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)

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.
Pharmacol Res 1997 Sep
PMID:Action of capparis decidua against alloxan-induced oxidative stress and diabetes in rat tissues. 936 67

Mineral dust exposure can result in emphysema and chronic airflow obstruction. We postulated that dust-induced emphysema has a pathogenesis similar to that in cigarette smoke-induced emphysema, namely, excess release of proteolytic enzymes from dust-evoked inflammatory cells, and inactivation of alpha-1-antitrypsin (A1AT) by dust-catalyzed formation of oxidants. To test this theory we examined the antiproteolytic activity of A1AT exposed to quartz in vitro and found that it was decreased in a dose-response fashion. Catalase prevented this effect, which suggested that it was mediated by quartz-generated hydrogen peroxide. We also showed that a variety of dusts could oxidize methionine to methionine sulfoxide in vitro, using either pure amino acid or whole protein. The relative order of activity was coal > quartz > titanium dioxide. Lastly, we used a new high-performance liquid chromatography technique to demonstrate that quartz, coal, and titanium dioxide produced connective tissue breakdown in rat lungs, as determined by the appearance of desmosine and hydroxyproline in lavage fluid after dust instillation. On a particle-for-particle basis, the order of dust potency was similar to that for methionine oxidation. Connective tissue breakdown was associated with elevations of both polymorphonuclear leukocytes and macrophages in lavage fluid, and it is unclear whether one or both of these types of inflammatory cell mediates this process. These observations support our theory that dust-induced emphysema and smoke-induced emphysema occur through similar mechanisms.
Environ Health Perspect 1997 Sep
PMID:Mechanisms of mineral dust-induced emphysema. 940 Jul 26

Transforming growth factor beta1 (TGF-beta1) is a multifunctional, profibrotic cytokine involved in cellular growth and differentiation. We have previously described a cell surface-associated H2O2-generating NADH:flavin:O2 oxidoreductase (referred to as NADH oxidase) activity in human lung fibroblasts induced by TGF-beta1 (Thannickal, V. J., and Fanburg, B. L. (1995) J. Biol. Chem. 270, 30334-30338). In this study, the potential for regulation of this novel TGF-beta1-activated oxidase in fibroblasts by protein tyrosine phosphorylation was examined. Immunoblots using anti-phosphotyrosine antibody demonstrated a time-dependent but delayed phosphorylation of two proteins of 115 and 103 kDa in cells stimulated with TGF-beta1 (2 ng/ml). Similar to the effect on TGF-beta1-induced H2O2 production, phosphorylation of these proteins was blocked by the addition of actinomycin D. The protein-tyrosine kinase inhibitors genistein and herbimycin A inhibited TGF-beta1-induced protein tyrosine phosphorylation, NADH oxidase activation, and H2O2 production in a dose-dependent manner. Catalase, diphenyliodonium (an inhibitor of flavoenzymes), and suramin (an inhibitor of receptor activation, added 4 h after TGF-beta1) had no effect on the induction of protein tyrosine phosphorylation. Phosphorylation of the 115- and 103-kDa proteins preceded the generation of H2O2 production and returned to control levels when H2O2 was undetectable at 48 h after TGF-beta1 exposure. These results suggest that protein tyrosine phosphorylation by a nonreceptor protein-tyrosine kinase(s) regulates the activity of the TGF-beta1-responsive H2O2-generating NADH oxidase in human lung fibroblasts. Additionally, this study demonstrates that TGF-beta1, which binds to a serine-threonine kinase receptor, is able to induce protein tyrosine phosphorylation in a delayed manner via a signaling pathway that requires transcriptional activation.
J Biol Chem 1998 Sep 04
PMID:Tyrosine phosphorylation regulates H2O2 production in lung fibroblasts stimulated by transforming growth factor beta1. 972 2

Alloxan is known to induce diabetes in experimental animals through destruction of insulin-producing 3-cells of pancreas. The mechanism of DNA damage induced by alloxan was investigated using 32P-labeled human DNA fragments. Cu(II)-dependent DNA damage increased with the concentration of alloxan and NADH. Alloxan induced DNA cleavage frequently at thymine and cytosine residues in the presence of NADH and Cu(II). Catalase and bathocuproine, a Cu(I)-specific chelator, almost completely inhibited DNA damage, suggesting the involvement of H2O2 and Cu(I). Alloxan induced Cu(II)-dependent production of 8-oxodG in calf thymus DNA in the presence of NADH. UV-visible and electron spin resonance (ESR) spectroscopic studies showed that superoxide anion radical and alloxan radical were generated by the reduction of alloxan by NADH, and also by the autoxidation of dialuric acid, the reduced form of alloxan. These results suggest that the copper-oxygen complex derived from the reaction of H2O2 with Cu(I) participates in Cu(II)-dependent DNA damage by alloxan plus NADH and dialuric acid. The mechanism of DNA damage is discussed in relation to diabetogenic action of alloxan.
Free Radic Biol Med 1998 Sep
PMID:Metal-mediated DNA damage induced by diabetogenic alloxan in the presence of NADH. 974 96

Unlike the mature animal, immature mice transgenic for copper/zinc superoxide dismutase (SOD1) have greater brain injury after hypoxia-ischemia than their wild-type nontransgenic littermates. To assess the role of oxidative stress in the pathogenesis of this injury, we measured histopathological damage, lipid peroxidation products, enzymatic activities of catalase and glutathione peroxidase, and hydrogen peroxide (H2O2) concentration in these animals before and after hypoxic-ischemic injury. Lipid peroxidation products were significantly increased 2 hours after the insult in both transgenic and nontransgenic brains in hippocampus, the most damaged brain region. Catalase activity did not increase in response to SOD1 overexpression or injury in either group. However, glutathione peroxidase activity, unchanged in response to overexpression, decreased significantly 24 hours after injury in both groups. At 24 hours after injury, greater H2O2 accumulation was observed in transgenic brains. Because SOD1 dismutates superoxide to H2O2, overexpression of SOD1 in the presence of developmentally low activities of the catalytic enzymes glutathione peroxidase and catalase leads to an increased production of H2O2, and may explain the increased brain injury observed after hypoxia-ischemia in neonatal SOD1 mice.
Ann Neurol 1998 Sep
PMID:Copper/zinc superoxide dismutase transgenic brain accumulates hydrogen peroxide after perinatal hypoxia ischemia. 974 2

In view of the accumulation of H2O2 in the myocardium due to ischemia-reperfusion and changes in beta-adrenoceptor mechanisms in the ischemic-reperfused heart, we investigated the effects of H2O2 on the beta-adrenoceptor, G-protein and adenylyl cyclase complex. Rat hearts were perfused with 1 mM H2O2 for 10 min before isolating membranes for measuring the biochemical activities. The stimulation of adenylyl cyclase by different concentrations of isoproterenol was depressed upon perfusing hearts with H2O2. Both the affinity and density of beta1-adrenoceptors as well as the density of the beta2-adrenoceptors were decreased whereas the affinity of beta2-adrenoceptors was increased by H2O2 perfusion. Competition curves did not reveal any effect of H2O2 on the proportion of coupled receptors in the high affinity state. The basal as well as forskolin-, NaF- and Gpp(NH)p-stimulated adenylyl cyclase activities were depressed by perfusing the heart with H2O2. Catalase alone or in combination with mannitol was able to significantly decrease the magnitude of alterations due to H2O2. The positive inotropic effect of 1 microM isoproterenol was markedly attenuated upon perfusing hearts with 200-500 microM H2O2 for 10 min. These results suggest that H2O2 may depress the beta1-adrenoceptor, Gs-proteins and catalytic subunit of the adenylyl cyclase enzyme and thus may play an important role in attenuating the beta-adrenoceptor linked signal transduction due to ischemia-reperfusion injury.
Mol Cell Biochem 1998 Sep
PMID:Role of H2O2 in changing beta-adrenoceptor and adenylyl cyclase in ischemia-reperfused hearts. 977 90

UV radiation generates reactive oxygen species, which may be involved in polymorphic light eruption. The endogenous enzymatic defense system includes catalase in the epidermis. Thirteen patients with a history of polymorphic light eruption, but free from lesions, and 13 controls were investigated from November to March. Catalase was analysed in the upper horny layer according to Colin et al.'s spectrophotometric technique. In polymorphic light eruption, catalase values were about 30% lower than in control subjects. Such deficiency was observed in patients free from the disease and not recently sun-exposed. The diminished skin catalase in irradiated polymorphic light eruption makes it possible that a longer restoration time of catalase is involved in the pathogenesis.
Acta Derm Venereol 1998 Sep
PMID:Catalase in the stratum corneum of patients with polymorphic light eruption. 977 48

Catalase I of Bacillus stearothermophilus has high catalatic and low peroxidatic activities. The mutant from the first random mutant population, D130N, which has higher peroxidatic and lower catalatic activities than those exhibited by the wild-type enzyme, was subjected to second random mutagenesis in observance of the change in reaction specificity. From the second mutant population, the mutant I108T/D130N/I222T was selected and examined. The reaction specificity of the purified enzymes revealed that catalase I being originally 98% catalase and 2% peroxidase was brought to 58% specificity to peroxidase after two-step adaptive walks. From the statistical analysis of the two random mutant populations, the average degree of nonadditivity of the mutational effects was estimated to be 0.13 irrespective of the properties of the enzyme. It was demonstrated that the distribution pattern of a property of the second mutant population can be predicted well from the data of the first mutant population by taking into consideration the degree of nonadditivity. The strategy for an efficient adaptive walk in directed evolution of enzymes through the prediction of appropriate mutation rate and effective sample size for further mutation and selection was presented and discussed.
Protein Eng 1998 Sep
PMID:Nonadditivity of mutational effects on the properties of catalase I and its application to efficient directed evolution. 979 28

Vasoactivities of 6-nitronorepinephrine were investigated using rat aorta. 6-Nitronorepinephrine (> 100 microM) caused dose-dependent contraction in both endothelium-intact and -denuded aorta, although the latter showed greater contraction than the former. Prazosin (> 3 nM), an alpha1-adrenoceptor antagonist, attenuated significantly the 6-nitronorepinephrine-induced contractions, thereby suggesting the alpha1-adrenoceptor involvement. Aortic rings prepared from reserpine-pretreated rats showed the 6-nitronorepinephrine-induced a contraction to the extent similar to those from untreated rats, suggesting that endogenous norepinephrine does not play a role in the 6-nitronorepinephrine-induced contraction. 6-Nitronorepinephrine (> 10 microM) potentiated norepinephrine-induced contraction only in the presence of endothelium. The augmentation was attenuated by catalase (1200 U/ml). H2O2 (10-300 microM) augmented the norepinephrine-induced contraction only in the endothelium-intact rat aortic rings. 6-Nitronorepinephrine attenuated significantly acetylcholine-induced relaxation. Catalase prevented the 6-nitronorepinephrine-induced inhibition of the acetylcholine-induced relaxation. These results suggest that 6-nitronorepinephrine has a weak alpha1-adrenoceptor agonistic property and that the endothelium-dependent potentiation by 6-nitronorepinephrine of the norepinephrine-induced contraction is mediated through production of H2O2.
Eur J Pharmacol 1998 Sep 18
PMID:Endothelium-independent and -dependent vasoactivity of 6-nitronorepinephrine. 979 36

To clarify the mechanism of carcinogenesis by hair dyes, we compared the extent of DNA damage induced by mutagenic m-phenylenediamine and 4-methoxy-m-phenylenediamine, using 32P-5'-end-labeled DNA fragments obtained from the human c-Ha-ras-1 protooncogene and the p53 tumor suppressor gene. Carcinogenic 4-methoxy-m-phenylenediamine caused DNA damage at thymine and cytosine residues in the presence of Cu(II). Catalase and bathocuproine, a Cu(I)-specific chelator, inhibited 4-methoxy-m-phenylenediamine-induced DNA damage, suggesting the involvement of H2O2 and Cu(I). Superoxide dismutase (SOD) enhanced the DNA damage. Formation of 8-hydroxy-2'-deoxyguanosine (8-OH-dG) was induced by 4-methoxy-m-phenylenediamine in the presence of Cu(II). UV-visible spectroscopic studies have shown that Cu(II) mediated autoxidation of 4-methoxy-m-phenylenediamine and SOD accelerated the autoxidation. On the other hand, non-carcinogenic m-phenylenediamine did not cause clear DNA damage and significant autoxidation even in the presence of Cu(II). These results suggest that carcinogenicity of m-phenylenediamines is associated with ability to cause oxidative DNA damage rather than bacterial mutagenicity.
Free Radic Res 1998 Sep
PMID:DNA damage induced by m-phenylenediamine and its derivative in the presence of copper ion. 980 51


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