Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.15.1.1 (superoxide dismutase)
58,858 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

G-6-Pase activity was investigated in the microsomal fraction from rat liver in the presence of carbon tetrachloride and/or propyl gallate (PG), reduced glutathione (GSH) and superoxide dismutase. Results obtained "in vitro" demonstrated that CCl4 induced a 60% inhibition of the microsomal enzyme activity. Moreover, a marked inhibition of G-6-Pase activity was found also when propyl gallate and reduced glutathione were added, at different concentrations, to incubation mixture. In addition, these drugs were unable to interfere with the dangerous effect exerted on the enzymatic activity by the haloalkane. Additional experiments carried out "in vivo" with propyl gallate produced evidence that intraperitoneal administration of the antioxidant was followed by a significant inhibition of G-6-Pase activity, while the damaging action of CCl4 was unaffected. Some possible explanations of these results are reported.
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PMID:[Interference of antioxidants E/O of some free radical "scavengers" with the activity of glucose-6-phosphatase after administration of carbon tetrachloride]. 23 43

It seems that superoxide dismutase plays the key role in protecting aerobes against O2 toxicity, but there is a whole range of ancillary mechanisms: enzymes to remove H2O2 (catalase, peroxidases) and hence to control formation of .OH from O2, which requires H2O2; antioxidants (ascorbate, GSH, alpha-tocopherol, carotenoids), which also react with singlet oxygen and/or .OH and often inhibit lipid peroxidation and last, but not least in animals, glutathione peroxidase, which controls the rate of lipid peroxidation. These mechanisms cope well at normal O2 concentrations but are insufficient at higher levels.
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PMID:Biochemical mechanisms accounting for the toxic action of oxygen on living organisms: the key role of superoxide dismutase. 35 40

The levels of lipid peroxides, determined as thiobarbituric acid reactive substances (TBARS), and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), were examined in the blood from stroke-prone spontaneously hypertensive rats (SHRSP), with and without cerebral lesions, and normotensive Wistar Kyoto (WK) rats. The levels of TBARS in the blood from healthy SHRSP were not significantly different from those of WK rats, while the values of SHRSP (male) with stroke were more than twice as high as those of healthy SHRSP. The activities of SOD and GSH-Px in stroke SHRSP were also statistically different from those of healthy SHRSP.
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PMID:Fluctuation of lipid peroxides and related enzyme activities at time of stroke in stroke-prone spontaneously hypertensive rats. 46 20

The effect of dietary selenium and vitamin E on the important cellular antioxidant defense systems was studied in rat erythrocytes. Weanling male Sprague-Dawley rats were fed a basal selenium and vitamin E deficient diet and supplemented with either none or 0.5 ppm selenium and either none or 45 ppm vitamin E for 35 or 40 days. Depletion of dietary selenium resulted in marked decrease of glutathione (GSH) peroxidase in the red cells, but the levels of GSH, catalase and superoxide dismutase were not significantly altered. The red cells of rats fed the basal diet deficient in both selenium and vitamin E had significantly lower levels of GSH and GSH peroxidase, but not of catalase and superoxide dismutase, than in those fed the basal diet and supplemented with either selenium, vitamin E or both. The results suggest that depletion of dietary selenium and vitamin may have a precipitate effect on lowering the levels of GSH and GSH peroxidase in rat erytyrocytes.
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PMID:Effect of dietary selenium and vitamin E on the antioxiant defense systems of rat erythrocytes. 46 73

Toxic doses of butylated hydroxytoluene (BHT), a phenolic antioxidant commonly used as a food additive, are known to produce lung damage. In this study, 3 days after a single ip injection of 62.5, 215, or 500 mg/kg BHT in mice there was a dose-dependent increase in lung weight. This concentration dependence with injected BHT was accompanied by increases in lung DNA and nonprotein sulfhydryl levels and in whole lung tissue enzyme activities of glutathione (GSH) peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase. The increased enzyme activities are considered to correspond to inflammatory and proliferative pulmonary changes resulting from acute lung cell injury and necrosis, which have been described previously, and cannot be construed as evidence for a primary oxidant-induced pulmonary lesion. The mechanism of BHT-induced lung changes may not be related to the antioxidant property of BHT, since vitamin E, n-propyl gallate, ethoxyquin, N,N'-p-phenylenediamine, and the structurally similar compound, butylated hydroxyanisole did not appear to produce the gross anatomical or biochemical lung changes observed with BHT.
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PMID:Effect of butylated hydroxytoluene and other antioxidants on mouse lung metabolism. 59 82

Neonatal rats (4--7 days old) and adult rats (approximately 80 days old) were continuously exposed to either 96--98% oxygen or air. Examination of the lungs of neonatal rats, who survived 5 days of oxygen exposure with no evidence of respiratory distress, showed significant increases in the pulmonary superoxide dismutase (SOD) activity (peak value: 144% of air-exposed controls), glutathione peroxidase (GP) activity (126%), glutathione reductase (GR) activity (122%), reduced glutathione (GSH) level (176%), and glucose-6-phosphate dehydrogenase activity (151%). Adult rats, most of whom succumbed within 3 days of oxygen exposure, did not show any significant increase in the activities of pulmonary SOD, GP, GR, and the level of GSH as compared to the air-exposed adult animals. Glucose-6-phosphate dehydrogenase was significantly elevated in the 72-hr oxygen-exposed adult rats. It is concluded that increases in the lung complement of SOD, GR, GP, and GSH in the neonatal rat during oxygen challenge may provide the mechanism(s) for their increased tolerance to hyperoxia-induced lung injury as compared to the adults.
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PMID:Oxygen toxicity: comparison of lung biochemical responses in neonatal and adult rats. 64 79

Paraquat is a widely used herbicide which causes lung injury in man characterized by progressive parenchymal damage that may lead to fatal respiratory failure. The precise mechanism of injury is unknown but is related to the cyclic oxidation and reduction of paraquat in cells with resultant production of free radicals of oxygen. In this study, superoxide dismutase (SOD), an enzyme that catalyzes the dismutations of superoxide free radical (O2-) to less toxic forms, plus reduced glutathione (GSH), and d-propranolol (PROP), were evaluated for their ability to protect against acute paraquat toxicity. Rats maintained at room air were given 50 mg paraquat dichloride/kg body weight in a single intraperitoneal (IP) injection 60 min prior to receiving either 0.2, 2, 10, or 20 mg/kg/d SOD, 3.6, 7.2, or 14.4 mmol/kg/d GSH, 2 or 20 mg/kg/d PROP, or an equal volume of normal saline (controls) LP. in divided doses for 3 d. SOD significantly prolonged and increased survival at doses of 2, 10, or 20 mg/kg/d (p less than 0.05). In addition, histologic lung morphology in SOD-treated rats showed only minimal intra-alveolar hemorrhage and hypercellularity 24, 48, and 168 h after paraquat challenge. Treatment with GSH, PROP or 0.2 mg/kg/d SOD was not protective. Duration of survival, percent survival, and lung morphology in these groups were not significantly different from controls. These results indicate that a) SOD protects against the development of acute paraquat toxicity in rats, b) one mechanism of paraquat poisoning is increased biologic production of O2-, and c) SOD may have a role in the therapy of paraquat poisoning in man.
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PMID:Prevention of acute paraquat toxicity in rats by superoxide dismutase. 65 8

The effects of dietary vitamin E on the important cellular antioxidant defense systems were studied in rat blood. One-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet and supplemented with either none or 45 ppm vitamin E for 4 months. The activity of glutathione (GSH) peroxidase was decreased significantly (p less than 0.05) in the red blood cells and plasma of vitamin E-deficient rats. The level of GSH in the red cells of vitamin E-deficient rats was also significantly decreased. No detectable GSH was found in the plasma of both groups of animals. The activities of catalase and superoxide dismutase were not significantly altered by the status of dietary vitamin E. Similar results were obtained when 2-month-old male rats were fed the respective diets for 3 months. The results suggest that the decreased levels of GSH and GSH peroxidase in the red cells of animals fed a vitamine E-deficient diet may in part contribute to their increased susceptibility to hemolytic agents.
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PMID:Dietary vitamin E and levels of reduced glutathione, glutathione peroxidase, catalase and superoxide dismutase in rat blood. 91 61

The purpose of this study was to investigate the hypothesis that paraquat pulmonary toxicity results from cyclic reduction-oxidation of paraquat with sequential generation of superoxide radicals and singlet oxygen and initiation of lipid peroxidation. In vitro mouse lung microsomes catalyzed an NADPH-dependent, single-electron reduction of paraquat. Incubation of paraquat with NADPH, NADPH-cytochrome c reductase, and purified microsomal lipid increased malondialdehyde production is a concentration dependent manner. Addition of either superoxide dismutase or a single oxygen trapping agent 1,3-dipheylisobenzo furan inhibited paraquat stimulated lipid peroxidation. In vivo, pretreatment of mice with phenobarbital decreased paraquat toxicity, possibly by competing for electrons which might otherwise reduce paraquat. In contrast, paraquat toxicity in mice was increased by exposure to 100% oxygen and by deficiencies of the antioxidants selenium, vitamin E, or reduced glutahione (GSH). Paraquat, given IP to mice, at 30 mg/kg, decreased concentrations of the water-soluble antioxidant GSH in liver and lipid soluble antioxidants in lung. Oxygen-tolerant rats, which hae increased activities of pulmonary enzymes which combat lipid peroxidation, were also tolerant to lethal doses of paraquat as indicated by an increased paraquat LT50. Furthermore, rats chronically exposed to 100 ppm paraquat in the water had elevated pulmonary activities of glucose-6-phosphate dehydrogenase and GSH reductase. These results were consistent with the hypothesis that lipid peroxidation is involved in the toxicity of paraquat.
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PMID:Paraquat toxicity: proposed mechanism of action involving lipid peroxidation. 101 17

Interactions between manganese (Mn) deficiency and streptozotocin (STZ)-diabetes with respect to tissue antioxidant status were investigated in male, Sprague-Dawley rats. All rats were fed either a Mn-deficient (1 ppm) or a Mn-sufficient (45 ppm) diet for 8 wk. Diabetes was then induced by tail-vein injection of STZ (60 mg/kg body weight), after which the rats were kept for an additional 4 or 8 wk. The control groups comprised rats not injected with STZ and fed either Mn-deficient or Mn-sufficient diets for a total of 12 wk. The Mn-deficient diet decreased the activities of manganese superoxide dismutase (MnSOD) in kidney and heart, and of copper-zinc superoxide dismutase (CuZnSOD) in kidney, in the non-diabetic animals. In the diabetic rats, the Mn-deficient diet induced more pronounced decreases in activities of these same enzymes, and also increased liver MnSOD activity. Plasma and hepatic vitamin E levels increased progressively with the duration of diabetes, independent of dietary Mn intake. Lipid peroxidation, as measured by H2O2-induced production of thiobarbituric acid reactive substances in erythrocytes, also increased, concomitant with decreased liver and kidney glutathione (GSH) levels. These findings demonstrate for the first time and interactive effective between Mn deficiency and STZ-diabetes, resulting in amplification of tissue antioxidant changes seen with either Mn deficiency or STZ-diabetes alone. This effect of Mn deprivation in experimental diabetes suggests a physiological role for Mn as an antioxidant nutrient.
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PMID:Tissue antioxidant status in streptozotocin-induced diabetes in rats. Effects of dietary manganese deficiency. 128 89


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