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)

Small dosages of endotoxin (100--500 micrograms/kg) provide significant protection against the acute manifestations of pulmonary O2 toxicity and lethality. Ninety-seven percent of endotoxin-treated adult rats survived a 72-h exposure to greater than or equal to 95% O2 with mimimal lung changes, compared to 32% of control animals (P less than 0.01). Exposure to greater than or equal to 95% O2 for 7 days resulted in a 20% survival rate in untreated control rats vs. 98% survival in endotoxin-treated rats (P LESS THan 0.01). Histological evaluation of lung from survivors revealed substantially less collagen and reticular fiber deposition in the endotoxin-treated animal lungs. Endotoxin treatment was associated with increased activity of the protectant antioxidant enzyme systems of the lung in an apparent dose-response manner. Endotoxin's protective activity against O2 toxicity does not appear to depend on an initial toxic insult to the lung like with alpha-naphthylthiourea, oleic acid, or alloxan treatment. The data support a protective role for endotoxin against the acute and the more chronic manifestations of O2-induced pulmonary injury.
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PMID:Endotoxin protection against oxygen-induced acute and chronic lung injury. 53 52

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

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

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

1. The in vitro effects of alloxan, dialuric acid and vanadium ions, alone or in combination, on lipid peroxidation and on antioxidant enzyme activity in rat liver and kidney were studied. 2. Unlike alloxan, alloxan-glutathione (GSH) and dialuric acid increased lipid peroxidation, which could be explained by the decreased activity of catalase and GSH peroxidase during incubation. 3. Vanadium(IV) ions increased the amount of thiobarbituric acid-reacting substances, but neither vanadium(IV) nor vanadium(V) changed the enzyme activity. 4. The combination of vanadium ions and alloxan-GSH or dialuric acid had no additive effect on lipid peroxidation. Vanadium ions decreased the dialuric acid-induced inhibition of catalase activity. 5. The present results suggest the therapeutic value of vanadium as an antidiabetic agent.
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PMID:In vitro effects of alloxan-vanadium combination on lipid peroxidation and on antioxidant enzyme activity. 970 25

Effects of cytotoxic agents and hydrogen peroxide were examined using pancreatic BRIN-BD11 cells and the parental insulinoma RINm5F cell line. Cell viability was determined using the MTT colorimetric assay and the TUNEL assay was used to assess apoptosis and acridine orange assay was used to determine levels of apoptosis versus necrosis. RT-PCR studies were employed to investigate the effects of the toxins on the expression of antioxidative enzymes, superoxide dismutase (SOD), glutathionine peroxidase (GPX) and catalase (CAT). Streptozotocin, hydrogen peroxide, alloxan and ninhydrin exerted time- and concentration-dependent toxic effects on BRIN-BD11 and RINm5F cells. RT-PCR showed that 90 minutes exposure of BRIN-BD11 cells or RINm5F cells to 5 mM ninhydrin down regulates SOD, GPX and CAT antioxidative enzymes. Glutathionine peroxidase gene expression was also down regulated in both types of cell by hydrogen peroxide. There were no significant differences in antioxidant gene expression after exposure to the other toxins under the conditions employed. TUNEL assay revealed that streptozotocin (8 mM) and hydrogen peroxide (125 microM) had no significant effect on the number of cells undergoing apoptosis. However after exposure to ninhydrin (5 mM) almost 100% of the non-viable BRIN-BD11 cells and around 50% of the RINm5F cells were dying by apoptosis. With the BRIN-BD11 cells there was around a 30% increase in the number of apoptotic cells compared with 50% in the RINm5F cells after exposure to alloxan (16 mM). The results indicate multiple effects of cytotoxic agents on functional integrity and antioxidant enzyme gene expression in clonal beta-cells.
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PMID:Effects of cytotoxic agents on functional integrity and antioxidant enzymes in clonal beta-cells. 1268 36

The effect of sulfur dioxide (SO2) on brain antioxidant status, lipid peroxidation, and somatosensory evoked potentials (SEPs) was investigated in diabetic rats. A total of 40 rats were divided into 4 equal groups: control (C), SO2 + C (SO2), diabetic (D), and SO2 + D (DSO2). Experimental diabetes mellitus was induced by i.v. injection of alloxan at a dose of 50 mg/kg body weight. Ten ppm SO2 was administered to the rats in the sulfur dioxide groups (SO2 and DSO2) in an exposure chamber. Exposure occurred 1 hr/day, 7 days/wk, for 6 wk; control rats were exposed to filtered air during the same time periods. Although SO2 exposure markedly increased copper, zinc Superoxide dismutase activity, it significantly decreased glutathione peroxidase activity in both the diabetic and nondiabetic groups, compared with the C group. Brain catalase activity was unaltered; however, brain thiobarbituric acid reactive substances (TBARS) were elevated in all experimental groups with respect to the C group. SEP components P1, N1, P2, and N2 were significantly increased in all experimental groups, compared with the C group, and these components were also prolonged in the DSO2 group with respect to the other groups. The authors' findings suggest that exposure to SO2, because it increases lipid peroxidation, can change antioxidant enzyme activities and affect SEP components in diabetic rats.
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PMID:Changes in somatosensory evoked potentials, lipid peroxidation, and antioxidant enzymes in experimental diabetes: effect of sulfur dioxide. 1274 14

The effect of sulfur dioxide (SO(2)) on hippocampus antioxidant status, lipid peroxidation and learning and memory was investigated in diabetic rats. A total of 40 rats were divided into four equal groups: Control (C), SO(2) + C (SO(2)), diabetic (DM) and SO(2) + D (DMSO(2)). Experimental diabetes mellitus (DM) was induced by i.v injection of alloxan with a dose of 50 mg/kg body weight. Ten ppm SO(2) was administered to the rats in the sulfur dioxide groups in an exposure chamber. Exposure occurred 1 h/d, 7 d/wk, for 6 wk; control rats were exposed to filtered air during the same time periods. SO(2) exposure, while markedly increasing Cu-Zn Superoxide dismutase activity, significantly decreased glutathione peroxidase activity in diabetic and non-diabetic groups compared with the C group; hippocampus catalase activity was unaltered. Hippocampus thiobarbituric acid reactive substances (TBARS) were found to be elevated in all experimental groups with respect to control group. The active avoidance training results indicated that diabetic condition has been associated with learning and memory impairment. SO(2) exposure caused deficits of learning and memory. Diabetes mellitus-induced impairment of learning and memory were potentiated by SO(2) exposure. These findings suggest that exposure to SO(2) by increasing lipid peroxidation, can change antioxidant enzyme activities and can elevated intensity of deficits of learning and memory in diabetic rats.
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PMID:Effect of sulfur dioxide on active and passive avoidance in experimental diabetes mellitus: relation to oxidant stress and antioxidant enzymes. 1761 16

The in vitro effects of alloxan and the product of its reduction dialuric acid (alone or in combination with copper ions) on lipid peroxidation, carbonyl content, GSH level and antioxidant enzyme activities in rat liver and kidney have been studied. The effects of Cu2+/alloxan and Cu2+/dialuric acid were compared with those of Fe3+/alloxan and Fe3+/dialuric acid. Unlike alloxan, dialuric acid increased liver and kidney lipid peroxidation; similar effects were registered in the presence of Fe3+. In the presence of Cu2+/dialuric acid, the lipid peroxidation was strongly inhibited and vice versa--the liver protein oxidation was increased. Alloxan and dialuric acid, as well as their combinations with Fe3+ had no effect on the total GSH level. Both substances did not affect the Cu2+-induced changes in GSH level, glucose-6-phosphate dehydrogenase and gluthatione reductase activities. In contrast, Cu2+ had no effect on dialuric-acid induced changes in gluthatione peroxidase and superoxide dismutase activities. The present in vitro results, concerning the metal dependence of the effects of alloxan and dialuric acid, are a premise for in vivo study of alloxan effects in metal-loaded animals.
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PMID:In vitro effects of alloxan/copper combinations on lipid peroxidation, protein oxidation and antioxidant enzymes. 1827 62

Hyperglycemia, abnormal lipid and antioxidant profiles are the most usual complications in diabetes mellitus. In the present study, the antihyperglycemic, antihyperlipemic and antioxidant potency of an ethanol extract of Costus speciosus root was investigated in alloxan-induced diabetic male (Charles Foster) rats. Four groups of alloxan diabetic rats (n = 6) were administered orally with different doses of Costus speciosus root extract (150, 300 and 450 mg/kg BW) and a standard drug, glibenclamide (600 microg/kg BW), for 4 weeks. Two groups of rats (n = 6) served as normal and diabetic controls. While the diabetic controls showed significant abnormal carbohydrate, lipid and antioxidant profiles, administration of 150 mg/kg BW dose neither improved glucose nor lipid metabolism and antioxidant levels. Administration of 300 and 450 mg/kg BW doses, however, resulted in a reversal of diabetes and its complications. Both doses significantly brought down blood glucose concentration (26.76%, 34.68%), increased glycogenesis and decreased glyconeogenesis bringing the glucose metabolism toward normalcy. These doses also reversed the hyperlipidemia by reducing plasma total lipid (12.87%, 178.24%), cholesterol (21.92%, 30.77%) and triglyceride (25.32%, 33.99%) and improved hepatic antioxidant enzyme activities. The high dose (450 mg/kg BW) was found to have more potential antioxidant activities compared with glibenclamide. It is concluded that Costus speciosus root extract possesses anti-hyperglycemic, antihyperlipemic and antioxidative effects, which may prove to be of clinical importance in the management of diabetes and its complications.
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PMID:Antihyperglycemic and hypolipidemic effects of Costus speciosus in alloxan induced diabetic rats. 1844 47


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