UNIPROT:P04040 - FACTA Search

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)

'Long-Life CiLi' ('CiLi') oral liquid, is composed of superoxide dismutase (SOD), polysacchairide, vitamin C, vitamin E and trace elements which were all extracted from a natural plant fruit Cili (Rosa roxburghii Tratt) in Guizhou, China. A set of indices were evaluated after administration of 'CiLi' 10 ml Bid, for two months in 50-75 years old healthy people, the mean value of NK cell activity (22.4 +/- 10.8-->27.5 +/- 12.9%, P < 0.05), SOD (453.0 +/- 24.2-->468.6 +/- 21.3 micrograms/gHb, P < 0.001), Catalase (15.5 +/- 1.7-->17.4 +/- 3.0 U/mgHb, P < 0.001) and GSH content (2.3 +/- 0.3-->2.6 +/- 0.5 mg/gHb, P < 0.001) in erythrocytes and 'delta CO, CI, SV, SI, LVET, LVETI and AC' values increased significantly, while the serum LPO level (4.20 +/- 0.78-->3.78 +/- 0.50 nmol/ml, P < 0.001), total microcirculation weighed value (1.87 +/- 1.0-->0.92 +/- 0.5, P < 0.001), delta PVR (-241.7 +/- 733.2-->187.9 +/- 938.2, P < 0.05) and the light reaction time (Simple RT, red light: 383 +/- 128-->332 +/- 68.9 ms, P < 0.05; selective RT: red light 709 +/- 287-->566 +/- 119 ms, P < 0.05; green light 639 +/- 162-->536 +/- 80 ms, P < 0.01) decreased significantly. There were no significant differences in the control group. The mean life span of fruit flies were significantly elongated for low, medium and high concentrations 'CiLi' treatment groups than in the control group (Female: 57.6 +/- 11.3-->62.1 +/- 12.8; 69.6 +/- 14.7; 62.6 +/- 12 days; P < 0.05 approximately 0.001. Male: 56.3 +/- 9.6-->64.9 +/- 12.4; 64.5 +/- 14.5; 64.8 +/- 14.1 days, P < 0.001). It is suggested that 'CiLi' has an aging retarding and geroprotection effect.
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PMID:The aging retarding effect of 'Long-Life CiLi'. 922 19

Cigarette smoking is associated with impaired endothelium-dependent vasodilation and reduced nitric oxide (NO) in the exhaled air of smokers. To explore the mechanism for the impairment of NO-mediated vasodilation, we studied the effect of cigarette smoke extract (CSE) on NO synthase (eNOS) activity and content in pulmonary artery endothelial cells (PAEC). Incubation of PAEC with CSE resulted in a time- and dose-dependent decrease in eNOS activity. The inhibitory effect of CSE on eNOS activity was not reversible. Both gas-phase and particulate-phase extracts of CSE contributed to the inhibition of eNOS activity. The protein kinase c (PKC) inhibitors staurosporine and chelerythrine did not affect the CSE-induced inhibition of eNOS activity. Catalase, superoxide dismutase (SOD), vitamin C, vitamin E, glutathione, and dithiothreitol (DTT) also did not prevent the CSE-induced inhibition of eNOS activity, and incubation of PAEC with 3 mM nicotine did not change the activity of eNOS. Treatment of PAEC with CSE also caused a nonreversible, time-dependent decrease in eNOS protein content detected by Western blot analysis, and in eNOS messenger RNA (mRNA) detected by Northern blot analysis. Treatment of PAEC with CSE had no effect on cell protein or glutathione contents or on lactate dehydrogenase (LDH) release. These results indicate that exposure to CSE causes an irreversible inhibition of eNOS activity in PAEC, and suggest that the decreased activity is secondary to reduced eNOS protein mass and mRNA. The decrease in eNOS activity may contribute to the high risk of pulmonary and cardiovascular disease in cigarette smokers.
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PMID:Effect of cigarette smoke extract on nitric oxide synthase in pulmonary artery endothelial cells. 980 47

Oxidative stress parameters were evaluated in rat testes after chronic iron intoxication and vitamin E supplementation. Male Wistar rats were fed during 6 weeks with the following diets: C = rat chow; I = C + 25 mg carbonyl-iron/g diet; A = C + 0.2 mg alpha-tocopheryl acetate/g diet; and the combination of I and A (IA). After the treatment, no changes in final body weight, testis weight and protein content were observed. Total iron content in testes from the I group was 33% higher compared to the C group (216 +/- 10 nmol/g of tissue). The content of alpha-tocopherol (alphaT) was 2.5-fold higher in the A and IA groups compared to the C group (12.8 +/- 0.7 nmol/g tissue). The content of ubiquinol-9 (13.0 +/- 1.7 nmol/g tissue) and ubiquinol-10 (3.3 +/- 0.5 nmol/g tissue) was similar among the groups. Superoxide dismutase activity was 13 and 16% lower in the A and IA groups with respect to the C group (12.9 +/- 0.7 U/mg protein). Catalase activity was 26 and 33% lower in the I and IA groups than in the C (0.19 +/- 0.01 pmol/mg protein) and A (0.21 +/- 0.01 pmol/mg protein) groups, respectively. Glutathione peroxidase was 24 and 23% higher in the IA group than in the C (11.4 +/- 0.3 mU/mg protein) and I (11.5 +/- 1.0 mU/mg protein) groups, respectively. The testes content of 2-thiobarbituric acid-reactive substances (TBARS) and protein-associated carbonyl groups were 37 and 16% higher, respectively, in the I group than in the C group. These increased in TBARS and carbonyls, were not observed in the IA group. No diet-associated changes were observed in the steady state levels of 8-oxo-2'-deoxyguanosine in testes DNA (4.2 +/- 0.2 residue/10(5) dG). The present data suggest that this model of chronic iron overload produced a mild oxidative damage in rat testes that was partially prevented by alphaT supplementation.
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PMID:Oxidative stress in testes of rats subjected to chronic iron intoxication and alpha-tocopherol supplementation. 1043 81

Supplying adequate iron (Fe) to neonatal pigs to support normal growth and hematological and antioxidant status, while preventing iron toxicity, is a challenge for producers. Three experiments were conducted to determine the effect of frequency and route of Fe administration with or without vitamin E (E) and selenium (Se) on growth, Fe, and antioxidant status of neonatal pigs. In Exp. 1, 12 pigs from dams with reduced E status were fed a semipurified diet without added Fe from d 3 to d 14 of age. At d 6 of age, pigs received the following i.m. injections: 1) FE, 1 mL containing 200 mg of Fe (iron dextran); 2) FEE, treatment FE plus 1 mL containing 300 IU of vitamin E (d-alpha tocopherol); or 3) FESEE, 1.03 mL containing 200 mg of Fe (iron dextran), .15 mg of Se (sodium selenite), and 15 IU of vitamin E (d-alpha tocopherol). Pigs were weighed daily and blood was collected at 3, 7, and 14 d of age. From d 8 to 14, growth was depressed (P < .05) in pigs injected with FESEE. At 14 d of age, pigs injected with FE or FEE had increased (P < .05) hemoglobin (Hb) concentration. Ceruloplasmin activity (CP) was greater (P < .05) at d 7 of age than at d 3 or 14 regardless of treatment. In Exp. 2, 3-d-old pigs (n = 94) received the following: 1) FE, 200 mg Fe (iron dextran) i.m.; (2) FEE, treatment FE plus 300 IU vitamin E i.m.; 3) EFE, 300 IU vitamin E i.m. followed by 200 mg Fe (iron dextran) i.m. 24 h later; or 4) OFE, 100 mg Fe and 10 mg Cu orally. On d 21 of age, one-half of the pigs in each treatment received a second dose of their respective treatment. Blood samples (n = 60) were obtained on d 3 and 21 of age. Pigs injected with FE, FEE, or EFE had greater (P < .05) Hb at d 21 than pigs given OFE. Copper/zinc superoxide dismutase (Cu/ZnSOD) activity was greater (P < .05) at d 21 with OFE than with the other treatments. At 65 d of age, ADG did not differ among treatments. In Exp. 3, pigs (n = 150, in three farrowing groups) were injected with 200 mg of Fe (iron dextran) on d 1 or d 1 and 14. Blood samples were obtained on d 7 and 21 of age. Hemoglobin concentration on d 21 was improved equally by both treatments. Catalase and Cu/ZnSOD activities were increased (P < .05) on d 21 of the experiment compared with d 7 regardless of treatment. Growth was not affected by injection frequency. Results from these experiments indicate that one Fe injection (200 mg) for pigs from sows fed adequate vitamin E will result in adequate growth and hemoglobin concentration with today's improved genetics.
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PMID:Effect of vitamin E and selenium on iron utilization in neonatal pigs. 1043 23

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

The cytotoxic effects of ginkgetin, a natural biflavone isolated from Selaginella moellendorffii Hieron, were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in three different human cell lines: ovarian adenocarcinoma (OVCAR-3), cervical carcinoma (HeLa) and foreskin fibroblast (FS-5). The concentrations of ginkgetin required to induce 50% death (EC50) in OVCAR-3, HeLa, and FS-5 were 3.0, 5.2, and 8.3 microg/ml, respectively. Morphological changes in cells and their nuclei, DNA fragmentation with a characteristic pattern of inter-nucleosomal ladder, and double-stranded DNA breaks were detected following treatment with 3 microg/ml of this biflavone for 24 h. Incubation with 5 microg/ml ginkgetin led to increased intracellular levels of hydrogen peroxide as early as 30 min. The cytotoxicity of ginkgetin was partially inhibited by pretreating cells with vitamin C, vitamin E or catalase. Catalase not only afforded the best protective effect among three antioxidants, but also reduced both the DNA fragmentation and double-stranded DNA breakage induced by ginkgetin. Moreover, the involvement of caspase(s) in ginkgetin-induced apoptosis was demonstrated by the activation of caspase 3 after drug treatment and the suppression of cell death by a broad-spectrum caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk). However, the protective effects of z-VAD-fmk and catalase were not additive. Taken together, our results indicated that the apoptosis induced by ginkgetin (especially at 5 microg/ml) is mediated mainly through the activation of caspase(s) by the hydrogen peroxide generated possibly through autooxidation of this biflavone.
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PMID:Studies on the cytotoxic mechanisms of ginkgetin in a human ovarian adenocarcinoma cell line. 1093 37

beta-Amyloid is cytotoxic to neurons in culture by increasing hydrogen peroxide and altering calcium homeostasis. We have evaluated the cytotoxicty of beta-amyloid peptides (betaA(25-35) and betaA(1-40)) and generation of hydrogen peroxide on cortical cultured astrocytes. Twenty-four hours after a single addition of either betaA(25-35) or betaA(1-40) there was a concentration-dependent decrease in viability. This toxicity never exceeded 50% of the population independently of exposure time and concentrations. The subpopulation of astrocytes resistant to betaA(25-35) effects were also insensitive to peroxide. Catalase or vitamin E showed no protective effect against betaA(25-35) toxicity. Dithiothreitol (DTT), N-acetylcysteine (NAC), and cyclosporine A significantly prevented the toxic effects of both betaA(25-35) and peroxide. Inhibition of peroxide detoxifying enzymes increased betaA(25-35) and peroxide toxicity. Exposure to betaA(25-35) or betaA(1-40) increased peroxide production at 2 and 24 h, which was prevented by DTT and NAC, but not vitamin E. Despite the inability of added catalase to reduce betaA toxicity, these results suggest that betaA-induced cytotoxicity to astrocytes in culture is, as in neurons, mediated by generation of hydrogen peroxide.
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PMID:beta-amyloid peptides are cytotoxic to astrocytes in culture: a role for oxidative stress. 1096 10

Impairment of mitochondrial functions has been found in ethanol-induced liver injury. Ethanol can be oxidized to the 1-hydroxyethyl radical (HER) by rat liver microsomal systems. Experiments were carried out to evaluate the ability of HER to cause mitochondrial swelling as an indicator of the mitochondrial permeability transition (MPT). Electron spin resonance (ESR) spectroscopy was used to detect HER and to study its interaction with mitochondria. The ESR signal intensity of the spin adduct formed from alpha-(4-pyridyl-1-oxide) N-tert-butylnitrone (POBN) and HER generated from either a thermic decomposition of 1,1'-dihydroxyazoethane (DHAE) or a Fenton reaction system containing ethanol was markedly diminished by the addition of mitochondria, indicating an interaction between HER and mitochondria. Exposure of rat liver mitochondria to HER generated from either system caused swelling, as reflected by a decrease in absorbance at 540 nm, in a HER concentration-dependent and a cyclosporin A-sensitive manner. Mitochondrial swelling was also induced in the Fenton reaction system without ethanol. The DHAE-dependent generation of HER in mitochondrial suspension resulted in a decrease of membrane protein thiols and collapse of the membrane potential (delta psi). The swelling induced by HER was prevented by glutathione and vitamin E, but not by superoxide dismutase. Catalase did not prevent the swelling caused by the acetaldehyde/hydroxylamine O-sulfonate (HOS) system, but was inhibitory in the Fenton reaction system with or without ethanol. These results indicate that HER, as well as hydroxyl radical, can induce the MPT, and suggest the possibility that the collapse of delta psi caused by HER may, at least in part, contribute to impairment of mitochondrial function caused by ethanol and in ethanol-induced liver injury.
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PMID:Mitochondrial permeability transition induced by 1-hydroxyethyl radical. 1128 Dec 95

beta-Amyloid (betaA) is cytotoxic to neurons in culture by increasing hydrogen peroxide and altering calcium homeostasis. We have evaluated betaA-induced cytotoxicity, peroxide generation and glutamate (Glu) uptake in cultured astrocytes. Twenty-four hours after a single addition of either betaA25-35 or betaA1-40there was a concentration-dependent decrease in viability. Catalase or vitamin E showed no protective effect against betaA25-35 Dithiothreitol (DTT), N-acetylcysteine (NAC) and cyclosporine A significantly prevented the toxic effects of both betaA25-35 and peroxide, while inhibition of peroxide detoxifying enzymes enhanced toxicity. Exposure to betaA25-35 or betaA1-40 increased peroxides at 2 h and 24 h, which was prevented by DTT and NAC, but not vitamin E. betaA25-35 inhibited Glu uptake in astrocytes and neurons in culture. Following exposure of neurons to betaA for 24 h there was decreased uptake and increased Glu levels in the culture medium, that resulted in gradual excitotoxicity.
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PMID:beta-Amyloid-induced cytotoxicity, peroxide generation and blockade of glutamate uptake in cultured astrocytes. 1138 55

One-day-old chicks were reared using diets that differed in their vitamin E and/or selenium content. In chicks depleted of both selenium and vitamin E, signs of exudative diathesis on the superficial pectoralis muscle were observed. The purpose of this research was to determine the defective points of the antioxidant defense system, which made this tissue highly susceptible to nutritionally-induced oxidative stress. Vitamin E, and selenium in lower magnitude, were the factors that strikingly affected the course of mitochondrial lipid peroxidation. Animals fed diets deficient in vitamin E and selenium displayed the lowest reduced glutathione level and glutathione peroxidase activity. The decreased levels of reduced glutathione were not due to a defective activity of glutathione reductase, which was increased in both mitochondria and cytosol. The absence of vitamin E was linked to lowering of mitochondrial thiol levels. The Glutathione peroxidase/Cu,Zn-superoxide dismutase ratio was 2.8 in animals fed selenium and vitamin E, and decreased to 0.13 in animals deficient in both nutrients. This change was indicative of oxidant-induced damage mediated by hydrogen peroxide. Catalase activity increased in an attempt to counteract the decrease in glutathione peroxidase activity. The results obtained showed that alpha-tocopherol and Se deficiencies caused multiple alterations in the antioxidant system and adversely affected the redox state of chicken superficial pectoralis muscle.
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PMID:Effect of vitamin E and selenium on resistance to oxidative stress in chicken superficial pectoralis muscle. 1142 88

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