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)

Both alpha-linolenic (ALA) and eicosapentaenoic acids (EPA) were toxic to SP 2/0 mouse myeloma cells in vitro. On the other hand, linoleic acid (LA), gamma-linolenic acid (GLA), di-homo-gamma linolenic acid (DGLA), arachidonic acid (AA), docosahexaenoic acid (DHA) and oleic acid (OA) were much less effective in their growth suppressive actions. Both nordihydroguaiaretic acid (NDGA) and Indomethacin (IM) could block the action of the fatty acids indicating a role for prostaglandins (PGs) and leukotrienes (LTs) in the growth suppressive action of ALA and EPA. Superoxide dismutase (SOD) completely blocked, while vitamin E and reduced glutathione (GSH) could prevent to a limited extent the anti-proliferative effects of ALA and EPA. Catalase, mannitol, chlorpromazine (CPZ) and trifluoperazine (TFP) did not block the cytotoxic actions of ALA and EPA. N(G)-mono-methyl L-arginine (N(G)MMA), an analogue of L-arginine, which inhibits nitric oxide synthase, was ineffective in preventing the cytotoxicity induced by ALA and EPA. Fatty acid analysis of the various lipid fractions of SP 2/0 cells treated with ALA and EPA showed significant incorporation of these fatty acids in the cell membrane lipid pools. These results suggest that ALA and EPA induced suppression of SP 2/0 cell proliferation is cyclo-oxygenase (CO), lipoxygenase (LO) and superoxide dependent. Lipid peroxidation has only a limited role in this process. Both calmodulin dependent process and L-arginine derived nitric oxide do not seem to have a role in the cytotoxic action of ALA and EPA in these cells.
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PMID:Cytotoxic action of alpha-linolenic and eicosapentaenoic acids on myeloma cells in vitro. 915 Mar 74

Current models of Cr(VI) carcinogenesis suggest an important role for Cr(IV) as an intermediate, toxic, carcinogenic species, but direct chemical evidence has been lacking. This is because Cr(IV) is a highly reactive oxidation state of Cr and few Cr(IV)-based compounds are known that can be used as a model compound containing a biological ligand. This study reports the isolation of such a stable Cr(IV) complex. The Cr(IV)-GSH complex has been synthesized through the reaction of Cr(VI) with GSH. Its electron paramagnetic resonance (EPR) spectrum exhibits g = 1.9629 and a peak-to-peak line width of 480 G in aqueous medium as well as in the powder form. Magnetic susceptibility measurements showed that the compound has a magnetic moment of 2.53 Bohr magneton per Cr, establishing that the Cr ion has two unpaired electrons, hence its identity as Cr(IV). The Cr(IV)-GSH complex is able to generate hydroxyl (.OH) radical in the presence of molecular oxygen in aqueous medium. Catalase inhibited the .OH radical generation while H2O2 enhanced it, indicating that the .OH radical was generated via a Fenton-like reaction, H2O2 being generated as an intermediate in the reduction of molecular oxygen. Metal ion chelators, deferoxamine and 1,10-phenanthroline, attenuated the generation of Cr(IV)-mediated .OH radical. In the case of deferoxamine, a deferoxamine-derived free radical was generated as shown by EPR measurements. The results imply that Cr(IV) may play an important role in the mechanism of Cr(VI)-induced carcinogenesis and Cr(IV)-GSH can be used as a model compound to study the role of Cr(IV) in this mechanism.
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PMID:Synthesis of Cr(IV)-GSH, its identification and its free hydroxyl radical generation: a model compound for Cr(VI) carcinogenicity. 919 34

'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

The regulating mechanism of hyperoxia-induced ICAM-1 expression has not been elucidated. We studied the effect of antioxidants, including superoxide dismutase (SOD), catalase and N-acetylcysteine (NAC), on hyperoxia-induced ICAM-1 expression in human pulmonary artery endothelial cells (HPAEC) and human umbilical vein endothelial cells (HUVEC). Cells were cultured to confluence and exposed to either hyperoxic or normoxic gas with or without various kinds of antioxidants. The levels of ICAM-1 expression in the endothelial cells and the concentrations of reduced (GSH) and oxidized glutathione (GSSG) in the media were examined by flow cytometry and by spectrophotometry, respectively. After 48-hour exposure to hyperoxia, ICAM-1 expression was increased (HPAEC; 161 +/- 21% and HUVEC; 163 +/- 16%) and total glutathione concentration in the media was decreased as compared with normoxia. SOD did not change the GSH and GSSG concentrations in the media. Catalase dose-dependently decreased the supernatant GSSG concentration in both HPAEC and HUVEC, while the GSH concentration was nearly constant. NAC dose-dependently increased the supernatant GSH concentrations in both HPAEC and HUVEC. There was no difference in the supernatant GSSG concentrations between the NAC-treated HPAEC and HUVEC. There was no difference in ICAM-1 expression in either HPAEC or HUVEC with SOD treatment. ICAM-1 expressions in 100 U/ml (236 +/- 20%) and 1,000 U/ml (315 +/- 36%) of catalase were increased in HPAEC, and that in 1,000 U/ml (440 +/- 209%) of catalase was increased in HUVEC. Five and 10 U/ml of NAC decreased ICAM-1 expression in HPAEC (141 +/- 26% and 113 +/- 11%) and HUVEC (119 +/- 23% and 106 +/- 7%), respectively. These results suggest that extracellular glutathione may play a role in regulating hyperoxia-induced ICAM-1 expression in HPAEC and HUVEC.
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PMID:Effect of antioxidants on hyperoxia-induced ICAM-1 expression in human endothelial cells. 926 67

To clarify whether the changes of free radicals and its scavengers are induced by thyroid disorders, we measured levels of free radical scavengers and checked O2 radical generating systems in the human thyroid gland. Thyroid specimens from patients with Graves' disease, follicular adenoma, and papillary and follicular carcinomas contained significantly higher concentrations of xanthine oxidase (XOD) and gluthathione peroxidase (GSH-PX), compared to those in the normal thyroid tissue. Catalase concentration was significantly lower in thyroid specimens from patients with Graves' disease and significantly lower in thyroid specimens from patients with follicular adenoma, compared to those in the normal thyroid tissue. Cu/Zn superoxide dismutase (Cu/Zn SOD) concentration was significantly lower in the specimens from follicular adenoma and papillary carcinoma and Mn SOD concentration was significantly higher in the specimens from papillary carcinoma than those in the normal thyroid tissue. The lipid peroxide concentration, expressed as malondialdehyde (MDA) concentration, was significantly higher in the specimens from papillary carcinoma than those in the normal thyroid tissue. These findings suggest that the levels of free radicals are increased and are scavenged and catalyzed in the thyroid of Graves' disease, whereas free radicals and lipid peroxide are not completely scavenged in papillary carcinoma tissues, suggesting that these substances affect some role in cell function of thyroid tumors.
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PMID:Changes in free radical scavengers and lipid peroxide in thyroid glands of various thyroid disorders. 928 68

This study investigates the interactive effects of chronic ethanol ingestion and exercise training on the antioxidant system and lipid peroxidation in cortex, cerebellum, medulla, striatum and hypothalamus of the rat brain. Exercise training (6.5 weeks) significantly increased superoxide dismutase (SOD) activity in striatum, the region associated with motor activity, but decreased SOD activity in other brain regions. Catalase (CAT) activity decreased significantly in hypothalamus, the region associated with behavior, due to exercise. The training significantly increased glutathione peroxidase (GSH-Px) activity in brain regions studied with the exception of cerebellum. In addition, glutathione reductase (GR) activity increased in brain regions, with the exception of medulla. The training significantly decreased malondialdehyde (MDA) levels in all brain regions studied, which is due to training adaptation. Ethanol (20%) (2.0 g kg[-1], p.o. for 6.5 weeks) significantly decreased SOD activity in all regions except cortex, CAT activity in cortex, striatum and hypothalamus, GSH-Px activity in cerebellum and GR activity in medulla. Similarly, ethanol significantly decreased the GSH level in cortex, medulla and striatum and the GSH/GSSG ratio in medulla and cerebellum. Conversely, ethanol significantly augmented GR activity in cortex, cerebellum and striatum. When ethanol and exercise were combined, there was significantly increased SOD and CAT activity in striatum, GSH-Px activity in cortex, striatum and hypothalamus and GR activity in cortex and striatum. The GSH level was significantly depleted in cortex, striatum and medulla. Combining training and ethanol also decreased MDA levels in medulla and cerebellum. In conclusion, the sensitivity of specific brain regions in reaction to chronic ethanol ingestion or training is a function of variability in antioxidant system activity. Thus, exercise training protects specific brain regions against ethanol-induced oxidative injury.
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PMID:Interaction of exercise training and chronic ethanol ingestion on antioxidant system of rat brain regions. 933 46

Effects of antioxidants, reactive oxygen species (ROS) scavengers, and Ca2+ on cisplatin-induced renal cell injury were studied in rabbit renal cortical slices in vitro. Cisplatin induced LDH release and lipid peroxidation, inhibition of PAH uptake, and GSH depletion. These changes were significantly prevented by thiols (DTT and GSH), antioxidants (DPPD and BHA), and an iron chelator (deferoxamine). Superoxide dismutase partially reduced the cisplatin-induced LDH release without affecting the lipid peroxidation and the GSH depletion. Catalase did not affect the LDH release and the lipid peroxidation induced by cisplatin. Hydroxyl radical scavengers prevented the lipid peroxidation, whereas they did not alter the LDH release, the inhibition of PAH uptake, and the GSH depletion induced by cisplatin. Removal of Ca2+ or addition of EGTA to the incubation medium did not alter cisplatin effects on LDH release and lipid peroxidation. Buffering intracellular Ca2+ with quin-2/AM or inhibition of intracellular Ca2+ release with TMB-8 significantly reduced the cisplatin effect on LDH release without any effect on the lipid peroxidation and the GSH depletion. Ruthenium red attenuated the LDH release, the lipid peroxidation, and the inhibition of PAH uptake mediated by cisplatin. La3+ prevented the cisplatin effect on the LDH release, whereas it did not affect the lipid peroxidation, the inhibition of PAH uptake, and the GSH depletion by cisplatin. These results suggest that cisplatin induces a lethal cell injury by lipid peroxidation-dependent and -independent mechanisms and that the cell injury and the lipid peroxidation by cisplatin are iron-dependent. In addition, the data indicate that the Ca2+ released from intracellular stores, but not the Ca2+ moved from extracellular space, plays a role in the cisplatin-induced cell injury independent of lipid peroxidation.
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PMID:Effects of antioxidants and Ca2+ in cisplatin-induced cell injury in rabbit renal cortical slices. 934 94

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.
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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.
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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.
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PMID:Distinct mechanisms of site-specific DNA damage induced by endogenous reductants in the presence of iron(III) and copper(II). 971 16


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