Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alloxan-induced diabetic rats were treated with insulin (i.p.) or with Capparis decidua powder as a hypoglycaemic agent mixed with diet. The effect was assessed on lipid peroxidation (LPO) and the antioxidant defense system in rat tissues. The increased levels of blood glucose in diabetes produce superoxide anions and hydroxyl radicals in the presence of transition metal ions which cause oxidative damage to cell membranes. The heart tissue showed an increased lipid peroxidation (LPO) in diabetic rats while no significant change was observed in the liver and kidney. The treatment with C. decidua lowered LPO in these tissues even more effectively than insulin-treated rats. The superoxide dismutase (SOD) activity increased in the heart and kidneys in the diabetic group of rats probably to increase dismutation of superoxide anions. However, treatment with C. decidua decreased SOD activity in the liver and kidney and was comparable to control rats. Catalase (CAT) activity was not significantly affected in any of the tissues in diabetic and insulin-treated animals, however, CAT activity markedly increased in tissues with C. decidua treatment. Total and Se-dependent glutathione peroxidase (GSH-Px) in the heart was markedly lowered in diabetic rats which recovered with insulin as well as with C. decidua treatment. The increase in GSH-Px and CAT activity with C. decidua treatment may lower H2O2 toxicity and reduce oxidative stress in diabetes. However, glutathione (GSH) content in the heart and kidney and glutathione reductase (GSH-R) activity in all the tissues studied increased in diabetic rats while treatment with insulin lowered GSH content and GSH-R activity in these tissues. The treatment with C. decidua also decreased GSH-R activity in the kidney and heart which resulted in the decrease in GSH content in these tissues. The changes such as the increase in kidney and heart SOD may be an adaptive response in order to neutralize superoxide anions. The increase in GSH content and GSH-R activity in the tissue are in response to neutralize superoxide anions and to counteract oxidative stress in diabetes. Glutathione S-transferase (GST) was not significantly affected in diabetic rat tissue, however, heart GST increased with antidiabetic treatments. The increase in glucose-6-phosphate dehydrogenase (G6PDH) in the kidney and heart of diabetic rats subsequently decreased with C. decidua treatment. The increase in G6PDH in tissues may increase NADPH generation required for GSH-R activity and GSH production. It is suggested that these changes initially counteract the oxidative stress in diabetes, however, a gradual decrease in the antioxidative process may be one of the factors which results in chronic diabetes. The data indicate that C. decidua may have potential use as an antidiabetic agent and in lowering oxidative stress in diabetes.
 ...
PMID:Action of capparis decidua against alloxan-induced oxidative stress and diabetes in rat tissues. 936 67

Oxidant injury is considered to be an important mechanism in the pathophysiology of acute renal failure. It has been thought that decrease in extracellular and intracellular fluid and endotoxemia seen in obstructive jaundice may cause an increase in production of oxygen free radicals and impairment in antioxidant defense mechanism. This study is designed to investigate the possible role of oxidant injury in renal failure seen in jaundiced patients. In this study, 28 rats were divided into four groups: Control (C)(N = 7); Renal ischemia (RI)(N = 7); Obstructive jaundice+renal ischemia (OJ+RI)(N = 7); Obstructive jaundice (OJ)(N = 7). All groups were compared with each other according to renal failure findings and enzyme activities, such as Xanthine oxidase (XOD), Superoxide Dismutase (SOD) and Catalase in renal cortex and Glutathione Peroxidase (GSH-Px), in blood at 3rd day after ischemia and reperfusion. Renal failure findings monitored by blood urea and creatinine levels, seemed more evident in OJ+RI than RI group (p < 0.05). When compared with RI, in OJ+RI group, increase in XOD activity at 3rd day was statistically significant [0.259 +/- 0.01 U/g (tissue) and 0.362 +/- 0.03 U/g (tissue) respectively] (p < 0.05). SOD and GSH-Px activities of each ischemic group at 3rd day were decreased compared to non-ischemic groups. This fall was significant (p < 0.05). But there was no statistical difference between jaundiced and non-jaundiced groups. Alterations in catalase activities also had no statistical significance. These findings may suggest that the injury induced by oxygen free radicals at re-oxygenation of tissue after ischemia may also play a role in the pathogenesis of acute renal failure developed in obstructive jaundice.
 ...
PMID:The role of oxygen free radicals in acute renal failure complicating obstructive jaundice: an experimental study. 951 37

The ability of Cu(II) and Fe(III) to promote site-specific DNA damage in the presence of endogenous reductants was investigated by using 32P-5'-end-labeled DNA fragments obtained from the human p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene. Ascorbate induced metal-dependent DNA damage most efficiently (ascorbate > GSH > NADH). Cu(II) induced endogenous reductants-dependent DNA damage more efficiently than Fe(III). Endogenous reductants plus Fe(III) caused DNA cleavage at every nucleotide, without marked site preference. DNA damage by Fe(III) was inhibited by hydroxyl free radical (.OH) scavengers and catalase. These results suggest that endogenous reductants plus Fe(III) generate free or extremely near free .OH via H2O2 formation, and that .OH causes DNA damage. In the presence of 50 microM Cu(II) in bicarbonate buffer, ascorbate caused DNA cleavage frequently at sites of two or more adjacent guanine residues. In contrast, in the presence of 20 microM Cu(II), ascorbate caused DNA cleavage frequently at thymine residues. Catalase and a Cu(I)-specific chelator inhibited DNA damage by Cu(II), whereas .OH scavengers did not. Fe(III)-dependent 8-oxo-7,8-dihydro-2'-deoxyguanosine formation was inhibited by .OH scavengers, whereas no inhibition by .OH scavengers was observed with Cu(II). These results suggest that .OH is the main active species formed with Fe(III), whereas copper-peroxide complexes with a reactivity similar to .OH participate in Cu(II)-dependent DNA damage. The polyguanosine sequence specificity of DNA damage in the presence of high concentrations of Cu(II) can be explained by the preferential binding of Cu(II) to guanine residues.
 ...
PMID:Distinct mechanisms of site-specific DNA damage induced by endogenous reductants in the presence of iron(III) and copper(II). 971 16

The study was carried out on 25 women with breast cancer, 25 with fibrocystic breast disease and 19 healthy subjects. Antioxidant enzyme activities and total antioxidant status (AOX) were measured in erythrocyte and plasma of patients and healthies. Among the studied parameters, the erythrocyte Glutathione Peroxidase (GSH-Px) and Catalase (CAT) activities of patients with breast cancer were significantly different as compared to the control group values (p < 0.002 and p < 0.001) respectively. There was no correlation between total antioxidant status and any of these enzymes in erythrocyte and plasma activities of subjects. However, the positive correlation was found between erythrocyte and plasma Superoxide Dismutase [SOD(CuZn)] activities in all groups. Our results indicate that enzymatic and nonenzymatic antioxidants are differentially altered in human breast tumors. Since the total antioxidant status measurement isn't sufficient to evaluate the oxidant damage in breast disease, antioxidant enzymes must be measured separately in order to get additional information.
 ...
PMID:Plasma and erythrocyte total antioxidant status in patients with benign and malign breast disease. 992 72

Using cultured human endothelial cells, we investigated the contribution of concentrations of magnesium to the antioxidant system and oxidative stress. Cells were cultured at decreasing magnesium levels (569, 380, 190 and 95 microM) for 72 h. We then measured the amount of released hydrogen peroxide (H2O2) from the cells, the consumption of exogenous H2O2, the intracellular reduced glutathione (GSH) and the oxidized glutathione (GSSG) contents and the activities of glutathione reductase and catalase. Magnesium at a level of 949 microM was used as a control. The effect of magnesium deficiency on cellular membrane permeability was determined by measurement of the amount of [14C] amino acid mixture released from the cells. The results showed that during 72 h of magnesium-deficient treatment, the H2O2 release from the cells gradually increased and consumption of exogenous H2O2 was enhanced during the first 48 h of treatment. GSH content gradually decreased but GSSG was not affected. The activity of glutathione reductase was first stimulated and then inhibited. Catalase activity was gradually reduced. [14C]Amino acid mixture release from the cells continuously increased. We suggest that magnesium deficiency affected the intracellular antioxidant system in cultured endothelial cells.
 ...
PMID:Influence of low magnesium concentrations in the medium on the antioxidant system in cultured human arterial endothelial cells. 1019 96

There is considerable interest in the role of the 1-hydroxyethyl radical (HER) in the toxic effects of ethanol. The goal of this study was to evaluate the effects of HER on classical antioxidant enzymes. The interaction of acetaldehyde with hydroxylamine-o-sulfonic acid has been shown to produce 1, 1'-dihydroxyazoethane (DHAE); this compound appears to be highly unstable, and its decomposition leads to the generation of HER. Addition of DHAE into a solution of PBN led to the appearance of the typical EPR spectra of PBN/HER adduct. No PBN/HER spin adduct was detected when DHAE was incubated with 0.1 M PBN in the presence of GSH. In the absence of PBN, DHAE oxidized ascorbic acid to semidehydroascorbyl radical, presumably via an ascorbate-dependent one-electron reduction of HER back to ethanol. Catalase was progressively inactivated by exposure to DHAE-generated HER in a time and HER concentration-dependent manner. Ascorbic acid and PBN gave full protection to catalase against HER-dependent inactivation. The antioxidants 2-tert-butyl-4-methylphenol, propylgallate, and alpha-tocopherol-protected catalase against inactivation by 84, 88, and 39%, respectively. Other antioxidant enzymes were also sensitive to exposure to HER. Glutathione reductase, glutathione peroxidase, and superoxide dismutase were inactivated by 46, 36, and 39%, respectively, by HER. The results reported here plus previous results showing HER interacts with GSH, ascorbate, and alpha-tocopherol suggest that prolonged generation of HER in cells from animals chronically exposed to ethanol may lower the antioxidant defense status, thereby contributing to mechanisms by which ethanol produces a state of oxidative stress and produces toxicity.
 ...
PMID:Interaction of 1-hydroxyethyl radical with antioxidant enzymes. 1060 Jan 75

This study investigated the response of the antioxidant defense system in brain subcellular fractions after oral graded doses of ethanol to rat. Four groups of male Fischer-344 rats were orally administered saline, ethanol 2 g, 4 g, and 6 g/kg, respectively, and sacrificed 1 hour post treatment. Brain cytosol, synaptosomes, microsomes and mitochondria were separated by density gradient differential centrifugation and assayed for antioxidant system. A significant and dose-dependent-decrease in superoxide dismutase (SOD) activity was observed in all brain subcellular fractions. Catalase (CAT) activity was significantly decreased in brain mitochondria (67% and 80% of control) at higher doses of ethanol; whereas, CAT activity was significantly increased in cytosol, synaptosomes and microsomes. Glutathione peroxidase (GSH-Px) activity was significantly increased in all brain subcellular fractions except in cytosol at higher dose of ethanol. Malondialdehyde (MDA) content was significantly increased in all brain subcellular fractions showing dose response of ethanol-induced oxidative stress. The increase in MDA levels in the brain synaptosomes and microsomes were higher at 6 g dose of ethanol (155% and 163% of control) when compared to mitochondria and cytosol. Glutathione (GSH) levels were significantly increased in brain cytosol and microsomes at higher dose of ethanol (164% and 159% of control); whereas, the GSH concentration was significantly decreased in brain synaptosomes and mitochondria. The antioxidant enzyme (AOE) activity ratios (GSH-Px/SOD and GSH-Px + CAT/SOD) were dose dependently increased in all brain subcellular fractions, particularly in synaptosomes. The GSH/GSSG ratio was dose dependently increased in brain microsomes. The perturbations in the antioxidant defense system and enhanced lipid peroxidation following graded doses of ethanol ingestion indicate a dose-dependent-oxidative 2133stress response in brain subcellular compartments of rats.
 ...
PMID:Dose response of ethanol ingestion on antioxidant defense system in rat brain subcellular fractions. 1069 79

The lipid metabolism in sperm cells is important both as one of the main sources for energy production and for cell structure. The double leaflets of the membrane should be considered not simply as a passive lipid film, but as a very specialized structure. The complete maturation of the sperm cell membrane is attained after testicular lipid biosynthetic processes and after passage through the epididymis. A special composition of membrane phospholipids, rich in polyunsaturated fatty acids (PUFA), and the different composition of sperm and immature germ cell membrane are described and discussed. Testis germ cells as well as epididymal maturing spermatozoa are endowed with enzymatic and non-enzymatic scavenger systems to prevent lipoperoxidative damage. Catalase, superoxide dismutase and GSH-dependent oxidoreductases are present in variable amounts in the different developmental stages. Phospholipid hydroperoxide GSH peroxidase (PHGPx) activity and alpha tochopherol of epididymal spermatozoa are considered in detail. Their distribution and roles in caput and cauda epididymal sperm cells are discussed. Seminal plasma also has a highly specialized scavenger system that defends the sperm membrane against lipoperoxidation and the degree of PUFA insaturation acts to achieve the same goal. Systemic predisposition and a number of pathologies can lead to an anti-oxidant/pro-oxidant disequilibrium. Scavengers, such as GSH, can be used to treat these cases as they can restore the physiological constitution of PUFA in the cell membrane. The results of GSH therapy are presented and discussed.
 ...
PMID:Lipoperoxidation damage of spermatozoa polyunsaturated fatty acids (PUFA): scavenger mechanisms and possible scavenger therapies. 1070 76

Alpha-lipoic acid (alpha-LA) is an important antioxidant drug with chelating properties. In experiments performed in male mice (CD-1, Charles River) the effects of cadmium on lipid peroxidation (LP), GSH level, the activity of catalase and glutathione peroxidase (GSH-Px) in liver homogenates were studied. Mice were injected with CdCl2 x 2.5 H2O at a dose of 40 micromol x kg(-1) s.c. Alpha-LA was administered simultaneously i.p. at the dose corresponding to alpha-LA-to-Cd molar ratio of 5:1. The experiments were completed at 24 h. Cadmium increased LP to 200.7% of controls. This effect was prevented by alpha-LA treatment (p < or = 0.05). GSH level was decreased to 81.7% of controls and it was not affected by alpha-LA. GSH-Px activity diminished by Cd administration was corrected by alpha-LA (p < 0.001). Catalase activity decreased by Cd remained unaffected. The administration of alpha-LA alone enhanced LP and the activity of catalase. As estimated by AAS, Cd content in the liver, the kidneys, the brain and the testes remained unaffected by alpha-LA treatment. In the acute toxicity experiment, the mortality associated with cadmium was decreased by alpha-LA administration. The results suggest that the toxicity of Cd was decreased mainly by the antioxidant activity of alpha-LA rather than by cadmium removal from tissues.
 ...
PMID:The influence of alpha-lipoic acid on the toxicity of cadmium. 1070 16

The paper outlines the modification of some antioxidant enzymes and of reduced glutathione studied on physical training induced oxidative stress model. We also assessed vitamin E and C effect. Biochemical determinations were performed on heart homogenate and erythrocytes. Catalase and glutathione peroxidase activity diminished and superoxide dismutase activity increased to a different extent in both tissue samples, while coupled vitamin E and C protection to these tissues equally varied. The glutathione (GSH) pool decreased in erythrocytes and was moderately enhanced in the heart. Either in red blood cells or heart tissue GSH level constancy was maintained by simultaneous administration of vitamins through the experiment (training period). Malondialdehyde concentration revealed a slightly pro-oxidative behaviour of this couple of vitamins that explained the only partial recovery of enzymatic activity to normal values as well as a moderate lipid peroxidation process. Both phenomena were better expressed in erythrocytes.
 ...
PMID:[The effect of the combination of vitamin E and C on the oxidative stress parameters in physical exercise]. 1075 79


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>