DPH). Both transplant groups showed no difference in TBARS, lipid standardised vitamin E, copper or selenium compared to controls. Zinc was significantly increased in both the cyclosporin and azathioprine groups compared to controls (P < 0.05). SOD was reduced in both transplant groups compared to controls (P < 0.001). GSHPx was elevated in both groups compared to controls but only reached significance in the azathioprine treated group (P < 0.005). GSHRx was slightly elevated in both transplant groups but did not reach significance. Erythrocyte membrane anisotropy was decreased in the cyclosporin treated group (P < 0.05). There was no difference in the azathioprine group compared to controls. The present results suggest an adaptive response to increased oxidative stress in both transplant groups sufficient to minimise markers of oxidative stress (TBARS and anisotropy). The results also suggest no significant difference between the two immunosuppressive regimes with regard to oxidative stress.
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PMID:Oxidative stress in cyclosporin and azathioprine treated renal transplant patients. 926 98

This study shows that superoxide dismutase is present in the thyroid gland of pigeons as a constitutive enzyme serving as an antioxidant against oxygen toxicity. Exogenous administration of thyrotropin induced thyroidal superoxide dismutase with a simultaneous burst in superoxide anion radical levels during the initial phase of hormone treatment. The superoxide radical generated was completely scavenged by SOD during the late phase of TSH-treatment, presumably as an adaptive measure to check the oxygen burst. TSH failed to augment serum T3 levels, although the thyroxine level in the serum was elevated. The peak level of SOD activity profile in the thyroid gland correlated very well with the peak level of thyroxine concentrations in the serum of pigeon. It is reasonable to postulate that the thyroidal SOD in homeotherms serves a dual role, firstly as a strategic antioxidant enzyme to protect the thyroid gland against the degenerative influence of toxic oxyradicals and secondly to provide H2O2 for thyroid hormone biosynthesis. Our results confirm the previous observations that TSH is mainly thyrotropic in birds and that it has no influence on the peripheral activation of thyroxine to triiodothyronine by stimulating the extra thyroidal 5'-deiodinase activity.
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PMID:Regulation of superoxide anion radical-superoxide dismutase system in the avian thyroid by TSH with reference to thyroid hormonogenesis. 934 97

The current study was designed to test the hypothesis that endurance training improves the ability of the diaphragm muscle to resist exercise-induced oxidative stress. Twenty-eight male Wistar rats were assigned to either untrained or trained groups. Trained rats were treadmill-trained for 9 wk. Each group was subdivided into acutely exercised or nonexercised groups. Diaphragm muscle from each rat was analyzed to determine the levels of certain antioxidant enzymes: Mn-superoxide dismutase (Mn-SOD), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase, and catalase. In addition, interleukin-1 and myeloperoxidase levels were determined. Endurance training upregulated all of the antioxidant enzymes. Conversely, acute exercise increased glutathione peroxidase and catalase in untrained rats, while it had no overt effect on any antioxidant enzymes in trained rats. Both Mn-SOD and Cu,Zn-SOD contents and activities were increased with endurance training. However, the mRNA expressions of both forms of SOD did not show any significant change with endurance training. Acute exercise also increased the levels of interleukin-1 and myeloperoxidase in untrained rats but not in trained rats. Moreover, acute exercise significantly increased the ability of neutrophils to produce superoxide, especially in untrained rats. The results from this study demonstrate that endurance training can upregulate certain antioxidant enzyme activities in rat diaphragm muscle, indicating the potential for improvement of the resistance to intracellular reactive oxygen species. The results of this study also suggest that acute exercise may cause oxidative damage in rat diaphragm through the activation of the inflammatory pathway and that endurance training may minimize such an extracellular oxidative stress by acute exercise.
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PMID:Endurance training improves the resistance of rat diaphragm to exercise-induced oxidative stress. 937 79


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