Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microglial cells are the resident immune cells of the central nervous system. These cells defend the central nervous system against invading microorganisms and clear the debris from damaged cells. Upon activation, microglial cells produce a large number of neuroactive substances that include cytokines, proteases, and prostanoids. In addition, activated microglial cells release radicals, such as superoxide and nitric oxide, that are products of the enzymes NADPH oxidase and inducible nitric oxide synthase, respectively. Microglia-derived radicals, as well as their reactive reaction products hydrogen peroxide and peroxynitrite, have the potential to harm cells and have been implicated in contributing to oxidative damage and neuronal cell death in neurological diseases. For self-protection against oxidative damage, microglial cells are equipped with efficient antioxidative defense mechanisms. These cells contain glutathione in high concentrations, substantial activities of the antioxidative enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, as well as NADPH-regenerating enzymes. Their good antioxidative potential protects microglial cells against oxidative damage that could impair important functions of these cells in defense and repair of the brain.
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PMID:Oxidative and antioxidative potential of brain microglial cells. 1611 27

The aim of this study was to analyse the effect of allelochemical stress on Lycopersicon esculentum growth. Our results showed that allelochemical stress caused by Sicyos deppei aqueous leachate inhibited root growth but not germination, and produced an imbalance in the oxidative status of cells in both ungerminated seeds and in primary roots. We observed changes in activity of catalase (CAT), ascorbate peroxidase (APX), superoxide dismutase (SOD), glutathione reductase (GR) and the plasma membrane NADPH oxidase, as well as in the levels of H(2)O(2) and O(2) (*-) in seeds at 12 and 24 h, and in primary roots at 48 and 72 h of treatment, which could account for the oxidative imbalance. There were changes in levels of expression of the mentioned enzymes, but without a correlation with their respective activities. Higher levels of membrane lipid peroxidation were observed in primary roots at 48 and 72 h of treatment. No effect on the expression of metacaspase and the PR1 was observed as indicators of cell death or induction of plant defence. This paper contributes to the understanding of plant-plant interactions through the phytotoxic allelochemicals released in an aqueous leachate of the weed S. deppei, which cause a negative effect on other plants.
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PMID:Allelochemical stress causes inhibition of growth and oxidative damage in Lycopersicon esculentum Mill. 1708 Dec 37

The present study aimed to investigate whether l-carnitine (LC) protects the vascular endothelium and tissues against oxidative damage in hypertension. Antioxidant enzyme activities, glutathione and lipid peroxidation were measured in the liver and heart of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Nitrite and nitrate levels and total antioxidant status (TAS) were evaluated in plasma, and the expression of endothelial nitric oxide synthase (eNOS) and p22phox subunit of NAD(P)H oxidase was determined in aorta. Glutathione peroxidase activity was lower in SHR than in WKY rats, and LC increased this activity in SHR up to values close to those observed in normotensive animals. Glutathione reductase and catalase activities, which were higher in SHR, tended to increase after LC treatment. No differences were found in the activity of superoxide dismutase among any animal group. The ratio between reduced and oxidized glutathione and the levels of lipid peroxidation were respectively decreased and increased in hypertensive rats, and both parameters were normalized after the treatment. Similarly, LC was able to reverse the reduced plasma nitrite and nitrate levels and TAS observed in SHR. We found no alterations in the expression of aortic eNOS among any group; however, p22phox mRNA levels showed an increase in SHR that was reversed by LC. In conclusion, chronic administration of LC leads to an increase in hepatic and cardiac antioxidant defense and a reduction in the systemic oxidative process in SHR. Therefore, LC might increase NO availability in SHR aorta by a reduction in superoxide anion production.
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PMID:L-carnitine attenuates oxidative stress in hypertensive rats. 1714 29

Nitric oxide (NO) is a highly reactive, membrane-permeable free radical, which has recently emerged as an important signalling molecule and antioxidant. Here we investigated the protective effect of NO against the toxicity caused by excess CuSO(4) (50 microM) in the adventitious roots of mountain ginseng. It was found that NO donor, sodium nitroprusside (SNP), was effective in reducing Cu-induced toxicity in the mountain ginseng adventitious roots. Protective effect of SNP, as indicated by extent of lipid peroxidation, was reversed by incorporation of 2-(4-carboxy-2-phenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (CPTIO), a NO scavenger, in the medium suggesting that the protective effect of SNP is attributable to NO released, which was revealed from in situ confocal laser scanning microscopic localization of NO in the adventitious roots of mountain ginseng. Results obtained in the present study suggest that reduction of excess Cu-induced toxicity by SNP is most likely mediated through the modulation in the activities of antioxidant enzymes involved in H(2)O(2) detoxification (catalase, peroxidase, ascorbate peroxidase) and in the maintenance of cellular redox couples (glutathione reductase), and contents of molecular antioxidants (particularly non-protein thiol, ascorbate and its redox status). Exogenous NO supply also improved the activity of superoxide dismutase, an enzyme responsible for O*(2) (-) dismutation, and NADPH oxidase, an enzyme responsible for O*(2) (-) generation, in excess Cu supplied adventitious roots of mountain ginseng.
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PMID:Modulation of copper toxicity-induced oxidative damage by nitric oxide supply in the adventitious roots of Panax ginseng. 1782 39

In the present study, we investigated the role of glucose-6-phosphate dehydrogenase (G6PDH) in regulating the levels of reduced form of glutathione (GSH) to the tolerance of calli from two reed ecotypes, Phragmites communis Trin. dune reed (DR) and swamp reed (SR), in a long-term salt stress. G6PDH activity was higher in SR callus than that of DR callus under 50-150 mM NaCl treatments. In contrast, at higher NaCl concentrations (300-600 mM), G6PDH activity was lower in SR callus. A similar profile was observed in GSH contents, glutathione reductase (GR) and glutathione peroxidase (GPX) activities in both salt-stressed calli. After G6PDH activity and expression were reduced in glycerol treatments, GSH contents and GR and GPX activity decreased strongly in both calli. Simultaneously, NaCl-induced hydrogen peroxide (H2O2) accumulation was also abolished. Exogenous application of H2O2 increased G6PDH, GR, and GPX activities and GSH contents in the control conditions and glycerol treatment. Diphenylene iodonium (DPI), a plasma membrane (PM) NADPH oxidase inhibitor, which counteracted NaCl-induced H(2)O(2) accumulation, decreased these enzymes activities and GSH contents. Furthermore, exogenous application of H2O2 abolished the N-acetyl-L: -cysteine (NAC)-induced decrease in G6PDH activity, and DPI suppressed the effect of buthionine sulfoximine (BSO) on induction of G6PDH activity. Western-blot analyses showed that G6PDH expression was stimulated by NaCl and H2O2, and blocked by DPI in DR callus. Taken together, G6PDH activity involved in GSH maintenance and H2O2 accumulation under salt stress. And H2O2 regulated G6PDH, GR, and GPX activities to maintain GSH levels. In the process, G6PDH plays a central role.
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PMID:Glucose-6-phosphate dehydrogenase plays a central role in modulating reduced glutathione levels in reed callus under salt stress. 1795 57

Cystathionine beta synthase deficiency induces hyperhomocysteinemia which is considered as a risk factor for vascular diseases. Studies underlined the importance of altered cellular redox reactions in hyperhomocysteinemia-induced vascular pathologies. Nevertheless, hyperhomocysteinemia also induces hepatic dysfunction which may accelerate the development of vascular pathologies by modifying cholesterol homeostasis. The aim of the present study was to analyze the modifications of redox state in the liver of heterozygous cystathionine beta synthase-deficient mice, a murine model of hyperhomocysteinemia. In this purpose, we quantified levels of reactive oxygen and nitrogen species and we assayed activities of main antioxidant enzymes. We found that cystathionine beta synthase deficiency induced NADPH oxidase activation. However, there was no accumulation of reactive oxygen (superoxide anion, hydrogen peroxide) and nitrogen (nitrite, peroxynitrite) species. On the contrary, hepatic hydrogen peroxide level was decreased independently of an activation of glutathione-dependent mechanisms. In fact, cystathionine beta synthase deficiency had no effect on glutathione peroxidase, glutathione reductase and glutathione S-transferase activities. However, we found a 50% increase in hepatic catalase activity without any variation of expression. These findings demonstrate that cystathionine beta synthase deficiency initiates redox disequilibrium in the liver. However, the activation of catalase attenuates oxidative impairments.
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PMID:Cystathionine beta synthase deficiency induces catalase-mediated hydrogen peroxide detoxification in mice liver. 1854 Nov 57

Zn phytotoxicity and its possible detoxifying responses in two ecotypes of Sedum alfredii Hance, i.e. hyperaccumulating ecotype (HE) and non-hyperaccumulating ecotype (NHE) were investigated. HE grew better with high Zn concentrations of 29.11gkg(-1) DW in shoots when exposed to 500microM Zn2+. Toxicity symptoms caused by Zn in root cells of both ecotypes mainly included plasmolysis, disruption of plasma membranes and increased cell vacuolation. At high supplied Zn concentration, chloroplasts suffered from structural disorganization in both ecotypes. Zn-induced hydrogen peroxide (H2O2) and superoxide radical (O(2)-) productions in leaves were determined by a histochemical method, which revealed that Zn stress may have involved NADPH oxidase, protein phosphatases and intracellular Ca2+ to activate the reactive oxygen species production. Inhibition of glutathione synthesis may have led to increased H2O2 and O(2)- accumulations in leaves of HE. In response to higher Zn concentrations, ascorbic acid significantly increased in both ecotypes and levels of glutathione increased in both leaves and roots of HE and in roots of NHE without any change in the leaves of NHE. The enzymatic activities like those of superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), guaiacol peroxidase (GPX, EC 1.11.1.7), ascorbate peroxidase (APX, EC 1.11.1.11), dehydroascorbate reductase (DHAR, EC 1.8.5.1), and glutathione reductase (GR, EC 1.6.4.2) in leaves of HE were all enhanced at supplied Zn concentration of 500microM, which may account for its better growth.
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PMID:Ultrastructural changes, zinc hyperaccumulation and its relation with antioxidants in two ecotypes of Sedum alfredii Hance. 1869 16

Abscisic acid (ABA) regulates the plant's adaptive responses to abiotic stresses. Over-expression of the 9-cis-epoxycarotenoid dioxygenase gene (SgNCED1) in the transgenic tobaccos increased ABA content and tolerance to drought and salt stresses. H2O2 and nitric oxide (NO) contents were enhanced in guard cells and mesophyll cells of the transgenic plants, accompanied with increased transcripts and activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX) and glutathione reductase (GR). The enhancements of H2O2 and NO and transcripts and activities of antioxidant enzymes in the transgenic plants were blocked by pre-treatments with inhibitor of ABA biosynthesis, scavengers of H2O2 and NO, and inhibitors of NADPH oxidase and NO synthase-like (NOS-like). The elevated production of NO in the transgenic plants was blocked by scavenger of H2O2 and inhibitors of NADPH oxidase, whereas H2O2 level was not affected by scavenger of NO and inhibitor of NOS-like, indicating that H2O2 is essential for the elevated production of NO. The results demonstrate that the increased drought and salt tolerance in the transgenic plants is associated with ABA-induced production of H2O2 via NADPH oxidase and NO via NOS-like, which sequentially induce transcripts and activities of SOD, CAT, APX and GR.
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PMID:Increased abscisic acid levels in transgenic tobacco over-expressing 9 cis-epoxycarotenoid dioxygenase influence H2O2 and NO production and antioxidant defences. 1918 89

Previously the authors have designed and synthesized a library of antioxidative glutathione analogues called UPF peptides which are superior to glutathione in hydroxyl radical elimination. This paper is a follow-up study which investigated the effects of the most promising members of the library (UPF1 and UPF17) on oxidative stress-related enzymes. At concentrations used in vivo experiments neither UPF peptide influenced the activity of glutathione peroxidase (GPx) when purified enzyme or erythrocyte lysate was used. At higher concentrations they inhibited GPx activity. UPF peptides had no effect on glutathione reductase (GR) activity. Also they, as well as glutathione itself, slightly increased MnSOD activity in human brain mitochondria and inhibited oxidative burst caused by neutrophil NAD(P)H oxidase. RT-PCR measurements showed that UPF1 and UPF17 have no effect on GPx and MnSOD expression level in human blood mononuclear cells. The results of this study confirm that investigated UPF peptides do not interfere with the enzymatic mechanisms of antioxidative defence and can be used as themselves or as a lead for the protector molecule design against excessive oxidative stress.
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PMID:Characterization of UPF peptides, members of the glutathione analogues library, on the basis of their effects on oxidative stress-related enzymes. 1942 27

Using in vitro systems, numerous authors have cited the sensitivity of pollen tube growth to high temperature as a major cause of low yields for crops with valuable reproductive structures. We investigated the hypothesis that in vivo fertilization efficiency would be negatively affected by heat stress-induced changes in energy reserves and calcium-mediated oxidative status in the pistil. Gossypium hirsutum plants exposed to optimal (30/20 degrees C) or high day temperature (38/20 degrees C) conditions during flowering were analyzed for fertilization efficiency via UV microscopic observation of pollen tube-containing ovules and for soluble carbohydrates, adenosine triphosphate (ATP), calcium, antioxidant enzyme activity and NADPH oxidase (NOX; EC 1.6.3.1) activity in the pistil. Leaf measurements included gas exchange, chlorophyll content, quantum efficiency and ATP content of the subtending leaf on the day of anthesis. In the pistil fertilization efficiency, soluble carbohydrates, ATP content and NOX activity declined significantly, whereas water soluble calcium and glutathione reductase (EC 1.8.1.7) activity increased, and superoxide dismutase (EC 1.15.1.1) activity remained unchanged. In leaves, heat stress decreased photosynthesis, quantum efficiency and chlorophyll content, but increased stomatal conductance. We conclude that decreased source leaf activity either inhibits pollen development, tube growth through the style or guidance to the ovules as a result of an insufficient energy supply to the developing pistil. We further conclude that a calcium-augmented antioxidant response in heat-stressed pistils interferes with enzymatic superoxide production needed for normal pollen tube growth and fertilization of the ovule.
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PMID:Heat stress-induced limitations to reproductive success in Gossypium hirsutum. 1965 31


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