Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P06889 (
Mol
)
630,302
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The sequence of the major soluble protein component of the cuticle of filarial nematodes is homologous to that of bovine
glutathione peroxidase
, for which an X-ray structure is available. Due to the high degree of sequence identity (42%), it has been possible to build an apparently reliable three-dimensional model of the gp29 cuticular protein from Brugia spp. that will aid studies of the molecule both as a target immunogen and secreted enzyme. The modelled core of the gp29 structure is conserved compared to the bovine enzyme, consisting of a beta-sheet surrounded by alpha-helices. Experimental data showed that Brugia spp. gp29 has four subunits, and a tetrameric form of gp29 has also been modelled. The two N-linked glycosylation sites per subunit were predicted to lie on the surface of the tetramer. Most of the variation in amino acid sequence compared to that of mammalian enzymes, occurs in the surface loops, several of which are larger and more exposed in gp29. Deglycosylated gp29 was demonstrated to be immunogenic in human infection, and six likely B-cell epitopes have been predicted on the basis of a high protrusion index and sequence variability.
Mol
Biochem Parasitol 1993 Mar
PMID:Molecular modelling and epitope prediction of gp29 from lymphatic filariae. 768 45
The effect of the antipsychotic agents chlorpromazine (CPZ) and Li2CO3 on superoxide dismutase (SOD, EC 1.15.1.1) and
glutathione peroxidase
(GPx, EC 1.11.1.9) activities of brain, liver and erythrocyte of rats was investigated. The short-term treatment (7 days) either with CPZ (10 mg/kg body weight) or with Li2CO3 (2 mEq Li/kg body weight) did not affect enzymatic activities. In contrast, the long-term administration of CPZ (1 month) decreased the SOD activity in brain and erythrocytes while Li2CO3 had no effect. GPx activity and lipid peroxidation of brain and liver homogenates were not affected by either acute or chronic administration of these agents.
Biochem
Mol
Biol Int 1994 Dec
PMID:The effect of chlorpromazine and Li2CO3 on the superoxide dismutase and glutathione peroxidase activities of rat brain, liver and erythrocytes. 769 80
It has been documented that cytokines can induce the formation of reactive oxygen species (ROS) in the liver, and that an inflammatory reaction can locally increase the production of ROS, but it remains unknown whether in vivo a subcutaneous (s.c.) inflammatory reaction can induce the formation of ROS in the liver. To determine in vivo whether an inflammatory reaction, able to decrease the amount of hepatic cytochrome P450, enhances the presence of ROS in the liver, turpentine was injected s.c. to rabbits, which were sacrificed 48 hours later. Control rabbits received saline s.c. The amount and activity of cytochrome P450, as well as several parameters reflecting the presence of ROS were assessed in the liver. Total amount of cytochrome P450 was reduced, as was its activity, assessed by the rates of hydroxylation of aniline and of demethylation of aminopyrine. Moreover, lipid peroxidation increased, while the activity of the enzymatic scavengers, i.e. catalase,
glutathione peroxidase
and superoxide dismutase decreased. In addition, hepatic concentrations of reduced glutathione were diminished. On the other hand, the activity of the xanthine oxidase system was enhanced by almost 200%. These results strongly suggest an increased presence of ROS. The changes in the amount of cytochrome P450 were inversely correlated with lipid peroxidation. In conclusion, these results show that in vivo an inflammatory reaction, that reduces total cytochrome P450 and its activity, produces simultaneously an oxidative stress in the liver.
Res Commun
Mol
Pathol Pharmacol 1995 Feb
PMID:Inflammation-induced decrease in hepatic cytochrome P450 in conscious rabbits is accompanied by an increase in hepatic oxidative stress. 774 59
The involvement of reactive oxygen species in chromate-induced genotoxicity has been postulated. Because intracellular antioxidants help in eliminating the reactive species of oxygen, we have investigated both the prooxidant and antioxidant status of human leukemic T-lymphocyte MOLT4 cells exposed to nontoxic levels of chromium(VI) in culture. The cells treated with 0-->200 microM potassium chromate in a salts/glucose medium for 2 h were found to contain significantly lower levels of both small molecular weight and macromolecular antioxidants. In particular, the levels of glutathione and ascorbate were found to decrease with increased doses of chromate exposure in a dose-dependent manner. As little as 10 microM chromate was found to decrease these small molecular weight antioxidants significantly (p < 0.01). The macromolecular antioxidants, such as
glutathione peroxidase
, catalase, glutathione reductase, glucose-6-phosphate dehydrogenase and superoxide dismutase were also significantly (p < 0.01) decreased by exposing the cells to as little as 10 microM chromate. Concomitantly, there was a dose-dependent increase in intracellular H2O2 accumulation in cells exposed to chromium(VI). These results indicate that chromate-induced genotoxicity may be due, at least in part, to decreased levels of intracellular antioxidants in conjunction with an increased production of the reactive oxygen species.
Mol
Cell Biochem 1995 Jan 12
PMID:Alterations in the prooxidant and antioxidant status of human leukemic T-lymphocyte MOLT4 cells treated with potassium chromate. 775 43
Effects of hypoxia-reoxygenation (H-R) on myocytes isolated from 10 week hypertrophied and sham control rat hearts were studied. Myocyte hypertrophy was indicated by an increase in cell size. Superoxide dismutase (SOD) and
glutathione peroxidase
(GSHPx) enzyme activities were significantly higher and lipid peroxidation (TBARS) was lower in hypertrophied myocytes prior to any H-R. Hypertrophied myocyte population showed significantly less damage to cell morphology due to H-R. In sham as well as hypertrophied myocytes, Na+ and Ca2+ contents were increased by H-R, but Ca2+ accumulation was significantly less in the hypertrophied myocytes. Both SOD and GSHPx activities were depressed by the oxidative stress in the sham myocytes whereas these activities were not significantly changed in the hypertrophied myocytes. Catalase activity in the prehypoxic sham and hypertrophied myocytes was comparable and this activity did not change during H-R. There was a significant increase in lipid peroxidation due to H-R but this change was less in hypertrophied myocytes. This study shows less vulnerability of hypertrophied myocytes to oxidative stress and an increase in endogenous antioxidant reserve may have an important role in mediating this protection.
J
Mol
Cell Cardiol 1995 Jan
PMID:Endogenous antioxidants in isolated hypertrophied cardiac myocytes and hypoxia-reoxygenation injury. 776 Mar 50
The molecular regulation of seed dormancy was investigated using differential display to visualize and isolate cDNAs representing differentially expressed genes during early imbibition of dormant and nondormant Avena fatua L. embryos. Of about 3000 cDNA bands examined, 5 cDNAs hybridized with mRNAs exhibiting dormancy-associated expression patterns during the first 48 h of inhibition, while many more nondormancy-associated cDNAs were observed. Dormancy-associated clone AFD1 hybridized with a 1.5 kb mRNA barely detectable in dry dormant and nondormant embryos that became more abundant in dormant embryos after 24 h of imbibition. Clone AFD2 hybridized with two mRNAs, a 1.3 kb message constitutively expressed in dormant and nondormant embryos and a 0.9 kb message present at higher levels in dormant embryos after 3 h of imbibition. Nondormancy-associated clones AFN1, AFN2 and AFN3 hybridized with 1.5 kb, 1.7 kb and 1.1 kb mRNAs, respectively, that were more abundant in nondormant embryos during imbibition. Expression patterns of some mRNAs in dormant embryos induced to germinate by GA3 treatment were different than water controls, but were not identical to those observed in nondormant embryos. DNA sequence analysis revealed 76% sequence identity between clone AFN3 and a Citrus sinensis
glutathione peroxidase
-like cDNA, while significant sequence similarities with known genes were not found for other clones. Southern hybridization analyses showed that all clones represent low (1 to 4) copy number genes.
Plant
Mol
Biol 1995 Apr
PMID:Characterization of cDNA clones for differentially expressed genes in embryos of dormant and nondormant Avena fatua L. caryopses. 778 76
Adaptation to various forms of stress has been found to be associated with increased cellular tolerance to myocardial ischemia. In this study, the effects of myocardial adaptation to oxidative stress was examined by injecting rats with endotoxin (0.5 mg/kg) and its non-toxic derivative, lipid A (0.5 mg/kg). Both compounds exerted oxidative stress within 1 h of treatment as evidenced by enhanced malonaldehyde formation. The oxidative stress disappeared steadily and progressively with time in concert with the appearance of the induction of glutathione and antioxidative enzymes that included superoxide dismutase, catalase,
glutathione peroxidase
and glutathione reductase. After 24 h of endotoxin or lipid A treatment, the amount of oxidative stress and antioxidant enzyme levels were significantly lower and higher, respectively, compared to those at the baseline levels. Corroborating these results, both endotoxin and lipid A provided protection against myocardial ischemia and reperfusion injury as evidenced by a significantly improved postischemic recovery of left ventricular functions. The data presented here demonstrates that a controlled amount of oxidative stress induces the expression of intracellular antioxidants that can result in enhanced myocardial tolerance to ischemia. This suggests that myocardial adaptation to oxidative stress may be a potential tool for reduction of ischemic/reperfusion injury.
Mol
Cell Biochem 1995 Mar 09
PMID:Oxidative stress adaptation improves postischemic ventricular recovery. 779 47
It is now clear that peroxisomes play a crucial role in many cellular processes, including the beta-oxidation of very long chain fatty acids. Recently, mammalian peroxisomes have been shown to contain the antioxidant enzymes, superoxide dismutase and
glutathione peroxidase
, in addition to catalase. The presence of these enzymes in peroxisomes suggests that peroxisomes undergo oxidative stress in normal and disease states. As an indicator of the potential impact of an oxidative stress on peroxisomal functions, we evaluated the effect of endotoxin exposure on the beta-oxidation enzyme system in rat liver. Peroxisomes were isolated from liver homogenates by differential and density gradient centrifugations. Endotoxin treatment decreased the beta-oxidation of lignoceric acid to 56% of control values (p < 0.01). The specific activity of the rate limiting enzyme in the system, acyl-CoA oxidase, was decreased to 73% of control values (p < 0.05). Immunoblot analysis revealed a 25% decrease in the 21KD subunit of the acyl-CoA oxidase protein. In contrast, the protein levels of the other enzymes in the pathway, trifunctional protein and 3-ketoacyl-CoA thiolase, were increased by 10 and 15%, respectively. These findings suggest that impairment of beta-oxidation of lignoceric acid by endotoxin treatment is due primarily to a reduction in the activity and protein level of the key enzyme, acyl-CoA oxidase. Oxidative stresses such as endotoxin exposure may have deleterious effects on important peroxisomal functions, such as beta-oxidation of very long chain fatty acids.
Mol
Cell Biochem 1994 Jun 29
PMID:Impairment of peroxisomal beta-oxidation system by endotoxin treatment. 783 45
The effect of dietary vitamin E supplementation upon macrophage metabolism and function was examined in aged rats fed a balanced or a polyunsaturated-rich diet. The following parameters were studied: number of cells in the intraperitoneal cavity, maximal activity of hexokinase, citrate synthase, glucose-6-phosphate dehydrogenase,
glutathione peroxidase
and phosphate-dependent glutaminase. The consumption of glucose and the production of lactate, hydrogen peroxide and thiobarbituric reactive substances were measured in control ONCO-BCG injected rats. The results indicated that vitamin E has no significant effect on the values of the parameters studied in the macrophages of rats fed a balanced diet both for 3 (mature) or 17 months (aged). This antioxidant did not provoke any response on the changes caused by ageing the animals. However, several of the metabolic and functional alterations in macrophage induced by the polyunsaturated-rich diets were reversed by the inclusion of vitamin E in the diet. These changes were associated with macrophage migration capacity, citrate synthase and glucose-6-phosphate dehydrogenase activities and the content of lipid peroxides. The findings suggest that vitamin E has a beneficial effect for macrophage metabolism and function, but the effects are confined to particular circumstances.
Biochem
Mol
Biol Int 1994 Aug
PMID:Effect of dietary vitamin E supplementation on macrophage metabolism during ageing. Study in rats fed fat-rich diets during ageing. 784 17
The growth of fibroblasts, which were isolated from human, rabbit, rat, mouse, and chick embryos, was inhibited partially under 50% oxygen and nearly completely under 95% oxygen. There was species difference in the resistivity of these cells against oxygen-induced growth inhibition. The extent of the resistivity was in the following order: chick cells > rat cells > human cells > rabbit cells approximately mouse cells. The order of their ability to recover from oxygen-induced growth inhibition was similar to the above order of species. There was also species difference in their antioxidant enzyme activities, including superoxide dismutase, catalase, and
glutathione peroxidase
activities, and their reduced glutathione concentration. Chick cells, having the highest resistivity against oxygen-induced growth inhibition, were at the lowest activity levels of antioxidant enzymes and at the highest concentration level of reduced glutathione. The species difference in resistivity against oxygen-induced growth inhibition seems to depend on the reduced glutathione concentration, but not on the antioxidant enzyme activities.
Comp Biochem Physiol B Biochem
Mol
Biol 1995 Jan
PMID:Species difference in the resistibility of embryonic fibroblasts against oxygen-induced growth inhibition. 785 38
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>