Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Generation of reactive oxygen species by photosensitization is the corner stone of photodynamic therapy of tumors. Cell damage may be mediated by free radical species and lipid peroxidation of their membranes. The effects of oxygen active species (.OH and O(2)(.-) radicals) photogenerated by the novel photosensitizer m-chloroperbenzoic acid (m-CPBA) on human erythrocyte integrity and stability were studied. The biological toxicity of the reactive oxygen species on human red blood cells (RBCs) was evident by increased osmotic fragility, spherocytosis and haemolysis. The haemolysis was increased in concentration and time dependent manner. The lipid peroxidation product thiobarbituric acid reactive substances (TBARS) was elevated in m-CPBA photosensitized RBCs indicating increased oxidative stress. This was accompanied with a depletion of erythrocyte glutathione (GSH). These effects were blunted by hydroxyl radical scavengers, thiourea and mannitol, which might indicate the production of (.)OH radical by photosensitization with m-CPBA. The antioxidant enzyme activities such as superoxide dismutase (SOD), catalase (CAT), peroxidase (Px) and glutathione peroxidase (GSH-Px) were elevated in RBCs treated with m-CPBA in the presence and absence of hydroxyl radical scavengers, mannitol and thiourea. These results suggested that the main oxygen radical photogenerated from m-CPBA is O(2)(&z.rad;-) radical, which is transformed to (.)OH radical probably by hydrogen abstraction. This is probably the main damaging oxygen species and played an essential role in oxidative haemolysis mediated by peroxidation of membrane lipids of human erythrocytes. This study provides an investigational promising data for photodynamic therapy.
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PMID:Photosensitization induced reactive oxygen species and oxidative damage in human erythrocytes. 1096 Jul 65

To investigate the antioxidant defense system, chilling stress-induced changes of antioxidant enzymes were examined in the leaves of cucumber (Cucumis sativus L.). Chilling stress preferentially enhanced the activities of the superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR) and peroxidase specific to guaiacol, whereas it induced the decrease of catalase activity. In order to analyze the changes of antioxidant enzyme isoforms against chilling stress, foliar extracts were subjected to native PAGE. Leaves of cucumber had four isoforms of Mn-SOD and two isoforms of Cu/Zn-SOD. Fe-SOD isoform was not observed in this plant. Expression of Cu/Zn-SOD and Mn-SOD was preferentially enhanced by chilling stress. Expression of Mn-SOD-2 and -4 was enhanced after 48 h of the poststress period. Five APX isoforms were presented in the leaves of cucumber. The intensities of APX-4 and -5 were enhanced by chilling stress, whereas that of APX-3 was significantly increased in the poststress periods after chilling stress. Gel stained for GR activity revealed six isoforms in the plant. Activation levels for most of GR isoforms were higher in the stressed-plants than the control and poststressed-plants, but that of GR-1 isoform was significantly higher in the poststressed-plants than chilling stressed-plants. These results collectively suggest that chilling stress activates the enzymes of an SOD/ascorbate-glutathione cycle under catalase deactivation in the leaves of cucumber, but the response timing of enzyme isoforms against various environmental stresses is not the same for all isoforms of antioxidant enzymes.
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PMID:Chilling stress-induced changes of antioxidant enzymes in the leaves of cucumber: in gel enzyme activity assays. 1101 Oct 95

Three terrestrial plant species, oat (Avena sativa ), Chinese cabbage (Brassica campestris cv. chinensis) and lettuce (Lactuca sativa), were exposed to different concentrations of herbicide TCA (sodium trichloroacetate) in a growth test according to guideline OECD # 208. Classical (i.e. germination and biomass) and biochemical (i.e., antioxydant enzyme activities) endpoints were investigated. Germination rate decreased significantly at 3.9 mg TCA kg dry soil(-1) (for oat and lettuce) and 62.5 mg TCA kg dry soil(-1) (for Chinese cabbage). Biomass decreased significantly only at 1.9 mg TCA kg dry soil(-1) (for oat and lettuce) and 15.6 mg TCA kg dry soil(-1) (for Chinese cabbage). The activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), peroxidase (EC 1.11.1.7) and glutathione reductase (EC 1.6.4.2) increased significantly at the lowest concentration of TCA tested, i.e. 0.03 mg TCA kg dry soil(-1) (for oat and lettuce) and 0.48 mg TCA kg dry soil(-1) (for Chinese cabbage). Our results showed a ranking of sensitivity among the different endpoints for the three plant species: enzyme activities>biomass>germination rate. The increase in antioxidant enzyme activities observed in this study ensured the detoxification of increased levels of active oxygen species, and presumably prevented the plants from undergoing oxidative stress damage. Thus, the use of enzyme activities will permit the detection of early injury in plant growth testing.
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PMID:Classical and biochemical endpoints in the evaluation of phytotoxic effects caused by the herbicide trichloroacetate. 1106 42

There is an individual susceptibility to diabetic nephropathy, and oxidative stress is believed to play an important role in the pathogenesis of diabetic complications. Active oxygen species induce antioxidant enzyme expression in tissues, an effect considered to be a defensive mechanism. To test whether altered intracellular antioxidant enzyme production might explain the predisposition to diabetic nephropathy, we studied the effect of long-term (12 weeks) exposure to normal (5 mmol/l) or high (22 mmol/l) glucose concentrations on fibroblast antioxidant enzyme gene expression and protein activity in type 1 diabetic patients with and without nephropathy, nondiabetic nephropathic patients, and nondiabetic control subjects. Under conditions of normal glucose concentration in the culture media, CuZnSuperoxide-dismutase, MnSuperoxide-dismutase, catalase, and glutathione-peroxidase activity and mRNA expression were not different among the four groups. Under high-glucose conditions, CuZnSuperoxide-dismutase mRNA and activity increased similarly in all groups (P < 0.001 vs. basal), whereas MnSuperoxide-dismutase did not change. In contrast, catalase mRNA and activity as well as glutathione-peroxidase mRNA and activity increased in fibroblasts from type 1 diabetic patients without nephropathy (P < 0.001), in fibroblasts from nondiabetic nephropathic patients (P < 0.001), and in fibroblasts from nondiabetic control subjects (P < 0.001), but not in fibroblasts from type 1 diabetic patients with nephropathy. Exposure to high glucose concentrations significantly increased lipid peroxidation in cells, higher levels being found in cells from diabetic patients with nephropathy (P < 0.001). These data, while confirming that exposure to high glucose concentrations induces an antioxidant defense in skin fibroblasts from normal subjects, demonstrate a failure of this defensive mechanism in cells from type 1 diabetic patients with nephropathy, whereas skin fibroblasts from diabetic patients without complications or from nondiabetic nephropathic patients have an intact antioxidant response to glucose-induced oxidative stress.
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PMID:Defective intracellular antioxidant enzyme production in type 1 diabetic patients with nephropathy. 1111 22

We have previously demonstrated that the loss of glutathione (GSH) and GSH-peroxidase (GSH-PX) in banked red blood cells (RBCs) is accompanied by oxidative modifications of lipids, proteins and loss of membrane integrity. The objective of this study was to determine whether artificial increases in antioxidant (GSH) or antioxidant enzyme (catalase) content could protect membrane damage in the banked RBCs following an oxidant challenge. RBCs stored at 1-6 degrees C for 0, 42 and 84 days in a conventional additive solution (Adsol) were subjected to oxidative stress using ferric/ascorbic acid (Fe/ASC) before and after enriching them with GSH or catalase using a hypotonic lysis-isoosmotic resealing procedure. This lysis-resealing procedure in the presence of GSH/catalase raised intracellular GSH and catalase concentrations 4-6 fold, yet produced only a small reduction in mean cell volume (MCV), mean cell hemoglobin (MCH) and mean cell hemoglobin concentrations (MCHC). Indicators of oxidative stress and membrane integrity were measured, including acetylcholinesterase (AChE) activity, GSH concentration, phosphatidylserine (PS) externalization (prothrombin-converting activity) and transmembrane lipid movements (14C-lyso phosphatidylcholine flip-flop and PS transport). GSH-enrichment protected AChE activity in fresh (0 day) and stored (42 and 84 days) RBCs from Fe/ASC oxidation by 10, 23 and 26%, respectively, compared with not-enriched controls. Following oxidative stress, the rate of transbilayer lipid flip-flop did not increase in fresh cells, but increased 9.3% in 42-day stored cells. Phosphatidylserine exposure, as measured by prothrombinase activity, increased 2.4-fold in fresh and 5.2-fold in 42-day stored cells exposed to Fe/ASC. Previous studies have shown that 42-day storage causes a moderate decrease in PS transport (approximately 50%), whereas transport rates declined by up to 75% in stored RBCs when challenged with Fe/ASC. GSH-enrichment prevented the increase in passive lipid flip-flop and the increase in prothrombinase activity, but offered no protection against oxidative damage of PS transport. In contrast to these effects, catalase-enrichment failed to protect GSH levels and AChE activity upon oxidative stress. Membrane protein thiol oxidation was assessed by labeling reactive protein thiols with 5-acetalamidofluorescein followed by immunoblotting with antifluorescein antibodies. Significant oxidation of membrane proteins was confirmed by a greater loss of thiols in stored RBCs than in fresh RBCs. These results demonstrate that it may be possible to prevent storage-mediated loss of AChE, increased lipid flip-flop, and increased PS exposure, by maintaining or increasing GSH levels of banked RBCs.
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PMID:Glutathione loading prevents free radical injury in red blood cells after storage. 1120 85

The role of abscisic acid (ABA) in the signal transduction pathway associated with NaCl-induced up-regulation of antioxidant enzyme activity was examined in a NaCl-tolerant cotton callus cell line treated with NaCl, ABA, paraquat, or H2O2 in the presence and absence or fluridone, an inhibitor of terpene, and therefore, ABA synthesis. Treatment with NaCl resulted in a rapid increase (within 30 minutes) in the ABA levels of the callus tissue, and the NaCl, ABA, and paraquat treatments induced rapid increases in the activities of superoxide dismutase, catalase, peroxidase, and glutathione reductase. Pre-treatment with fluridone significantly suppressed the NaCl-induced increases, but only slightly delayed the increases in tissue subjected to exogenous ABA treatment. This implies that ABA is involved in the signal transduction pathway associated with the NaCl-induced up-regulation of these antioxidant enzymes. Pre-treatment with fluridone had no effect on the paraquat-induced increases, suggesting that these enzymes can also be up-regulated by a pathway other than the one mediated by ABA. Both the NaCl and paraquat treatments produced significant increases in the superoxide levels within the callus, but the increase resulting from the paraquat treatment was significantly higher than the increase resulting from the NaCl treatment. These data suggest that NaCl stress results in the production of reactive oxygen intermediates (ROI) which signals the induction of an ABA-dependent signaling pathway. The production of very high levels of ROI, such as those that occur with paraquat treatment or perhaps during periods of prolonged or extreme stress, may induce an ABA-independent signaling pathway.
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PMID:Involvement of abscisic acid-dependent and -independent pathways in the upregulation of antioxidant enzyme activity during NaCl stress in cotton callus tissue. 1120 86

Sunflower (Helianthus annuus L. cv. SH222) plants and calli were exposed to KCl stress for three weeks. Calli were more tolerant to KCl than plants. KCl stress decreased NO(-)(3), Mn, Fe and B levels in whole plants and P, Ca and Mg in shoots. NO(-)(3), P, Ca, Mg, Mn, and B levels decreased in 100 mM-stressed calli. Chlorophyll content, F:(m) and (F:(m)-F:(0))/F:(m) ratio decreased in stressed leaves, while F:(0) increased only in leaves exposed to severe stress (100 and 150 mM). Membrane permeability and lipid peroxidation increased in plants under all stress conditions and in 100 and 150 mM stressed calli, but remained unchanged in 25 mM stressed calli. Salt stress also induced changes relating to antioxidant enzymes: plants under all stress conditions showed a decrease in catalase, peroxidase and SOD activities. Calli under moderate stress (25 mM KCl) showed an increase of catalase, peroxidase and SOD activities, but the activities of peroxidase and SOD decreased when calli were exposed to higher KCl concentrations. The decrease of antioxidant enzyme activities is in tune with lipid peroxidation and membrane permeability increases. On the other hand, calli adapted for 6 months to 100 mM KCl showed an increase of these enzyme activities compared to unstressed calli, while MDA production and membrane permeability were not significantly affected.
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PMID:In situ and in vitro senescence induced by KCl stress: nutritional imbalance, lipid peroxidation and antioxidant metabolism. 1128 80

Mangroves have been observed to possess a tolerance to high levels of heavy metals, yet accumulated metals may induce subcellular biochemical changes, which can impact on processes at the organism level. Six month-old seedlings of the grey mangrove, Avicennia marina (Forsk.) Vierh, were exposed to a range of Cu (0-800 micrograms/g), Pb (0-800 micrograms/g) and Zn (0-1000 micrograms/g) concentrations in sediments under laboratory conditions, to determine leaf tissue metal accumulation patterns, effects on photosynthetic pigments (chlorophyll a, chlorophyll b and carotenoids), and the activity of the antioxidant enzyme peroxidase. Limited Cu uptake to leaves was observed at low sediment Cu levels, with saturation and visible toxicity to Cu at sediment levels greater than 400 micrograms/g. Leaf Pb concentrations remained low over a range of Pb sediment concentrations, up to 400 micrograms/g Pb, above which it appeared that unrestricted transport of Pb occurred, although no visible signs of Pb toxicity were observed. Zn was accumulated linearly with sediment zinc concentration, and visible toxicity occurring at the highest concentration, 1000 micrograms/g Zn. Significant increases in peroxidase activity and decreases in photopigments were found with Cu and Zn at concentrations lower than those inducing visible toxicity. Significant increases in peroxidase activity only, were found when plants were exposed to Pb. Positive linear relationships between peroxidase activity and leaf tissue metal concentrations were found for all metals. Significant linear decreases in photosynthetic pigments with increasing leaf tissue metal concentrations were observed with Cu and Zn only. Photosynthetic pigments and peroxidase activity may be applicable as sensitive biological indicators of Cu and Zn stress, and peroxidase activity for Pb stress in A. marina.
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PMID:Photosynthetic pigments and peroxidase activity as indicators of heavy metal stress in the Grey mangrove, Avicennia marina (Forsk.) Vierh. 1138 78

In order to investigate the relations of iodine deficiency and/or goiter with selenium (Se) and antioxidant enzyme (AOE) status, we determined the relevant parameters of goitrous high school children living in an endemic goiter area of Turkey. Subjects were selected by a simple random sampling technique after screening the whole population of the high schools of two towns by neck palpation. The results of the goitrous group (n = 48, aged 15-18 yr) were compared with those of nongoitrous control children (n = 49) from the same populations, and with an outside control group (n = 24) from a lower-goiter-prevalence area. The overall prevalence of goiter was 39.6% in the high school population of the area. Activities of erythrocyte AOE (glutathion peroxidase, catalase, and superoxide dismutase) and concentrations of plasma and erythrocyte Se and urinary iodine were found to be significantly lower in goitrous children than both in-region and out-region of the control groups. When the whole study group was reclassified according to the severity of iodine deficiency, it was found that the AOE and Se status of those control children without goiter but with high iodine deficiency was significantly higher than goitrous children, although they did not differ from nondeficient control group. This might be the result of the possibility that goitrous children are exposed of oxidative stress, which may introduce alterations to the antioxidant defense system and/or the antioxidant status is relatively lower in goitrous children than those children who are highly iodine-deficient but did not develop goiter. The results of this study seem to support the view that the risk of goiter development may be higher in highly iodine-deficient children with lower enzymatic antioxidant and Se status.
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PMID:Status of selenium and antioxidant enzymes of goitrous children is lower than healthy controls and nongoitrous children with high iodine deficiency. 1169 77

Recently, we have reported that erythropoietin (Epo) provides neuroprotection in 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP)-induced neurotoxicity in vivo. In the present study, we investigated the effects of single Epo administration on brain antioxidant enzyme (superoxide dismutase (SOD) and glutathion peroxidase (GSHPx)) activities in this model in C57BL/6 mice. We found that MPTP treatment decreased GSHPx activity in both substantia nigra and striatum, and Epo restores nigral GSHPx activity decreased by MPTP. SOD enzyme activity was not significantly changed by MPTP and Epo treatment. Further, Epo stimulated astroglial GSHPx production in neonatal murine astroglial cell culture suggesting that the possible cell source for the stimulation of GSHPx activity by Epo in the MPTP-induced neurotoxicity model are astroglia. In conclusion, modulation of the astroglial antioxidant defense system might be one of the mechanisms by which Epo exerts a beneficial effect in MPTP-induced Parkinsonism.
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PMID:Erythropoietin restores glutathione peroxidase activity in 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine-induced neurotoxicity in C57BL mice and stimulates murine astroglial glutathione peroxidase production in vitro. 1187 60


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