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:1.11.1.9 (glutathione peroxidase)
22,002 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of technical pentachlorophenol in drinking water (20 mg/l) to male Wistar rats caused significant liver concentration of tetrachlorophenol which remained stable during the exposure of 14 weeks. Pentachlorophenol and tetrachlorophenol accumulated to some extent in the perirenal fat whereas only pentachlorophenol could be found in brain. A period of four weeks of chlorophenol-free diet was sufficiently long to allow removal of the major part of the chlorophenol burden. The neurochemical effects included increased acid proteinase activity at the 8th week of exposure. It levelled off while superoxide dismutase activity increased to twice the control level. Glial glutathione peroxidase activity did not change whereas glial glutathione concentration was below the control range at the 12th week of exposure. Cerebral diaphorase activity was below the control range initially, and its activity increased above the control level during the recovery period whereas other biochemical changes levelled off.
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PMID:Neurochemical effects of peroral administration of technical pentachlorophenol. 44 21

Chlorine dioxide (Cl02) has been proposed as an alternative disinfectant to chlorine to avoid formation of organohalides. Cl02 and metabolites, chlorite (Cl0-2) and chlorate (Cl0-3) in drinking water produced decreases in rat and chicken blood GSH. The GSH dependent system was studied in rat and chicken blood after chronic treatment for 6 months with CL02 (0, 1, 10, 100, 1000 MG/L), Cl0-2 or Cl0-3 (10, 100 mg/l) in drinking water. There was a 60% increase in GSH reductase in the Cl02 treatment groups of rats and chickens. A similar increase was shown in rats treated with Cl0-2 but with Cl0-3 no change was observed. GSH peroxidase was without change in rat but chickens drinking 1000 mg/l Cl02 had decreased activity. Catalase was significantly higher than control in rat and chicken in the 1000 mg/l groups. However, catalase activity was decreased in rat treated with Cl0-2 and at the same time that GSH was decreased. These studies support the view that catalase is the first line of defense against the oxidative stress of Cl02 in rat and chicken erythrocytes.
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PMID:Effect of chlorine dioxide and metabolites on glutathione dependent system in rat, mouse and chicken blood. 54 25

Studies were conducted in an attempt to define a biochemical index of selenium toxicity rather than weight loss, liver disease and death. Rats, maintained on selenium deficient diets, received in drinking water various levels of selenium as Na2SeO3(0.1, 1.0, 1.5, 2.0 ppm). Changes in selenium dependent glutathione peroxidase (GSH-Px) activities and specific activities (nCi75Se/ug Se) were determined in liver, kidney and plasma at baseline and two and ten weeks after repletion. In intial selenium deficient rats, GSH-Px activities were markedly depressed and specific activities elevated as compared to 0.1 ppm controls. After two weeks, liver and plasma GSH-Px activiities increased, and plasma, liver and kidney specific activities decreased in a concentration dependent manner. In kidney, there were no differences in enzyme activity at either two or ten weeks. At ten weeks, liver GSH-Px activities continued to increase in the 1.0 ppm group, but were depressed at both the 1.5 and 2.0 ppm levels. Specific activities were also depressed in liver and excretion was not increased at these levels. This suggests a biochemical toxicity in liver at levels above 1.0 ppm after ten weeks, prior to the onset of gross pathological changes.
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PMID:The effects of different levels of selenium administered to rats in drinking water on distribution and glutathione peroxidase. 68 71

The activities of 2Cu,2Zn-superoxide dismutase, ferroxidase (ceruloplasmin), catalase and glutathione peroxidase were measured in the blood of rats during copper depletion. Two control groups of animals were used; one received the regular diet containing all essential components including copper and the other group was maintained on a diet, containing 1% the amount of copper in normal diet, copper being supplied as Cu(Leu)2 in the drinking water. Both groups showed no detectable differences, either in the copper content of blood or in the measured four enzymic activities. Excessive copper (injected intraperitoneally) caused only an insignificant rise in the enzymic activities (0-10%) compared to either control. After starting copper depletion ferroxidase activity decreases to 15% on the 15th day, while the 2Cu,2Zn-superoxide dismutase activity decreases to 40% on the 45th day. Ferroxidase activity shows rapid but transient changes immediately after perturbation in plasma copper levels. By contrast, the 2Cu,2Zn-superoxide dismutase activity more closely parallels the overall copper deficiency. Dietary repletion with copper raises the 2Cu,2Zn-superoxide dismutase activity to 94% and the ferroxidase activity to 80% of the control values within 36 h. Apart from the copper-dependent anemia catalase activity was decreased. However, 15 days after the start of the copper depletion catalase activity rises again and reaches the control value on the 40th day and a 30% stimulation was even seen on the 58th day. Upon copper repletion catalase activity reaches 166% of the control within 14 days. No copper-dependent differences of glutathione peroxidase activity were seen regardless whatever copper level was present in the rats.
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PMID:Copper deficiency and erythrocuprein (2Cu, 2Zn-superoxide dismutase). 97 14

Dietary Se (0.5 ppm Se supplied as sodium selenite to a casein-based diet containing 0.02 ppm Se and lacking in vitamin E) prevented the growth depression observed in rats receiving 76 ppm Ag in the water supply and markedly improved growth and survival of those given 751 ppm Ag. The Ag concentration of liver and possibly of kidney was increased by Se. Liver glutathione peroxidase activities from rats fed 0.5 ppm Se and given 76 and 751 ppm Ag for 52 days in their water were, respectively, 30% and 4% of those from control rats fed 0.5 ppmSe without Ag. In rats fed a diet, adequate in vitamin E (100 IU/kg) and Se (0.5 ppm as sodium selenite), administration of 751 ppm Ag in the water for 15 wk reduced liver GSH-Px activity to 5% of that from control rats receiving no Ag. GSH-Px activity of erythrocytes and kidney was decreased by Ag to 37% and 38%, respectively, of control values. It is concluded that in vivo administration of Ag dramatically decreased liver GSH-Px in rats fed Se-supplemented diets with or without vitamin E. Furthermore, supplemental Se (0.5 ppm) prevented the growth depression and mortality caused by Ag in rats fed a diet lacking vitamin E, while increasing the Ag concentration of liver and kidney.
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PMID:Alleviation of silver toxicity by selenite in the rat in relation to tissue glutathione peroxidase. 112 24

Effects of Buyang Huanwu decoction (BYHWD) on the change of oxygen free radical and cell ultrastructure were observed in rats with acute brain edema induced by pertussis vaccine (PV). The results showed that BYHWD could decrease significantly the contents of brain tissue protein and malondialdehyde, and raise the declining of superoxide dismutase and glutathione peroxidase activities. Also, BYHWD could reduce markedly the transport of pinosome in the left cerebral capillary endothelial cell, and lessen slightly the swelling of cerebral perivascular astrocyte processes and mitochondria in neuron. There was no significant reduction of water content in the left hemisphere on intravenous administration of BYHWD before and after injecting PV; while that in the right hemisphere, it was less remarkable in BYHWD group than that in control (P < 0.05). Hence, it suggests that BYHWD had the evident effects in antagonizing the damage of blood brain barrier and encephalic cell caused by free radical in brain edema.
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PMID:[Effects of buyang huanwu decoction on changes of oxygen free radical and cell ultrastructure in rats with experimental brain edema]. 129 71

The mechanisms of formation and removal of active oxygen species and lipid peroxides in biological systems have been briefly reviewed. Cytotoxic active oxygen species can be classified into two types: (a) radical species such as O2-. (superoxide) and HO. (hydroxyl radical) and (b) non-radical species such as H2O2 (hydrogen peroxide) and 1O2 (singlet oxygen). The direct or indirect attack of active oxygen species on polyunsaturated fatty acids, essential constituents of biological membranes, has been shown to result in the formation of a number of peroxidative lipid breakdown-products: LOOH (lipid hydroperoxide), LOO. (lipid peroxyl radical) and LO. (lipid alkoxyl radical). The lipid peroxide decomposition is probably dependent on the presence of ferric-ferrous ions. These processes are called lipid peroxidation reactions. In recent years, there has been a renewed interest in the role played by lipid peroxidation in many disease states. The multiple lines of defense against toxic oxygen intermediates consist of enzymatic systems, glutathione peroxidase, catalase and superoxide dismutase, and furthermore involves antioxidant capacities such as those of vitamin E and vitamin C. In biological systems, there are naturally occurring lipid-soluble (vitamin E and ubiquinone) and water-soluble (vitamin C, reduced glutathione and uric acid) antioxidants. Therefore, so long as homeostasis is maintained between the rate of radical generation and the rate of radical dissipation, the cellular generation of radicals may not be harmful. In contrast, this balance can be disturbed if cellular defenses are decreased or if there is a significant increase in the flux of radical generation. Once lipid peroxidation is initiated, the reactive intermediate formed induces cell damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Formation and removal of active oxygen species and lipid peroxides in biological systems]. 132 2

The molecular structure of plasma and erythrocyte selenium-dependent glutathione peroxidase (GSH-Px) was studied in rats drinking water containing [75Se]selenious acid, 1.3 mg Se/L. Substantial differences were found using three-step fractionation, including gel filtration of crude plasma and erythrocyte lysate, gel filtration of 75Se-GSH-Px treated by mercaptoethanol, and SDS-electrophoresis. Native plasma 75Se-GSH-Px, which exhibited a molecular weight (M(r)) of approx. 700,000, could be destroyed by mercaptoethanol action, resulting in disintegration of enzyme into several different 75Se-protein fragments and release of part of low-mol-wt 75Se. Native erythrocyte 75Se-GSH-Px M(r) value was found to be 113,000; two 75Se-protein fragments arose after mercaptoethanol treatment without 75Se release from the enzyme. The 75Se-subunits of 22,500 and 21,900 were isolated from plasma and erythrocyte 75Se-GSH-Px, respectively. Another minor 75Se-GSH-Px was identified in erythrocyte lysate (M(r) 214,000, subunit 22,100), which was considered to be a dimer of the above-mentioned erythrocyte enzyme. It can be assumed, based on these data, that native plasma GSH-Px, in contrast to erythrocyte enzyme, represents a high-molecular wt complex composed of several tetramers linked with S-S bonds. A certain part of selenium present in this complex is probably not selenocysteine and may be released with the mercaptoethanol treatment.
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PMID:Comparison of molecular properties of rat plasma and erythrocyte selenium-dependent glutathione peroxidase. 138 17

Cellular protection against free radical reactions was measured in myocardium from ethanol-fed rats using ethanol administration in drinking water as a model of moderate alcohol intoxication. The activities of Cu,Zn-superoxide dismutase (SOD) and glutathione-S-transferase were higher in ethanol-fed rats than in controls, whereas Mn-SOD, catalase and glutathione peroxidase activities were not altered by ethanol treatment. Myocardial zinc was higher and selenium concentration lower in ethanol-fed rats than in controls. Ethanol consumption, which failed to modify the myocardial vitamin E level, did not result in increased lipid peroxidation, but decreased cytosolic and membraneous protein thiols.
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PMID:Effects of chronic ethanol administration on free radical defence in rat myocardium. 141 73

The purpose of the present investigation was to establish whether pretreatment with selenium enhances the stores of selenium-dependent glutathione peroxidase in the tissues and to verify if and to what extent alterations of mechanical and biochemical cardiac properties induced by ischemia in the myocardium may be thus prevented. Ten rats had sodium selenite (6 micrograms/day) added to their drinking water for 4 weeks, while 10 control rats received no treatment. At the end of 4 weeks, the hearts were perfused by the Langendorff technique with oxygenated Krebs-Henseleit solution at a rate of 10 ml/min for 30 minutes at 37 degrees C. Ischemia was then induced by reducing the perfusion to 1 ml/min for 60 minutes; reperfusion followed at the control rate for a further 30 minutes. Isometrically developed pressure and its maximum first derivative at different ventricular volumes was measured before and after the ischemic period. Lactate and creatine kinase activity were measured in the effluent throughout. Tissue concentrations of adenine nucleotides and creatine phosphate and lutathione peroxidase activity were estimated after reperfusion. The rats treated with selenium showed a wide-spread increase in the activity of Se-dependent glutathione peroxidase in all tissues. There was an improved recovery of ventricular contraction during reperfusion and an increased myocardial content of adenine nucleotides and creatine phosphate. During reperfusion, the loss of creatine kinase into the perfusate was less in the treated animals, and there was a similar trend for the production of lactate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of selenium in cardiac ischemia and reperfusion. 142 Sep 51


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