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

Incubation of human term placental mitochondria with Fe2+ and a NADPH-generating system initiated high levels of lipid peroxidation, as measured by the production of malondialdehyde. Malondialdehyde formation was accompanied by a corresponding decrease of the unsaturated fatty acid content. This NADPH-dependent lipid peroxidation was strongly inhibited by superoxide dismutase and singlet oxygen scavengers, markedly stimulated by paraquat, but was not affected by hydroxyl radical scavengers. Catalase enhanced the production of malondialdehyde by placental mitochondria. The effects of catalase and hydroxyl radical scavengers suggest that the initiation of NADPH-dependent lipid peroxidation is not dependent upon the hydroxyl radical produced via an iron-catalyzed Fenton reaction. These studies provide evidence that hydrogen peroxide strongly inhibits NADPH-dependent mitochondrial lipid peroxidation. The inhibitory effect of superoxide dismutase and stimulatory effect of paraquat, which was abolished by the addition of superoxide dismutase, suggests that superoxide may promote NADPH-dependent lipid peroxidation in human placental mitochondria.
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PMID:The involvement of superoxide and iron ions in the NADPH-dependent lipid peroxidation in human placental mitochondria. 282 15

The oxygen paradox refers to the abrupt release of cytoplasmic enzymes and severe cellular disruption that occurs following reoxygenation of anoxic perfused hearts. In this study, the ability of a series of oxygen-derived free radical inhibitors and scavenging agents to protect isolated perfused rat hearts from the oxygen-induced enzyme release following 30 or 60 mins of anoxic perfusion (oxygen paradox) and cumene hydroperoxide-induced injury was evaluated. Malondialdehyde (MDA) release, an indicator of lipid peroxidation, and creatine kinase (CK) release, an indicator of cellular injury, were monitored. We evaluated five agents previously reported to scavenge or inhibit the formation of oxygen free radicals. The putative hydroxyl radical scavengers dimethylthiourea (DMTU) and mannitol; catalase, an agent protective against peroxide injury; allopurinol, an inhibitor of xanthine oxidase; and albumin, a non-specific protein control, were evaluated. Coronary flow rates and myocardial temperature were continuously monitored to ensure uniform perfusion conditions. The MDA assay was carefully monitored by constructing standard curves on each experimental day. Addition of 20 microM cumene hydroperoxide to oxygenated perfused hearts caused peroxidative cell injury as evidenced by significant MDA and CK release in the coronary effluent. DMTU and catalase provided near complete protection from cumene hydroperoxide-induced cell injury but did not reduce CK release from hearts subjected to either the mild (30-min) or the severe (60-min) oxygen paradox (reoxygenation-induced injury). Allopurinol caused a significant reduction in MDA release but not CK release from oxygen paradox-injured hearts. Allopurinol and albumin had no significant effect on MDA release from cumene-hydroperoxide-injured hearts. Catalase (300 U/ml) caused a mild but not statistically significant reduction in MDA release from cumene hydroperoxide injury but did not provide protection from the oxygen paradox at either injury level. Mannitol (120 mM), in contrast to DMTU, was ineffective in reducing cumene-induced injury but showed a significant protective effect against oxygen paradox-induced damage. It is concluded that the ability of mannitol to reduce reoxygenation-induced CK release in the oxygen paradox may be due to its osmotic activity and consequent ability to prevent cellular swelling rather than its activity as an oxygen-free radical scavenger.
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PMID:Effects of the free radical scavenger DMTU and mannitol on the oxygen paradox in perfused rat hearts. 311 97

Xanthine (X) and xanthine oxidase (XO) were injected intratracheally (IT) in hamsters at Day 0 (38 mg X, 100 micrograms XO) and Day 5 (38 mg X, 250 micrograms XO). Control hamsters received saline or X (38 mg) plus boiled XO (100, 250 micrograms). Cytoplasmic superoxide dismutase (SOD) activity increased from control of 286 to 337 and 335 units/lung at Days 12 and 19, respectively, but decreased to 228 units/lung at Day 33; mitochondrial SOD activity increased at Day 12 from control of 57 to 71 units/lung and then decreased at Days 26 and 33 to 42 and 33 units/lung, respectively. Glutathione peroxidase (GP) and glutathione reductase (GR) activities rose from their control values of 1161 and 1151 to 1561 and 2287 units/lung at Day 12, respectively; thereafter, GR activity decreased to 512 and 462 units/lung at Days 19 and 26, respectively. Glutathione transferase declined at Day 12 but increased at Day 26 after initial treatment. Glucose-6-phosphate dehydrogenase activity declined from control of 1071 to 693 units/lung at Day 2 and returned to control thereafter. Catalase activity remained unaffected. Hydroxyproline was increased from 903 micrograms/lung in control to 1080, 1301, 1195, and 1148 micrograms/lung at Days 12, 19, 26, and 33, respectively. Malonaldehyde increased from 40 nmole/lung in control to 70 and 113 nmole/lung at Days 12 and 33, respectively. The ratio of right ventricle to left ventricle and septum increased significantly from control of 0.277 to 0.318 at Day 33. Histopathology at Days 2 and 4 revealed peribronchiolar and arteriolar inflammation, and diffuse alveolitis. By Day 12 there were thickened alveolar septa and foci of fibrotic consolidation.
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PMID:Effects of intratracheal administration of xanthine plus xanthine oxidase on lung antioxidant enzymes, lipid peroxidation, and collagen in hamsters. 319 17

1. The present study was undertaken to investigate the effects of hypobaric hypoxia, equivalent to an altitude of 5500 m, on antioxidant enzymes in rats. 2. Malondialdehyde levels in serum, heart, lung, liver and kidney of hypobaric-hypoxic rats were all significantly higher than in control rats by day 21 of exposure (P < 0.05), indicating increased oxidative stress. 3. Superoxide dismutase (SOD) catalyses the conversion of the superoxide anion to H2O2 and O2. The concentration of immunoreactive Mn-SOD in the serum of hypobaric-hypoxic rats was raised significantly from day 5 onwards, whereas in liver and lung, it had decreased significantly by day 21 (P < 0.05). 4. Glutathione peroxidase (GSH-Px) catalyses H2O2 and certain lipid peroxides. By day 21, GSH-Px activity had increased significantly in the heart and lungs, but decreased significantly in the liver (P < 0.05). 5. Catalase catalyses H2O2. Catalase activity in the liver and kidney of hypobaric-hypoxic rats was significantly decreased on day 1 (P < 0.05) though levels then recovered. 6. Mn-SOD mRNA in the liver of hypobaric-hypoxic rats was induced during the experiment, the effect being exceptionally marked, especially during the first 3 days of exposure to hypobaric hypoxia. 7. These results suggest that the liver may be more vulnerable than the other organs tested to oxidative stress under hypobaric hypoxia.
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PMID:Effects of hypobaric hypoxia on antioxidant enzymes in rats. 878 50

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.
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PMID:Dose response of ethanol ingestion on antioxidant defense system in rat brain subcellular fractions. 1069 79

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.
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PMID:[The effect of the combination of vitamin E and C on the oxidative stress parameters in physical exercise]. 1075 79

In this study we reviewed 20 patients with laryngeal squamous cell carcinoma to evaluate the oxidant and antioxidant status on tissue level. Superoxide Dismutase (SOD) and Catalase levels, two important antioxidant enzymes, and Malondialdehyde (MDA) levels, a valuable index of lipid peroxidation, were compared in cancerous and normal tissues of the patients. In cancerous tissue SOD activities were significantly lower than in the normal tissue, while there was no significant difference in MDA levels and Catalase activities. It was also observed that SOD activities significantly decreased as the histopathologic malignancy grades increased in cancerous tissue. These changes in oxidant and antioxidant status in carcinomatous tissue of the larynx are considered to be of great interest.
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PMID:Oxidant and antioxidant status in larynx squamous cell carcinomas. 1127 21

Effect of coconut protein in rats fed high fat cholesterol containing diet on the metabolism of lipids and lipid peroxides was studied. In addition, effect of coconut protein were compared with rats fed L-arginine. The results indicate that those fed coconut protein and those fed L-arginine showed significantly lower levels of total cholesterol, LDL+ VLDL cholesterol, Triglycerides and Phospholipids in the serum and higher levels of serum HDL cholesterol. The concentration of total cholesterol, triglycerides and phospholipids in the tissues were lower in these groups. There was increased hepatic cholesterogenesis which is evident from the higher rate of incorporation of labeled acetate into free cholesterol. Increased conversion of cholesterol to bile acids and increased fecal excretion of bile acids were observed. Feeding coconut protein results in decreased levels of Malondialdehyde in the heart and increased activity of Superoxide dismutase and Catalase. Supplementation of coconut protein causes increased excretion of urinary nitrate which implies higher rate of conversion of arginine into nitric oxide. In the present study, the arginine supplemented group and the coconut protein fed group produced similar effects. These studies clearly demonstrate that coconut protein is able to reduce hyperlipidemia and peroxidative effect induced by high fat cholesterol containing diet and these effects are mainly mediated by the L-arginine present in it.
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PMID:Hypolipidemic and antiperoxidative effect of coconut protein in hypercholesterolemic rats. 1188 11

Cisplatin-induced nephrotoxicity is closely associated with an increase in lipid peroxidation. In several previous reports it was claimed that acetylsalicylic acid (ASA) shows its therapeutic potential as a free radical scavenger. The aim of the study was to investigate effects of ASA on cisplatin induced nephrotoxicity in an experimental rat model. Control animals (n:7) were administered 1 mL saline solution intraperitoneal (i.p.). Cisplatin group (n:7) was treated with a single dose of cisplatin i.p. (6 mg/kg), ASA group (n:7) was treated with i.p. (2.5 mg/kg) per day during the study, cisplatin plus ASA group (n:7) was administered single dose cisplatin i.p. (6 mg/kg) plus ASA (2.5 mg/kg) during 5 days. At the end of the study, Catalase (CAT), Glutathione Peroxidase (GSH-Px), Superoxide Dismutase (SOD), Nitric Oxide Synthase (NOS) enzymes activities and Malondialdehyde (MDA), Antioxidant Potential (AOP) levels were measured in both erythrocytes and renal tissues. Urea and creatinine levels and renal tissue necrosis in cisplatin plus ASA group were significantly lower than cisplatin group (p = 0.000, p = 0.014, p = 0.015). SODr activities and MDAr levels of cisplatin plus ASA group were also significantly lower than cisplatin group (p = 0.000, p = 0.029). These results show that cisplatin and ASA combination decreases the levels of urea and creatinine, reduces necrosis and improves antioxidant enzyme activities, MDA and AOP in rat kidney.
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PMID:The protective effects of acetylsalicylic acid on free radical production in cisplatin induced nephrotoxicity: an experimental rat model. 1458 80

Age-related macular degeneration is the leading cause of legal blindness in the developed world, and yet its pathogenesis remains poorly understood. Oxidative stress may play a major role in the etiology and pathogenesis of age-related disorders such as age-related macular degeneration. Catalase is an antioxidant enzyme which plays an important role in the detoxification of free oxygen radicals. Malondialdehyde is a marker that shows free radical damage. We have measured the erythrocyte activity of catalase and the serum level of malondialdehyde in 30 patients with age-related macular degeneration and 60 healthy subjects. Patients with age-related macular degeneration showed significantly lower catalase activity compared to healthy subjects (p = 0.002). Plasma malondialdehyde level of the patient group was significantly higher than that of the controls (p = 0.038).
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PMID:Changes in antioxidant enzyme activity and malondialdehyde level in patients with age-related macular degeneration. 1510 17


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