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

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Query: EC:1.6.99.3 (diaphorase)
5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sterigmatocystin (Stg), a major secondary metabolite of Aspergillus versicolor and A. nidulans, is the precursor of aflatoxin B1. In this study, male albino rats were treated with Stg-contaminated diet for 30 days, resulting in reduced levels of glutathione, ascorbic acid, and alpha-tocopherol. The activity of catalase in liver was reduced, whereas an increase in the activities of superoxide dismutase and glutathione peroxidase was observed. The levels of cytochrome P450, cytochrome b5, cytochrome b5 reductase, cytochrome c reductase, hydroxyl radical, and hydrogen peroxide formation significantly increased in the Stg- treated rat liver microsomes. Hepatic parenchymal cell injury, necrosis, and Kupffer cells proliferation were noticed in histological sections of liver from animals treated with Stg. Overall results suggest that generation of free radicals imposes depletion of antioxidants. This led to enhanced lipid peroxidation. The observed elevation of hepatic thiobarbituric acid reactive substances appears to originate mainly from the damaged Kupffer cells. As a result, elevated levels of serum marker enzymes were also observed.
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PMID:Lipid peroxidation as a possible secondary mechanism of sterigmatocystin toxicity. 1172 90

Use of antioxidant enzymes as biomarkers often becomes a complicated process at application level because they show considerable seasonal fluctuation due to both natural and biological factors. In this study, we studied the consequences of seasonal variation of antioxidant enzymes [catalase (EC 1.11.1.6), superoxide dismutase (SOD, EC 1.15.1.1), glutathione peroxidase (GPX, EC 1.11.1.9) and microsomal NADPH-DT diaphorase (EC 1.6.99.2)] in the digestive gland of wild brackishwatcr oysters, Saccostrea cucullata for biomonitoring against polyaromatic hydrocarbon (PAH) contamination in Hooghly Estuary, north-eastern coast of India. As a general trend, maximum antioxidant enzyme activities were detected in pre-monsoon period or summer (March-June) followed by a gradual decrease during monsoon (July-October) with a minimum in post-monsoon period or winter (November-February) and this pattern was similar to tissue concentrations of PAHs also. The physiological fluctuations of the antioxidant defense systems were inversely-related to the lipid peroxidation indicating an enhanced susceptibility of oyster tissues to oxidative stress during post-monsoon or winter period. However, the oysters from polluted populations exhibited consistent very high PAHs load in their tissues as well as significant increases in the activities of antioxidant enzymes than in non-polluted populations in all three seasons. The results indicated that the antioxidant enzymes, catalase, SOD and microsomal NADPH-DT diaphorase in digestive gland of S. cucullata could be useful biomarkers of PAHs contamination. It also emphasized that seasonal variation of potential biomarkers like such enzymes should be incorporated into interpretation of biomonitoring studies by the use of appropriate controls and identical treatment in analysis of polluted and non-polluted samples.
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PMID:Antioxidant enzymes in brackishwater oyster, Saccostrea cucullata as potential biomarkers of polyaromatic hydrocarbon pollution in Hooghly Estuary (India): seasonality and its consequences. 1177 56

In brain mitochondria, state 4 respiration supported by the NAD-linked substrates glutamate/malate in the presence of EGTA promotes a high rate of exogenous H2O2 removal. Omitting EGTA decreases the H2O2 removal rate by almost 80%. The decrease depends on the influx of contaminating Ca2+, being prevented by the Ca2+ uniporter inhibitor ruthenium red. Arsenite is also an inhibitor (maximal effect approximately 40%, IC50, 12 microm). The H2O2 removal rate (EGTA present) is decreased by 20% during state 3 respiration and by 60-70% in fully uncoupled conditions. H2O2 removal in mitochondria is largely dependent on glutathione peroxidase and glutathione reductase. Both enzyme activities, as studied in disrupted mitochondria, are inhibited by Ca2+. Glutathione reductase is decreased by 70% with an IC50 of about 0.9 microm, and glutathione peroxidase is decreased by 38% with a similar IC50. The highest Ca2+ effect with glutathione reductase is observed in the presence of low concentrations of H2O2. With succinate as substrate, the removal is 50% less than with glutamate/malate. This appears to depend on succinate-supported production of H2O2 by reverse electron flow at NADH dehydrogenase competing with exogenous H2O2 for removal. Succinate-dependent H2O2 is inhibited by rotenone, decreased DeltaPsi, as described previously, and by ruthenium red and glutamate/malate. These agents also increase the measured rate of exogenous H2O2 removal with succinate. Succinate-dependent H2O2 generation is also inhibited by contaminating Ca2+. Therefore, Ca2+ acts as an inhibitor of both H2O2 removal and the succinate-supported H2O2 production. It is concluded that mitochondria function as intracellular Ca2+-modulated peroxide sinks.
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PMID:Respiration-dependent removal of exogenous H2O2 in brain mitochondria: inhibition by Ca2+. 1463 20

For many liver malignancies, major hepatectomy is the usual therapy. Although a normal liver has a tremendous capacity for regeneration, liver hepatectomy in humans is usually carried out on a diseased liver and, in such cases, liver regeneration takes place in a cirrhotic remnant. Mitochondrial function in cirrhotic livers shows a variety of changes compared to control livers. This study investigated how mitochondrial respiratory function and antioxidant capacity change following partial hepatectomy of cirrhotic livers, because liver regeneration requires greater energy demands and control of oxidative stress. Cirrhosis was induced in male Wistar-Furth rats by administration of thioacetamide. NADH-cytochrome c reductase activity, mitochondrial glutathione peroxidase activity and mitochondrial GSH levels were all significantly lowered in cirrhotic livers and in the cirrhotic remnants up to 72 h after 70% hepatectomy when compared to the corresponding controls. Lower respiratory control ratios with succinate as substrate were also observed from 6 to 48 h post-hepatectomy. At 24 h post-hepatectomy, higher levels of lipid peroxidation were observed. We conclude that, compared to the controls, cirrhotic livers have diminished oxidative phosphorylation capabilities due to changes in NADH and FADH(2)-linked respiration as well as impaired antioxidant defenses following partial hepatectomy. Both of these factors, if critical, could then impede liver regeneration.
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PMID:Mitochondrial respiratory function and antioxidant capacity in normal and cirrhotic livers following partial hepatectomy. 1474

We investigated the hypothesis that thallium (Tl) interactions with the glutathione-dependent antioxidant defence system could contribute to the oxidative stress associated with Tl toxicity. Working in vitro with reduced glutathione (GSH), glutathione reductase (GR) or glutathione peroxidase (GPx) in solution, we studied the effects of Tl+ and Tl3+ (1-25 microM) on: (a) the amount of free GSH, investigating whether the metal binds to GSH and/or oxidizes it; (b) the activity of the enzyme GR, that catalyzes GSH regeneration; and (c) the enzyme GPx, that reduces hydroperoxide at expense of GSH oxidation. We found that, while Tl+ had no effect on GSH concentration, Tl3+ oxidized it. Both cations inhibited the reduction of GSSG by GR and the diaphorase activity of this enzyme. In addition, Tl3+ per se oxidized NADPH, the cofactor of GR. The effects of Tl on GPx activity depended on the metal charge: Tl+ inhibited GPx when cumene hydroperoxide (CuOOH) was the substrate, while Tl(3+)-mediated GPx inhibition occurred with both substrates. The present results show that Tl interacts with all the components of GSH/GSSG antioxidant defence system. Alterations of this protective pathway could be partially responsible for the oxidative stress associated with Tl toxicity.
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PMID:In vitro interactions of thallium with components of the glutathione-dependent antioxidant defence system. 1562 16

The possibility that Tl(OH)3, the main Tl3+ specie present in water solutions, could interfere with the normal functioning of the glutathione-dependent antioxidant defense system was investigated. For this purpose, we used both the purified components of this system and rat brain cytosolic fractions. Tl(OH)3 (1-25 microM) significantly decreased the content of reduced glutathione (GSH) in both experimental systems, caused by GSH oxidation. In the same range of concentrations Tl(OH)3 inhibited glutathione peroxidase (GPx) activity in both models, using cumene hydroperoxide as the substrate. No alterations in the capacity of GPx activity to metabolize H2O2 were observed. Both in purified GR as well as in the cytosolic fraction, Tl(OH)3 (1-5 microM) inhibited GR activity, with a partial recovery of the activity at higher concentrations. While Tl(OH)3 inhibited the GR diaphorase activity of purified GR, in a concentration (1-25 microM) dependent manner, this effect was only observed in the cytosolic fractions at the highest concentration assessed (25 microM). Results indicate that, similarly to previous findings for Tl+ and Tl3+, Tl(OH)3 also alters the glutathione-dependent antioxidant defense system. The observed alterations of this important antioxidant protective pathway by the major Tl3+ specie in water solutions could be one mechanism involved in the oxidative stress associated to Tl-intoxication.
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PMID:Glutathione metabolism is impaired in vitro by thallium(III) hydroxide. 1566 76

White Spot Syndrome Virus (WSSV) is the major viral pathogen of culture shrimp. Although remarkable progress has been made in characterizing the WSSV genome, information concerning the antiviral process of host is still limited. To identify the genes differentially expressed along with their expression profile in the hemocytes of the virus-resistant shrimp, suppression subtractive hybridization (SSH) and differential hybridization (DH) were employed. Relying on the sequences identified in the subtractive cDNA library, 30 genes were characterized to be involved in the antiviral process as defense-relevant, among them, 22 are found for the first time in penaeid shrimp. The most interesting finding is that the interferon-like protein (IntlP) and (2'-5') oligo(A) synthetase-like protein (data not shown) known as the antiviral factors showed increased expression in virus-resistant shrimp and the non-specific antiviral activity of IntlP protein was verified by cytotoxicity experiment. A number of proteins with certain similarities to the components of the complement and cytokines system in vertebrates were also found in the subtracted library. The high expression of redox-related factors (NADH dehydrogenase, glutathione peroxidase and transcription factor AP-1 precursor), plasma defensive protein (C-type lectin and laminin-like protein) and translationally controlled tumor protein (TCTP) in the virus-resistant shrimp suggested that they are essential components participating in the antiviral process. Our work provides a wide array of genes differentially expressed in the virus-resistant shrimp, and a framework for further studies aimed at antiviral mechanism in shrimp.
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PMID:Differential profile of genes expressed in hemocytes of White Spot Syndrome Virus-resistant shrimp (Penaeus japonicus) by combining suppression subtractive hybridization and differential hybridization. 1578 Nov 31

The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSP) as well as of succinate dehydrogenase (SDG), NADH dehydrogenase (NDG) and fumarate hydratase (FHT) were examined in relation to mitochondrial ultrastructure changes in Aspergillus niger exposed to N,N-bis(3-aminopropyl)dodecylamine (Apd) that was shown to exhibit fungicidal activity. There was a progressive increase in SOD, CAT and GSP activities 1 and 4 h after 0.05 and 0.1 % Apd application. However, this was followed by a pronounced activity decrease when 0.05 % Apd treatment was prolonged by 1 d. The destructive effect on fungal morphology was observed when this fungicidal agent was applied at the concentration of 0.1 % for 1 d. In the treated hyphae mitochondria degenerated after all organelles. The morphological malformations of mitochondria had an impact on their metabolic state; however, the activities of SDG, NDG and FHT were affected to a different extent. In A. niger the fungicidal effect of Apd could be mediated by oxidative stress impairing the vital mitochondria-related cellular functions.
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PMID:Effects of N,N-bis(3-aminopropyl)dodecylamine on antioxidant enzyme activities, mitochondrial morphology and metabolism in Aspergillus niger. 1682 10

Mitochondria are an important intracellular source and target of reactive oxygen species. The life span of a species is thought to be determined, in part, by the rate of mitochondrial damage inflicted by oxygen free radicals during the course of normal cellular metabolism. In the present study, we have investigated the protective effect of squalene supplementation for 15 days and 30 days on energy status and antioxidant defense system in liver mitochondria of 18 young and 18 aged rats. The dietary supplementation of 2% squalene significantly minimized aging associated alterations in mitochondrial energy status by maintaining the activities of TCA cycle enzymes (isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase and malate dehydrogenase) and respiratory marker enzymes (NADH dehydrogenase and cytochrome-c-oxidase) at higher level in the liver mitochondria of aged rats compared with unsupplemented controls. It exerted an antioxidant effect by inhibiting mitochondrial lipid peroxidation (malondialdehyde) in liver of young and aged rats. Supplementation with squalene also maintained the mitochondrial antioxidant defense system at higher rate by increasing the level of reduced glutathione and the activities of glutathione-dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (superoxide dismutase and catalase) in the liver of young and aged rats. The results of this study provide evidence that dietary supplementation with squalene can improve liver mitochondrial function during aging and minimize the age-associated disorders in which reactive oxygen species are a major cause.
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PMID:Protective effect of dietary squalene supplementation on mitochondrial function in liver of aged rats. 1757 27

The modulatory efficacy of capsaicin on lung mitochondrial enzyme system with reference to mitochondrial lipid peroxidation (LPO), antioxidants, key citric acid cycle enzymes and respiratory chain enzymes during benzo(a)pyrene (B(a)P) induced lung cancer in Swiss albino mice was studied. Elevations in mitochondrial LPO along with decrements in enzymic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)), non-enzymic antioxidants (reduced glutathione (GSH), vitamin C, vitamin E and vitamin A), citric acid cycle enzymes (isocitrate dehydrogenase (ICDH), alpha-ketoglutarate dehydrogenase (alpha-KDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH)), and respiratory chain enzymes (NADH dehydrogenase and Cytochrome c oxidase) were observed in B(a)P (50mg/kg body weight) administered animals. CAP (10mg/kg body weight) pretreatment decreased lung mitochondrial LPO and augmented the activities of enzymic, non-enzymic antioxidants, citric acid cycle enzymes and respiratory chain enzymes to near normalcy revealing its chemoprotective function during B(a)P induced lung cancer.
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PMID:Stabilization of pulmonary mitochondrial enzyme system by capsaicin during benzo(a)pyrene induced experimental lung cancer. 1802 35


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