Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estradiol valerate (EV) treatment has been shown to result in the destruction of 60% of beta-endorphin neurons in the hypothalamic arcuate nucleus. Evidence suggests that the mechanism of EV-induced neurotoxicity involves the conversion of estradiol to catechol estrogen and subsequent oxidation to free radicals in local peroxidase-positive astrocytes. In this study, we examined whether treatment with the antioxidant, vitamin E, protects beta-endorphin neurons from the neurotoxic action of estradiol. Our results demonstrate that chronic vitamin E treatment prevents the decrement in hypothalamic beta-endorphin concentrations resulting from arcuate beta-endorphin cell loss, suggesting that the latter is mediated by free radicals. Vitamin E treatment also prevented the onset of persistent vaginal cornification and polycystic ovarian condition which have been shown to result from the EV-induced hypothalamic pathology.
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PMID:Vitamin E protects hypothalamic beta-endorphin neurons from estradiol neurotoxicity. 142 46

Sixty asymptomatic cigarette smokers were randomly allocated into three treatment groups. Smokers in Group 1 received 900 international units of Vitamin E (VE) daily for 6 wk, whereas 40 mg of beta-carotene (BC) daily was administered to those in Group 2 for the same period. Subjects in Group 3 were treated with a matched placebo. Plasma levels of VE and BC as well as circulating leukocyte counts, sister chromatid exchanges (SCEs), and the luminol-enhanced chemiluminescence (LECL) responses of blood phagocytes activated with phorbol myristate acetate (PMA) and FMLP with cytochalasin B (FMLP/CB) were measured prior to the administration of the antioxidant/placebo after 4 and 6 wk of supplementation and 12 wk after cessation of treatment. SCEs and leukocyte counts remained unchanged throughout the trial in all three treatment groups. Administration of VE for 4 wk was accompanied by decreased FMLP/CB-activated (p less than 0.005) and PMA-activated (p less than 0.005) LECL responses. However, with PMA as stimulant, the inhibition of LECL was transient, with partial recovery observed after 6 wk despite continued administration of VE. Administration of BC was associated with progressive inhibition of both FMLP/CB-activated (p less than 0.05 and p less than 0.01 after 4 and 6 wk, respectively) and PMA-activated (p less than 0.025 after 6 wk) LECL. No alterations in LECL responses were observed in Group 3 (placebo). VE appeared to inhibit the generation of oxidants by activated phagocytes, whereas BC scavenged oxidants generated by the myeloperoxidase/H2O2/halide system.
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PMID:Investigation of the effects of oral administration of vitamin E and beta-carotene on the chemiluminescence responses and the frequency of sister chromatid exchanges in circulating leukocytes from cigarette smokers. 216 23

The basic experimental data obtained at the Department of Coenzymes' Biochemistry of the A. V. Palladin Institute of Biochemistry of the Ukr. SSR Academy of Sciences as to the biological role of vitamin E are analyzed. Vitamin E, selenium and methionine are found to induce peculiar changes in the activity of glutathione-peroxidase, metabolism of sulphur-containing amino acids, biosynthesis of adenine nucleotides, proteins and nucleic acids. Participation of alpha-tocopherol and its active derivatives in the control of biosynthesis and intertransformation of ubiquinone and its cyclic isomer, ubichromenol, in the animal organism, is proved, which determines to a considerable extent the biological role of vitamin E in the bioenergy processes. It is substantiated in experiments that the detected wide range of the biological effect of vitamin E is associated with the control of RNA biosynthesis. Under these conditions the effect of vitamin E on the RNA synthesis does not depend on the manifestation of antioxidant properties of its molecule and in this sense it is a specific one. The results obtained are discussed for their significance in explanation of the molecular mechanism of the vitamin E action and in substantiation of the possibility to use the results in practical medicine and animal husbandry.
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PMID:[The role of vitamin E in the body]. 390 7

Metabolism of 2-amino-4-(5-nitro-2-furyl)thiazole (ANFT) by a variety of different peroxidases was examined. Metabolism of ANFT was measured by the binding of radiolabeled substrates to protein and DNA. Prostaglandin hydroperoxidase but not horseradish peroxidase, lactoperoxidase, or chloroperoxidase metabolically activated ANFT. All four peroxidases catalyzed the binding of benzidine to protein and DNA. With peroxide substrates, peroxidase-catalyzed binding of both carcinogens was observed with or without molecular oxygen. Arachidonic acid-dependent binding of ANFT and benzidine by prostaglandin endoperoxide synthetase was inhibited by anaerobic conditions and aspirin. Chloroperoxidase activation of benzidine was also inhibited by aspirin. Vitamin E inhibited activation of both carcinogens by all enzymes examined. Prostaglandin hydroperoxidase-catalyzed binding of benzidine to protein was inhibited by the 5-nitrofurans ANFT and 3-hydroxymethyl-1-(([3-(5-nitro-2-furyl)allydidene] amino))hydantoin and acetaminophen, while only acetaminophen inhibited horseradish peroxidase-catalyzed binding. These results indicate that different peroxidases may exhibit specificity with respect to their activation of carcinogens. Only prostaglandin hydroperoxidase activated the 5-nitrofuran ANFT, while a number of peroxidases activated the aromatic amine benzidine.
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PMID:Peroxidase metabolism of the urinary bladder carcinogen 2-amino-4-(5-nitro-2-furyl)thiazole. 640 25

An explanation of the functions of both vitamin E and selenium in metabolism and an account of the correlations between them is followed by reference to the results obtained by the authors of this paper from studies into the effects of dl-alpha-tocopherol on selenium levels in the M. longissimus dorsi, blood, and liver as well as on the activity of glutathione-peroxidase (EC 1.11.1.9) in erythrocytes of rabbit and rat, following application of therapeutic doses of selenium (0.5 mg/kg live weight). In both species selenium application increased the glutathione-peroxidase activity in erythrocytes. Vitamin E had no additional effect. Application of selenium was followed by rise in intraorganic selenium concentrations. In rabbit, the effect of vitamin T on intraorganic distribution of selenium caused an increased of the selenium level in the liver, but not in the muscles. No vitamin E effect was recordable in the rat. The findings are discussed, with conclusions being suggested for the treatment of metabolic disorders in the context of selenium and vitamin E and for non-invasive liver therapy.
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PMID:[Effect of dl-alpha-tocopherol on incorporation of selenium in "selenium-indicating" organs and on glutathione peroxidase activity in rat and rabbit erythrocytes following application of therapeutic doses of sodium selenite]. 722 95

The systemic vasculitides are characterized by necrotizing inflammation of blood vessels. Neutrophils are implicated in tissue damage by their presence at the site of injury. They can mediate injury by release of cellular contents including proteinases, cytokines and reactive oxygen species. Antioxidants such as vitamin E and N-acetyl cysteine (NAC) may therefore be predicted to ameliorate oxidative damage in vivo and could be a cheap and non-toxic form of therapy. We examined this hypothesis in an experimental model of vasculitis which has some similarities to human disease, and in which depletion of neutrophils ameliorates tissue injury. Mercuric chloride (HgCl2) treatment induces an autoimmune syndrome and necrotizing leucocytoclastic vasculitis in the Brown Norway (BN) rat; anti-myeloperoxidase (MPO) and anti-glomerular basement (GBM) antibodies are present, and vasculitis is reduced by antimicrobials. Methyl prednisolone given intravenously was effective in reducing tissue injury, demonstrating that the model was responsive to a treatment used in man. Vitamin E and NAC were given as daily injections intraperitoneally to BN rats either before, during or after HgCl2 administration. Serial blood samples were taken for anti-MPO and IgE antibodies, which were assayed by ELISA. Necropsies were performed on animals killed at peak disease. At doses of 50-200 mg/kg per day vitamin E had no beneficial effect on tissue injury, regardless of timing of treatment. NAC at 100 or 200 mg/kg also had no significant protective effect on vasculitis. Autoantibody and IgE levels were not affected by either methyl prednisolone or the antioxidants. The lack of benefit of vitamin E and NAC suggests that oxidative damage, whether generated by neutrophils or other cells, does not play a major role in the pathogenesis of vasculitis, and that antioxidant therapy is unlikely to be of benefit in systemic vasculitis in man.
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PMID:Use of methyl prednisolone and antioxidants in mercuric chloride-induced experimental vasculitis. 792 87

The effects of IRFI-048 (2,3-dihydro-5-methoxy-4,6,7-trimethyl-2-benzofuranyl acetic acid), a selective analogue of Vitamin E, on myocardial tissue injury were examined in anaesthetized rats subjected to 60-min occlusion of the left coronary artery followed by 60-min reperfusion. Infarct size (Evan's blue and tetrazolium stain), serum creatinphosphokinase (CPK), plasma malonaldehyde (MAL), cardiac myeloperoxidase (MPO) activity, and ST-segment of electrocardiogram (ECG) and survival rate were evaluated. Postischaemic reperfusion produced severe cardiac necrosis, caused neutrophil (PMNs) infiltration (evaluated by MPO activity) in the jeopardized tissue, increased serum CPK and plasma MAL, raised ST-segment of ECG, and decreased survival rate. IRFI-048, (200 and 400 mg/kg o.s.) given to the rats 6 h before occlusion, caused a reduction of necrotic area expressed as a percentage of either the area at risk or the total left ventricle, decreased MPO activity both in the area at risk (from 3.2 +/- 0.3 U x 10(-3)/g tissue to 1.1 +/- 0.4 U x 10(-3)/g tissue; p < .005) and in the necrotic area (from 5.7 +/- 0.9 U x 10(-3)/g tissue to 1.8 +/- 0.5 U x 10(-3)/g tissue; p < .001), attenuated the rise of ST-segment of ECG (from 0.51 +/- 0.14 mV in the vehicle group to 0.28 +/- 0.11 mV in the treated group; p < .005), reduced the increase of plasma MAL and serum CPK during reperfusion (from 42 +/- 5.3 nmol/ml to 15 +/- 3.1 nmol/ml and 139 +/- 13 IU/100 ml to 58 +/- 7.5 IU/100 ml, respectively; p < .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of myocardial infarct size in rat by IRFI-048, a selective analogue of vitamin E. 800 27

The protective effects of high dose antenatal vitamin E on hypoxemia in newborn rats were investigated. The subjects were 1-d-old Wistar rats weighing 5-6 g which were born to mothers weighing 245-250 g. Three groups of rat pups, each consisting of eight newborn rats, were used: nontreated control group, hypoxic group, and vitamin E group. The mothers of pups in the last group were given vitamin E (2000 mg/kg/d) antenatally on 3 consecutive days. Hypoxia was induced by breathing of a mixture of 8% oxygen and 92% nitrogen for 3 h. Then pups were allowed to inhale normal atmospheric air for 30 min. All rats were killed on the first day of life after the procedure of hypoxia and reoxygenation. The brains, lungs, livers, intestines, and kidneys were studied biochemically and histopathologically. The hypoxia-induced biochemical changes were determined by measuring lipid peroxidation and myeloperoxidase activity. Vitamin E effectively inhibited hypoxia-induced lipid peroxidation in liver and intestines, and decreased the levels of thiobarbituric acid-reactive substances in brain. In agreement with lipid peroxidation, tissue associated myeloperoxidase activity was increased in liver, intestines, and kidneys, but not in brain and lungs, of the hypoxic group. Histopathologic changes in intestines were epithelial separation and submucosal polymorphonuclear leukocyte infiltration. In the liver, leukocyte infiltration was observed only near the portal areas. These changes were not observed in the vitamin E group. It was concluded that high doses of antenatal vitamin E may protect the newborn rat pups against hypoxia-induced tissue injury.
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PMID:The effect of high dose antenatal vitamin E on hypoxia-induced changes in newborn rats. 855 34

The results of the present study revealed that peptides derived from bovine casein hydrolysates can promote peroxidase-dependent oxidation of human low-density lipoproteins (LDL). The reaction was independent of the free metal ions but required casein-derived peptides with tryosyl-residues, implying that the tyrosyl radical is a diffusible catalyst that conveys oxidizing potential from the active site of the heme enzyme to LDL lipids. This mechanism is independent of the peroxidase used to oxidize tyrosyl residues since myeloperoxidase and horseradish peroxidase mediate a similar LDL peroxidating process. Vitamin E, ascorbic acid, butylated hydroxytoluene and reduced glutathione delayed LDL oxidation and were consumed during the reaction, they transfered hydrogen to repair tyrosine.
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PMID:[Casein-derived peptides can promote human LDL oxidation by a peroxidase-dependent and metal-independent process]. 867 38

Zaprionus paravittiger fed with vitamin E supplemented diet (1, 5 and 10 micrograms/ml) showed an increase in median and maximum life spans. Further increase in concentration accelerated the mortality rate. Females exhibited longer life span as compared to males. Malondialdehyde (MDA) content and antioxidant enzymes (catalase and peroxidase) were measured in control and optimum concentration of vitamin E (5 micrograms/ml)-fed flies at various age intervals. MDA content showed an increase with age in control and vitamin E-fed group whereas catalase and proxidase activities showed a decrease with age. The females exhibited lower MDA content and higher activities of catalase and peroxidase as compared to males in control and vitamin E group. Vitamin E feeding caused a significant decrease in MDA and increase in catalase and peroxidase activities. These findings suggest that vitamin E has dose-dependent and sex-specific influence on longevity of Z. paravittiger and support the view that longevity and activity of antioxidant enzymes are positively linked.
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PMID:Effect of vitamin E on life span, malondialdehyde content and antioxidant enzymes in aging Zaprionus paravittiger. 893 Jun 18


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