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 defense system of aortic endothelial cells against oxidative stress was studied in alloxan-induced diabetic rabbits, and the effect of insulin on the antioxidant activities was estimated. Endothelial cells were prepared from 10 diabetic rabbits, 18 diabetic rabbits treated with insulin, and 10 age-matched controls after 17 days of diabetes. These cells were used for the estimation of glutathione (GSH) levels and its related enzyme activities. The antioxidant activities in these endothelial cells from diabetic rabbits were compared with those from control subjects. The concentration of GSH decreased in diabetic rabbits (1.6 +/- 0.2 nmol/mg protein [mean +/- SD] v 3.7 +/- 0.6 nmol/mg protein). Decreases in the activities of Cu, Zn-superoxide dismutase (Cu,Zn-SOD) (62.7 +/- 11.0 U/mg protein v 172.9 +/- 20.2 U/mg protein), catalase (7.6 +/- 2.1 U/mg protein v 12.3 +/- 3.2 U/mg protein), and GSH peroxidase (134.0 +/- 27.0 mU/mg protein v 179.1 +/- 26.2 mU/mg protein) were observed. The activities of other GSH-related enzymes such as GSH S-transferase or GSH reductase did not change in endothelial cells from diabetic rabbits. Most of these antioxidant activities were prevented when diabetic rabbits were treated with insulin (1 to 2 U/kg/d). These antioxidant activities were also determined in the diabetic liver and kidney. Similar decreases in the cellular defense activities and prevention of the decrease in activities by insulin were observed in the diabetic liver, while these antioxidant enzyme activities in the kidney were resistant to diabetic conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of insulin on impaired antioxidant activities in aortic endothelial cells from diabetic rabbits. 140 92

Tissue antioxidant status may be compromised under conditions of dietary restriction, either as the result of a deficiency in a specific cofactor required by a particular antioxidant enzyme or of more complex alterations of a generalized nature triggered by metabolic responses to starvation. Many similarities exist between insulin-reversible abnormalities in tissue antioxidant enzyme activities seen in experimental diabetes and in animals subjected to food deprivation-induced weight loss which is associated with hypoinsulinemia. The complex alterations in tissue antioxidant enzyme activities resulting from nutritional deficiency states, disease or drug administration may have important clinical consequences. Free radical-related processes have been implicated in the pathology of certain conditions in which weight loss is frequently recommended (e.g., diabetes and atherosclerosis). It will be important to investigate the possible adverse effects of this intervention on the underlying disease process involved. Glutathione-dependent hepatic detoxification processes are impaired under conditions of nutritional deficiency. This finding not only has important clinical implications but the standard practice of fasting small laboratory animals overnight to ensure reliable drug absorption can markedly influence the results of pharmacological/toxicological experiments. Further studies of the influence of nutritional status on free radical-related processes are likely to yield valuable information which may be applicable to a variety of research and clinical problems.
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PMID:Nutritional deficiency, starvation, and tissue antioxidant status. 307 49

Previous studies from our laboratory have demonstrated the presence of complex alterations in the activities of antioxidant enzymes in various tissues of rats with streptozotocin (STZ)-induced diabetes. In the present investigation, it is shown that rats made diabetic with alloxan (ALX), an agent differing from STZ both chemically and in its mechanism of diabetogenesis, show virtually identical tissue antioxidant enzyme changes which, as is the case with STZ, are preventable by insulin treatment. The finding that the patterns of antioxidant enzyme alterations in chemically-induced diabetes are independent of the diabetogenic agent used and the presence of similar abnormalities in tissues of spontaneously diabetic (BB) Wistar rats (particularly when diabetic control is less than optimal) suggest that the changes observed are a characteristic feature of the uncontrolled diabetic state and that these may be responsible for (or predispose to) the development of secondary complications in clinical diabetes. Comparative studies involving red cells of diabetic rats and human diabetics revealed a number of common changes, namely an increase in glutathione reductase activity, a decreased susceptibility to oxidative glutathione depletion (which was related to the presence of hyperglycemia) and an increased production of malondialdehyde (an indirect index of lipid peroxidation) in response to in vitro challenge with hydrogen peroxide. In the diabetic patients, the extent of this increase in susceptibility of red cell lipids to oxidation paralleled the severity of diabetic complications. Our results suggest that increased (or uncontrolled) oxidative activity may play an important role in the pathogenesis of complications associated with the chronic diabetic state.
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PMID:Antioxidant enzyme alterations in experimental and clinical diabetes. 323 Dec 24

We investigated the possible involvement of reactive oxygen radical-related processes in chronic (12-wk) diabetes induced in rats by streptozocin (STZ). Diabetes was associated with significantly increased activities of catalase (CAT), glutathione reductase (GSSG-RD), and CuZn-superoxide dismutase (SOD) in the pancreas and of CAT and GSSG-RD in the heart. On the other hand, the liver of diabetic rats showed a generalized decrease in CAT, glutathione peroxidase (GSH-PX), and SOD as well as in the levels of reduced glutathione (GSH). Diabetic kidney also showed decreases in CAT and SOD, but the activities of GSH-PX were increased. Insulin treatment (9-12 U/kg body wt) that was started after 8 wk of diabetes and continued for 4 wk reversed all of the foregoing alterations in tissue antioxidant status. Our results suggest the presence of increased oxidative stress in uncontrolled diabetes as manifested by the marked alterations in tissue antioxidant enzyme activities, the magnitude of which increased with the degree of emaciation. The complex patterns of changes observed in the various tissues examined are believed to be the result of compensatory increases in enzyme activities (usually involving enzymes whose activity in control tissues is low) and direct inhibitory effects, possibly resulting from an increased tissue-oxidant activity. Our findings support the view that tissue antioxidant status may be an important factor in the etiology of diabetes and its complications.
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PMID:Alterations in free radical tissue-defense mechanisms in streptozocin-induced diabetes in rat. Effects of insulin treatment. 330 71

Monolayer cultures of fetal rat mixed lung cells respond to sublethal concentrations (50%) of oxygen by a reduced growth rate. Exposure to 95% O2 causes growth arrest and cell loss. In the presence of serum the addition of dexamethasone (5.5 nM), tri-iodothyronine (5.5 nM), or insulin (5 microU/ml) appeared to increase the cytotoxicity of 95% O2. Under growth-arrested conditions, in the absence of serum or elevated O2 concentrations, all three agents influence cellular antioxidant enzyme activities. Dexamethasone (0.055 nM) increased CuZn superoxide dismutase activity by 72% and glutathione peroxidase activity by 94%. Triiodothyronine (5.5 nM) increased CuZn superoxide dismutase activity 93%. Insulin (5 microU/ml) increased CuZn superoxide dismutase activity 90%, and catalase activity 58%. Dexamethasone, but not tri-iodothyronine or insulin, seems to have a protective effect against subsequent acute hyperoxia under serum-free conditions. Local non-hormonal factors may also influence lung cell responses to acute increases in oxygen concentrations, since cells acutely exposed to 50% or 95% O2 release a transferable factor(s) into their culture medium which increases antioxidant enzyme activities of non-hyperoxic lung cells.
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PMID:Hormonal and local factors influence antioxidant enzyme activity of rat fetal lung cells in vitro. 352 18

T7 DNA polymerase reduced insulin at the same Km as thioredoxin, while the turnover number decreased. Recycling of the disulfide of thioredoxin subunit to its dithiol form was made by thioredoxin reductase. Incubation of T7 DNA polymerase with insulin decreases its ability to bind DNA and therefore inhibited polymerase and exonuclease activities. Thioredoxin reductase fully reversed this inhibition. Insulin did not induce dissociation of the T7 DNA polymerase subunits, which was tested by immunoadsorbent chromatography. No significant difference in single-stranded exonuclease compared to polymerase activity was seen in the flow through or the eluate, which had been expected if a dissociation of the subunits had occurred.
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PMID:Inhibition of the T7 DNA polymerase by insulin. 676 Nov 43

A reproducible scheme has been developed for the preparation of rat liver thioredoxin and thioredoxin reductase (EC 1.6.4.5) by using assays based on reduction of insulin and 5,5'-dithiobis(2-nitrobenzoic acid), respectively. Both proteins were purified to homogeneity, as judged from polyacrylamide gel electrophoresis. Thioredoxin had a molecular weight of 12 000 and contained about 110 amino acids including 4 half-cystines and an NH2-terminal valine. Peptide maps of reduced and carboxymethylated thioredoxin showed that the protein had the active center sequence -Cys-Gly-Pro-Cys-Lys-Met- characteristic of thioredoxins also from procaryotes. Prolonged air oxidation of fully reduced thioredoxin created inactive, aggregated disulfide-containing molecules. Thioredoxin reductase showed a subunit molecular weight of 58 000 and a native molecular weight of 116 000. The enzyme was highly specific for NADPH with a Km of 6 microM. It contained FAD as prosthetic group and was sensitive to inhibition by arsenite. Thioredoxin reductase had a Km of 2.5 microM for rat and calf liver thioredoxin and a Kcat of 3000 min-1.
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PMID:Rat liver thioredoxin and thioredoxin reductase: purification and characterization. 715 51

Pancreatic superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) activities were measured during the development of diabetes in diabetes-prone BB rats (BBdp) prior to insulin dependence. The pancreata from seven to eight BBdp rats of each sex were examined at ages 5, 7, 10, and 18 weeks and compared with age-matched control BB rats (BBc). At Week 18, BBdp rats had moderate to high insulitis but normal levels of blood glucose and insulin. Pancreatic CuZnSOD activity in BBdp rats was two times higher than the activity seen in BBc rats at age 5-10 weeks but then declined to the same level as seen in BBc rats at 18 weeks of age. MnSOD activity increased over time in the BBdp rats but remained very low in BBc rats. These changes in CuZnSOD and MnSOD activity resulted in BBdp rats having twice the pancreatic total SOD activity compared with BBc rats (P < 0.0001). Total GSHPx activity was significantly reduced in the pancreata from both male and female BBdp rats compared with their respective controls (P < 0.01 and P < 0.0001, respectively). The lower total GSHPx activity was due to reduced selenium-dependent GSHPx (SeGSHPx) activity. Erythrocyte and plasma activity of these enzymes was not different between rats with or without insulitis, indicating that differences in enzyme activities were confined to the pancreas. Thus, changes in pancreatic antioxidant enzyme activities occur prior to the development of diabetes symptoms in BBdp rats and may be related to the destruction of the pancreatic B cells and ultimate development of diabetes.
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PMID:Changes in pancreatic glutathione peroxidase and superoxide dismutase activities in the prediabetic diabetes-prone BB rat. 793 51

The effect of alloxan-induced diabetes on CuZn- and Mn-superoxide dismutase (SOD), catalase and glutathione peroxidase (GPX) activities, as well as the content of thiobarbituric acid reactive substances (TBARs) were examined in rat lymphoid organs (mesenteric lymph nodes (MLN), thymus and spleen) and, for comparison, red and white muscle fibres. The capacity for generation of reduced equivalents was also evaluated by measuring the activities of glucose-6-phosphate dehydrogenase (pentose-phosphate pathway-cytosol) and citrate synthase (Krebs cycle-mitochondria). Diabetes raised the capacity for the generation of reducing equivalents in the lymphoid organs: in the mitochondria of the thymus and spleen and in the cytosol of the mesenteric lymph nodes and thymus. In muscles, diabetes reduced CuZn-SOD activity in soleus and raised the activity in gastrocnemius, and depressed the activities of catalase in soleus and of glutathione peroxidase in both soleus and gastrocnemius. In relation to the lymphoid organs, the spleen showed a decrease in the antioxidant enzyme activities (except for glutathione peroxidase), whereas the thymus showed an increased level (except for Mn-SOD), and the MLN presented a reduction in Mn-SOD and catalase activities and an increase in GPX activity caused by diabetes. The content of TBARs in the tissues followed the changes in GPX activity inversely: i.e. a decrease in the lymphoid organs (except in the spleen) and an increase in the muscles of diabetic rats compared with the control group. All these changes found in diabetic rats were reversed by insulin treatment and were not modified by the normalization of glycaemia.
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PMID:Superoxide dismutase, catalase and glutathione peroxidase activities in the lymphoid organs of diabetic rats. 796 75

Insulin-dependent diabetes (IDD) in the nonobese diabetic (NOD) mouse is believed to result from the specific autoimmune destruction of pancreatic beta cells. The frequency of diabetes in the NOD mouse is sex-dependent, with approximately 90% of females and 40% of males developing clinical diabetes by 40 weeks of age. Recently, attention has focused on determining possible mechanisms for beta cell destruction. One potential mechanism is the toxic effect of free oxygen radicals produced as a result of the influx of inflammatory cells into the pancreas. A deficiency in available antioxidant enzymes could form a basis for diabetes susceptibility. To test the feasibility of this idea, we have compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase in isolated islets, pancreas, and other tissues of age- and sex-matched NOD, BALB/c, C57BL/10, and B10.GD mice. Enzyme profiles revealed that female NOD mice do not differ significantly in antioxidant enzyme activity from females of the other inbred strains. However, antioxidant enzyme activity in females was generally lower than in males regardless of mouse strain. While isolated islet cells exhibited somewhat lower levels of enzyme activity than other tissues, the islets of NOD mice proved to be no more deficient than those of BALB/c mice. Therefore, it is unlikely that any toxic effect of free oxygen radicals on the beta cells of NOD mice results directly or solely from an antioxidant enzyme deficiency. Nevertheless, one possible explanation for the lower incidence of diabetes in NOD males versus females may be the inherently higher male antioxidant enzyme activities.
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PMID:Antioxidant enzyme activities in IDD-prone and IDD-resistant mice: a comparative study. 846 25


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