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Dismutase
Kinds of Dismutase Terms modified by Dismutase Selected AbstractsCadmium Enhances Generation of Hydrogen Peroxide and Amplifies Activities of Catalase, Peroxidases and Superoxide Dismutase in MaizeJOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 1 2008P. Kumar Abstract Maize (Zea mays L. cv. 777) plants grown in hydroponic culture were treated with 50 ,m CdSO4. Growth and metabolic parameters indicative of oxidative stress and antioxidant responses were studied in leaves of plants treated with Cd. Apart from increasing lipid peroxidation and H2O2 accumulation, supply of Cd suppressed growth, fresh and dry mass of plants and decreased the concentrations of chloroplastic pigments. The activities of catalase (CAT; EC 1.11.1.6), peroxidase (POD; EC 1.11.1.7), ascorbate peroxidase (APX; EC 1.11.1.11) and superoxide dismutase (SOD; EC 1.15.1.1) were increased in plants supplied 50 ,m Cd. Localization of activities of isoforms of these enzymes (POD, APX and SOD) on native gels also revealed increase in the intensities of pre-existing bands. Stimulated activities of CAT, POD, APX and SOD in maize plants supplied excess Cd do not appear to have relieved plants from excessive generation of reactive oxygen species (ROS). It is, therefore, concluded that supply of 50 ,m Cd induces oxidative stress by increasing production of ROS despite increased antioxidant protection in maize plants. [source] Trends of Superoxide Dismutase and Soluble Protein of Aquatic Plants in Lakes of Different Trophic Levels in the Middle and Lower Reaches of the Yangtze River, ChinaJOURNAL OF INTEGRATIVE PLANT BIOLOGY, Issue 4 2009Ai-Ping Wu Abstract A limnological study was carried out to determine the responses of superoxide dismutase (SOD) activities and soluble protein (SP) contents of 11 common aquatic plants to eutrophication stress. Field investigation in 12 lakes in the middle and lower reaches of the Yangtze River was carried out from March to September 2004. Our results indicated that non-submersed (emergent and floating-leafed) plants and submersed plants showed different responses to eutrophication stress. Both SOD activities of the non-submersed and submersed plants were negatively correlated with their SP contents (P < 0.000 1). SP contents of non-submersed plants were significantly correlated with all nitrogen variables in the water (P < 0.05), whereas SP contents of submersed plants were only significantly correlated with carbon variables as well as ammonium and Secchi depth (SD) in water (P < 0.05). Only SOD activities of submersed plants were decreased with decline of SD in water (P < 0.001). Our results indicate that the decline of SOD activities of submersed plants were mainly caused by light limitation, this showed a coincidence with the decline of macrophytes in eutrophic lakes, which might imply that the antioxidant system of the submersed plants were impaired under eutrophication stress. [source] Bienzymatic Supramolecular Complex of Catalase Modified with Cyclodextrin-Branched Carboxymethylcellulose and Superoxide Dismutase: Stability and Anti-Inflammatory PropertiesMACROMOLECULAR BIOSCIENCE, Issue 1 2007Aymara Valdivia Abstract A bienzymatic supramolecular assembly of CAT and SOD is reported. CAT was chemically glycosilated with CD branched CMC and then associated with SOD modified with 1-adamantane carboxylic acid. SOD was remarkably resistant to inactivation by H2O2 and its anti-inflammatory activity was 4.5-fold increased after supramolecular association with the modified CAT form. [source] Level of Superoxide Dismutase, Glutathione Peroxidase and Uric Acid in Thioacetamide-Induced Cirrhotic RatsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2 2002H. ABUL Levels of superoxide dismutase and glutathione peroxidase were determined in blood and hepatic tissues of thioacetamide-induced cirrhotic rats and compared to levels in age-matched control animals. The plasma level of uric acid was also determined in these animals. A general decrease was noticed in the level of all the antioxidants examined as compared to the control. This decrease was statistically significant in the level of all the antioxidants studied, except for the level of superoxide dismutase in blood. A decrease in the antioxidant level may indicate an increase in free radical level and thereby an increase in cellular damage in cirrhotic rats. The changes in the level of antioxidants showed a direct correlation with the changes in the level of trace elements observed in our previous studies. These studies suggest that antioxidants alone or in combination with trace elements may have beneficial effects in treating liver cirrhosis. [source] Serum Copper/Zinc Superoxide Dismutase (Cu/Zn SOD) and Gastric Cancer Risk: a Case-Control StudyCANCER SCIENCE, Issue 10 2002Yingsong Lin We conducted a case-control study to evaluate the association between serum levels of copper/zinc superoxide dismutase (Cu/Zn SOD) and the risk of gastric cancer. Cases were 214 patients who had been diagnosed with gastric cancer and controls were 120 persons who underwent medical checkups. Serum levels of Cu/Zn SOD were determined by enzyme-linked immunosorbent assay (ELISA). Compared with the lowest quartile, the OR (odds ratio) was 4.54 (95% CI (confidence interval), 1.62,12.66) for the third quartile and 15.75 (95% CI, 5.84,42.46) for the highest quartile. With both early and advanced cancers, as well as with the intestinal and diffuse types, a significant increase in risk was observed with increasing levels of serum Cu/Zn SOD. Our case-control study showed that serum levels of Cu/Zn SOD were significantly elevated in gastric cancer patients compared with apparently healthy controls, and higher Cu/Zn SOD levels may be associated with an increased risk of gastric cancer. [source] New Insight into the Mode of Action of Nickel Superoxide Dismutase by Investigating Metallopeptide Substrate ModelsCHEMISTRY - A EUROPEAN JOURNAL, Issue 2 2009Daniel Tietze M. Abstract For the first time, the existence of a substrate adduct of a nickel superoxide dismutase (NiSOD) model, based on the first nine residues from the N terminus of the active form of Streptomyces coelicolor NiSOD, has been proven and the adduct has been isolated. This adduct is based on the cyanide anion (CN,), as a substrate analogue of the superoxide anion (O2.,), and the nickel metallopeptide H-HCDLPCGVY-NH2 -Ni. Spectroscopic studies, including IR, UV/Vis, and liquid- and solid-state NMR spectroscopy, show a single nickel-bound cyanide anion, which is embedded in the metallopeptide structure. This complex sheds new light on the question of whether the mode of action of the NiSOD enzyme is an inner- or outer-sphere mechanism. Whereas discussion was previously biased in favor of an outer-sphere electron-transfer mechanism due to the fact that binding of cyanide or azide moieties to the nickel active site had never been observed, our results are a clear indication in favor of the inner-sphere electron-transfer mechanism for the disproportionation of the O2., ion, whereby the substrate is attached to the Ni atom in the active site of the NiSOD. [source] Zinc diethyldithiocarbamate allergenicity: potential haptenation mechanismsCONTACT DERMATITIS, Issue 2 2008Itai Chipinda Background:, Zinc diethyldithiocarbamate (ZDEC) and its disulfide, tetraethylthiuram disulfide (TETD), are rubber accelerators and contact allergens that cross-react in some individuals. Objective:, This study explored potential protein haptenation mechanisms of ZDEC and its oxidation products. Methods:, ZDEC oxidation/reduction products and sites of protein binding were assessed using high-performance liquid chromatography and mass spectrometry. The murine local lymph node assay (LLNA) was employed to probe haptenation mechanisms of ZDEC by examining its allergenicity along with its oxidation products and through elimination of oxidation and chelation mechanisms by substituting cobalt for zinc [cobalt (II) dithiocarbamate, CoDEC]. Results:, Oxidation of ZDEC by hypochlorous acid (bleach, HOCl), iodine, or hydrogen peroxide resulted in production of TETD, tetraethylthiocarbamoyl disulfide, and tetraethyldicarbamoyl disulfide (TEDCD). Albumin thiols reduced TETD with subsequent mixed disulfide formation/haptenation. ZDEC directly chelated the copper ion on the active site of the superoxide dismutase, whereas CoDEC did not bind to Cu proteins or form mixed disulfides with free thiols. ZDEC, sodium diethyldithiocarbamate, TEDCD, and TETD were all positive in the LLNA except CoDEC, which was non-allergenic. Conclusion:, The thiol is the critical functional group in ZDEC's allergenicity, and haptenation is predominantly through chelation of metalloproteins and formation of mixed disulfides. [source] Reactive oxygen species in rostral ventrolateral medulla modulate cardiac sympathetic afferent reflex in ratsACTA PHYSIOLOGICA, Issue 4 2009M.-K. Zhong Abstract Aim:, The aim of the present study was to investigate whether reactive oxygen species (ROS) in rostral ventrolateral medulla (RVLM) modulate cardiac sympathetic afferent reflex (CSAR) and the enhanced CSAR response caused by microinjection of angiotensin II (Ang II) into the paraventricular nucleus (PVN). Methods:, Under urethane and ,-chloralose anaesthesia, renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the RSNA response to epicardial application of capsaicin (1.0 nmol). Results:, Bilateral RVLM microinjection of tempol (a superoxide anion scavenger) or polyethylene glycol-superoxide dismutase (PEG-SOD, an analogue of endogenous superoxide dismutase) attenuated the CSAR, but did not cause significant change in baseline RSNA and MAP. NAD(P)H oxidase inhibitors apocynin or phenylarsine oxide (PAO) also showed similar effects, but SOD inhibitor diethyldithio-carbamic acid (DETC) enhanced the CSAR and baseline RSNA, and increased the baseline MAP. Bilateral PVN microinjection of Ang II (0.3 nmol) enhanced the CSAR and increased RSNA and MAP, which was inhibited by the pre-treatment with RVLM administration of tempol, PEG-SOD, apocynin or PAO. The pre-treatment with DETC in the RVLM only showed a tendency in potentiating the CSAR response of Ang II in the PVN, but significantly potentiated the RSNA and MAP responses of Ang II. Conclusion:, These results suggest that the NAD(P)H oxidase-derived ROS in the RVLM modulate the CSAR. The ROS in the RVLM is necessary for the enhanced CSAR response caused by Ang II in the PVN. [source] Vascular endothelial growth factor prevents G93A-SOD1-induced motor neuron degenerationDEVELOPMENTAL NEUROBIOLOGY, Issue 13 2009J. Simon Lunn Abstract Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disorder characterized by selective loss of motor neurons (MNs). Twenty percent of familial ALS cases are associated with mutations in Cu2+/Zn2+ superoxide dismutase (SOD1). To specifically understand the cellular mechanisms underlying mutant SOD1 toxicity, we have established an in vitro model of ALS using rat primary MN cultures transfected with an adenoviral vector encoding a mutant SOD1, G93A-SOD1. Transfected cells undergo axonal degeneration and alterations in biochemical responses characteristic of cell death such as activation of caspase-3. Vascular endothelial growth factor (VEGF) is an angiogenic and neuroprotective growth factor that can increase axonal outgrowth, block neuronal apoptosis, and promote neurogenesis. Decreased VEGF gene expression in mice results in a phenotype similar to that seen in patients with ALS, thus linking loss of VEGF to the pathogenesis of MN degeneration. Decreased neurotrophic signals prior to and during disease progression may increase MN susceptibility to mutant SOD1-induced toxicity. In this study, we demonstrate a decrease in VEGF and VEGFR2 levels in the spinal cord of G93A-SOD1 ALS mice. Furthermore, in isolated MN cultures, VEGF alleviates the effects of G93A-SOD1 toxicity and neuroprotection involves phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling. Overall, these studies validate the usefulness of VEGF as a potential therapeutic factor for the treatment of ALS and give valuable insight into the responsible signaling pathways and mechanisms involved. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source] Oxidative stress, nitric oxide, and the mechanisms of cell death in Lurcher Purkinje cellsDEVELOPMENTAL NEUROBIOLOGY, Issue 8 2007Rebecca McFarland Abstract Oxidative stress is postulated to play a role in cell death in many neurodegenerative diseases. As a model of neonatal neuronal cell death, we have examined the role of oxidative stress in Purkinje cell death in the heterozygous Lurcher mutant (+/Lc). Lurcher is a gain of function mutation in the ,2 glutamate receptor (GluR,2) that turns the receptor into a leaky membrane channel, resulting in chronic depolarization of +/Lc Purkinje cells starting around the first week of postnatal development. Virtually, all +/Lc Purkinje cells die by the end of the first postnatal month. To investigate the role of oxidative stress in +/Lc Purkinje cell death, we have examined nitric oxide synthase (NOS) activity and the expression of two markers for oxidative stress, nitrotyrosine and manganese super oxide dismutase (MnSOD), in wild type and +/Lc Purkinje cells at P10, P15, and P25. The results show that NOS activity and immunolabeling for nitrotyrosine and MnSOD are increased in +/Lc Purkinje cells. To determine whether peroxynitrite formation is a prerequisite for +/Lc Purkinje cell death, +/Lc mutants were crossed with an ,-nNOS knockout mutant (nNOS,,/,) to reduce the production of NO. Analysis of the double mutants showed that blocking ,-nNOS expression does not rescue +/Lc Purkinje cells. However, we present evidence for sustained NOS activity and nitrotyrosine formation in the GluR,2+/Lc:nNOS,/, double mutant Purkinje cells, which suggests that the failure to rescue GluR,2+/Lc:nNOS,/, Purkinje cells may be explained by the induction of alternative nNOS isoforms. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007. [source] Advanced glycation end products-induced apoptosis attenuated by PPAR, activation and epigallocatechin gallate through NF-,B pathway in human embryonic kidney cells and human mesangial cellsDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 5 2010Yao-Jen Liang Abstract Background Diabetic nephropathy has attracted many researchers' attention. Because of the emerging evidence about the effects of advanced glycation end products (AGEs) and receptor of AGE (RAGE) on the progression of diabetic nephropathy, a number of different therapies to inhibit AGE or RAGE are under investigation. The purpose of the present study was to examine whether peroxisome proliferator-activated receptor , (PPAR,) agonist (L-165041) or epigallocatechin gallate (EGCG) alters AGE-induced pro-inflammatory gene expression and apoptosis in human embryonic kidney cells (HEK293) and human mesangial cells (HMCs). Methods The HEK cells and HMC were separated into the following groups: 100 µg/mL AGE alone for 18 h; AGE treated with 1 µM L-165041 or 10 µM EGCG, and untreated cells. Inflammatory cytokines, nuclear factor-,B pathway, RAGE expression, superoxide dismutase and cell apoptosis were determined. Results AGE significantly increased tumour necrosis factor-, (TNF-,), a major pro-inflammatory cytokine. The mRNA and protein expression of RAGE were up-regulated. These effects were significantly attenuated by pre-treatment with L-165041 or EGCG. AGE-induced nuclear factor-,B pathway activation and both cells apoptosis were also inhibited by L-165041 or EGCG. Furthermore, both L-165041 and EGCG increased superoxide dismutase levels in AGE-treated HEK cells and HMC. Conclusions This study demonstrated that PPAR, agonist and EGCG decreased the AGE-induced kidney cell inflammation and apoptosis. This study provides important insights into the molecular mechanisms of EGCG and PPAR, agonist in attenuation of kidney cell inflammation and may serve as a therapeutic modality to treat patients with diabetic nephropathy. Copyright © 2010 John Wiley & Sons, Ltd. [source] Protective effect of CPUX1, a progesterone, on hydrogen peroxide-induced oxidative damage in PC12 cells,DRUG DEVELOPMENT RESEARCH, Issue 8 2008Bian-sheng Ji Abstract The protective effect of CPUX1, a novel progesterone analog, on hydrogen peroxide (H2O2)-induced oxidative damage was investigated in rat pheochromocytoma (PC12) cells. Following the exposure of PC12 cells to H2O2, there was a reduction in cell survival and activities of superoxide dismutase (SOD) and mitochondrial membrane potential (MMP) accompanied by increased levels of lactate dehydrogenase (LDH) release, malondialdehyde (MDA) production, and intracellular reactive oxygen species (ROS) and intracellular [Ca2+]i levels. Preincubation of cells with CPUX1 prior to H2O2 exposure attenuated all these changes mentioned and had a protective effect against H2O2 -induced toxicity in PC12 cells, indicating that the compound may have potential therapeutic benefit for CNS disorders influenced by oxidative damage. Drug Dev Res 69: 2008 ©2008 Wiley-Liss, Inc. [source] Glutathione Peroxidase-Based Amperometric Biosensor for the Detection of S -NitrosothiolsELECTROANALYSIS, Issue 21 2006Mustafa Musameh Abstract A new biosensor is described for the detection of S -nitrosothiols (RSNOs) based on their decomposition by immobilized glutathione peroxidase (GPx), an enzyme containing selenocysteine residue that catalytically produces nitric oxide (NO) from RSNOs. The enzyme is entrapped at the distal tip of a planar amperometric NO sensor. The new biosensor shows good sensitivity, linearity, reversibility, and response times towards various RSNO species in PBS buffer, pH,7.4 . In most cases, the response time is less than 5,min, and the response is linear up to 6 ,M of the tested RSNO species. The lowest detection limit is obtained for S -nitrosocysteine (CysNO), at approx. 0.2,,M. The biosensor's sensitivity is not affected by the addition of EDTA as a chelating agent; an advantage over other potential catalytic enzymes that contain copper ion centers, such as CuZn-superoxide dismutase and xanthine oxidase. However, lifetime of the new sensor is limited, with sensitivity decrease of 50% after two days of use. Nonetheless, the new amperometric GPx based RSNO sensor could prove useful for detecting relative RSNO levels in biological samples, including whole blood. [source] Monitoring of protein profiles for the optimization of recombinant fermentation processes using public domain databasesELECTROPHORESIS, Issue 1-2 2003Karin Dürrschmid Abstract The expression of human superoxide dismutase in fed-batch fermentation of E. coli HMS174(DE3)(pET3ahSOD) was studied as model system. Due to the frequently used strong T7 promoter system a high metabolic load is exerted, which triggers stress response mechanisms and finally leads to the differentiation of the host cell. As a consequence, host cell metabolism is partly shifted from growth to survival accompanied by significant alterations of the protein pattern. In terms of process optimization two-dimensional electrophoresis deserves as a powerful tool to monitor these changes on protein level. For the analysis of samples derived from different states of recombinant protein production wide-range Immobiline Dry Strips pH 3,10 were used. In order to establish an efficient procedure for accelerated process optimization and to avoid costly and time-consuming analysis like mass spectrometry (MS), a database approach for the identification of significant changes of the protein pattern was evaluated. On average, 935 spots per gel were detected, whereby 50 are presumably stress-relevant. Out of these, 24 proteins could be identified by using the SWISS-2DPAGE database (www.expasy.ch/ch2d/). The identified proteins are involved in regulatory networks, energy metabolism, purine and pyrimidine nucleotide synthesis and translation. By this database approach, significant fluctuations of individual proteins in relation to recombinant protein production could be identified. Seven proteins show strong alterations (>100%) directly after induction and can therefore be stated as reliable marker proteins for the assessment of stress response. For distinctive interpretation of this highly specific information, a bioinformatic and statistic tool would be essential in order to perceive the role and contribution of individual proteins in stress response. [source] Comparative mutagenic effects of structurally similar flavonoids quercetin and taxifolin on tester strains Salmonella typhimurium TA102 and Escherichia coli WP-2 uvrAENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 6 2009Patrudu S. Makena Abstract Quercetin (QT) and Taxifolin (TF) are structurally similar plant polyphenols. Both have been reported to have therapeutic potential as anti-cancer drugs and antioxidants. Mutagenic effects of QT and TF were evaluated using Salmonella typhimurium TA102 and Escherichia coli WP-2 uvrA tester strains. Either in the presence or absence of S9 mix, QT was mutagenic to TA102 and WP2 uvrA. However, the mutagenicity of QT was significantly enhanced in the presence of S9 mix. Likewise, in the presence of Iron (Fe2+) and NADPH generating system (NGS) and absence of S9 mix, QT induced significantly high mutations in both TA102 and WP-2 uvrA. Mutagenicity of QT decreased in both strains in the presence of Iron (Fe2+) or NGS alone. TF was not mutagenic in the presence or absence of S9 mix in both TA102 and WP-2 uvrA 2, regardless of the presence of iron or NGS. Incorporation of antioxidants (ascorbate, superoxide dismutase (SOD), catalase (CAT)) and/or iron chelators (desferroxamine (DF) and ethylenediamine-tetraacetate (EDTA)) in the test systems markedly decreased QT-induced mutations in both tester strains. These results suggest that QT but not TF, could induce mutations in the presence or absence of rat liver S9 or Iron (Fe2+) and NGS in both tester strains by redox cycling and Fenton reactions to produce oxygen free radicals. Our results indicate that a minor structural variation between the two plant polyphenols could elicit a marked difference in their genotoxicities. These results provide a basis for further study into the potential use of QT in combination with iron supplements. Environ. Mol. Mutagen. 2009. © 2009 Wiley-Liss, Inc. [source] Evidence that 4-aminobiphenyl, benzidine, and benzidine congeners produce genotoxicity through reactive oxygen speciesENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 5 2007Patrudu S. Makena Abstract 4-Aminobyphenyl (4-Ab), benzidine (Bz), and Bz congeners were evaluated for their ability to induce genotoxicity through an oxidative mechanism. The mutagenicity of these compounds was tested in the presence and absence of Aroclor 1254-induced rat S9 mix using Salmonella typhimurium tester strain TA102, which is sensitive to agents producing reactive oxygen species (ROS). In the presence of S9, 4-Ab, Bz, N -acetyl-benzidine, and 3,3,-dimethoxybenzidine were strongly mutagenic in TA102, whereas, 3,3,,5,5,-tetra-methylbenzidine, 3,3,-dimethylbenzidine (O -tolidine), and N,N,-diacetylbenzidine were not mutagenic. In addition, 3,3,-dichlorobenzidine and 4,4,-dinitro-2-biphenylamine were directly mutagenic in TA102. Incorporation of the free radical and metal scavengers, catalase, superoxide dismutase (SOD), butylated hydroxytolune (BHT), and ethylenediamine tetraacetic acid (EDTA) reduced the mutagenic responses of 4-Ab and Bz, whereas heat-inactivated catalase and SOD had no effect. 4-Ab and Bz also induced lipid peroxidation in the presence of S9 mix as shown using the thiobarbituric acid reactive substances assay. The results of this study indicate that 4-Ab and Bz induce mutations through the induction of ROS. Environ. Mol. Mutagen., 2007. © 2007 Wiley-Liss, Inc. [source] Evaluation of the radioprotective effect of Liv 52 in miceENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 7 2006Ganesh C. Jagetia Abstract Liv 52 is a mixture of botanicals that is used clinically to treat various hepatic disorders. In this study, the radioprotective activity of Liv 52 was evaluated in mice given whole-body exposure to different doses of ,-radiation. In addition, a series of studies was conducted to explore the mechanism of radioprotection. Radioprotection was evaluated by the ability of Liv 52 to reduce both the frequency of bone marrow micronucleated erythrocytes and the lethality produced by 60Co ,-radiation. Mice were treated by oral gavage once daily for seven consecutive days with 500 mg/kg body weight Liv 52 or carboxymethylcellulose vehicle prior to radiation. Micronucleated polychromatic erythrocytes (MPCEs), micronucleated normochromatic erythrocytes (MNCEs), and the PCE/NCE ratio were measured at 0.25,14 days after exposure to whole-body radiation doses of 0, 0.5, 1.5, 3.0, or 4.5 Gy; animal survival was monitored after doses of 7, 8, 9, 10, 11, or 12 Gy. Pretreatment of mice with Liv 52 significantly reduced the frequency of radiation-induced MPCEs and MNCEs. Irradiation reduced the PCE/NCE ratio in a dose-related manner for up to 7 days following irradiation; Liv 52 pretreatment significantly mitigated against these reductions. Liv 52 treatment also reduced the symptoms of radiation sickness and increased mouse survival 10 and 30 days after irradiation. Liv 52 pretreatment elevated the levels of reduced glutathione (GSH), increased the activities of glutathione transferase, GSH peroxidase, GSH reductase, superoxide dismutase, and catalase, and lowered lipid peroxidation (LPx) and the activities of alanine amino transferase and aspartate aminotransferase 30 min after exposure to 7 Gy of ,-radiation. Liv 52 pretreatment also reduced radiation-induced LPx and increased GSH concentration 31 days following the exposure. The results of this study indicate that pretreatment with Liv 52 reduces the genotoxic and lethal effects of ,-irradiation in mice and suggest that this radioprotection may be afforded by reducing the toxic effects of the oxidative products of irradiation. Environ Mol. Mutagen., 2006. © 2006 Wiley-Liss, Inc. [source] Bentazon triggers the promotion of oxidative damage in the Portuguese ricefield cyanobacterium Anabaena cylindrica: Response of the antioxidant systemENVIRONMENTAL TOXICOLOGY, Issue 5 2010Victor Galhano Abstract Rice fields are frequently exposed to environmental contamination by herbicides and cyanobacteria, as primary producers of these aquatic ecosystems, are adversely affected. Anabaena cylindrica is a cyanobacterium with a significantly widespread occurrence in Portuguese rice fields. This strain was studied throughout 72 h in laboratory conditions for its stress responses to sublethal concentrations (0.75,2 mM) of bentazon, a selective postemergence herbicide recommended for integrated weed management in rice, with special reference to oxidative stress, role of proline and intracellular antioxidant enzymes in herbicide-induced free radicals detoxification. Activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione S -transferase (GST) increased in a time- and herbicide dose-response manner and were higher than those in the control samples after 72 h. A time- and concentration-dependent increase of malondialdehyde (MDA) levels and the enhanced cell membrane leakage following bentazon exposure are indicative of lipid peroxidation, free radicals formation, and oxidative damage, while increased amounts of SOD, CAT, APX, GST, and proline indicated their involvement in free radical scavenging mechanisms. The appreciable decline in the reduced glutathione (GSH) pool after 72 h at higher bentazon concentrations could be explained by the reduction of the NADPH-dependent glutathione reductase (GR) activity. The obtained results suggested that the alterations of antioxidant systems in A. cylindrica might be useful biomarkers of bentazon exposure. As the toxic mechanism of bentazon is a complex phenomenon, this study also adds relevant findings to explain the oxidative stress pathways of bentazon promoting oxidative stress in cyanobacteria. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2010. [source] Assessing the toxicity of TBBPA and HBCD by zebrafish embryo toxicity assay and biomarker analysisENVIRONMENTAL TOXICOLOGY, Issue 4 2009Jun Hu Abstract Tetrabromobisphenol A (TBBPA) and hexabromocyclododecane (HBCD) are two of the most widely used brominated flame retardants (BFRs). The biological toxicity effect of TBBPA and HBCD was studied by means of zebrafish embryo toxicity assays in combination with three biomarkers, including superoxide dismutase (SOD), lipid peroxidation, (LPO), and heat shock protein (Hsp70). The standard zebrafish embryo assay showed that high concentrations of TBBPA (,0.75 mg/L) can cause lethality or malformation. For HBCD within the concentration range (0.002,10 mg/L), no endpoint was observed. Furthermore, SOD activities of zebrafish embryos exposed to TBBPA were increased with the increasing concentrations. SOD activities in the group treated by HBCD showed an increase followed by a decline. Regardless of TBBPA or HBCD, LPO were increased along with the increase of the concentration. The change pattern of Hsp70 levels was the same with LPO. All these results showed that TBBPA and HBCD could cause oxidative stress and Hsp70 overexpression, inducing acute toxicity to zebrafish embryo in a short-term exposure. The study also indicates that the zebrafish embryo assay in combination with the biomarkers is effective in aquatic environmental toxicology and risk assessment. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Malathion-induced oxidative stress in human erythrocytes and the protective effect of vitamins C and E in vitroENVIRONMENTAL TOXICOLOGY, Issue 3 2009Dilek Durak Abstract Malathion is an organophosphate (OP) pesticide that has been shown to induce oxidative stress in erythrocytes through the generation of free radicals and alteration of the cellular antioxidant defense system. We examined the effect of several different doses of malathion (25, 75, 200 ,M), or malathion in combination with vitamin C (VC; 10 ,M) or vitamin E (VE; 30 ,M), on the levels of malondialdehyde (MDA), and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in human erythrocytes in vitro. Erythrocytes were incubated under various treatment conditions (malathion alone, vitamins alone, or malathion plus vitamin) at 37°C for 60 min, and the levels of MDA, and SOD, CAT and GPx activities, were determined. Treatment with malathion alone increased the levels of MDA and decreased SOD, CAT, and GPx activities in erythrocytes (P < 0.05). There were no statistical differences among VC-treated, VE-treated, or VC + VE-treated erythrocyes, as compared with nontreated control cells. Treatment of cells with malathion + VC, malathion + VE, or a combination of all three agents prevented malathion-induced changes in antioxidant enzyme activity and lipid peroxidation. However, this effect was seen only at low concentrations of malathion (25 and 75 ,M), and the combination of VC + VE had a more protective effect than VC or VE alone. These results indicated that the presence of vitamins at concentrations that are similar to the levels found in plasma have no effect on malathion-induced toxicity in erythrocytes at a concentration of malathion (200 ,M) that is typically used in pesticides. © 2008 Wiley Periodicals, Inc. Environ Toxicol, 2009. [source] Effect of di(n -butyl) phthalate on testicular oxidative damage and antioxidant enzymes in hyperthyroid ratsENVIRONMENTAL TOXICOLOGY, Issue 3 2007Ena Lee Abstract This study compared the effects of di(n-butyl) phthalate (DBP) on the oxidative damage and antioxidant enzymes activity in testes of hyperthyroid rats. Hyperthyroidism was induced in pubertal male rats by intraperitoneal injection of triiodothyronine (T3, 10 ,g/kg body weight) for 30 days. An oral dose of DBP (750 mg/kg) was administered simultaneously to normal or hyperthyroid (T3) rats over a 30-day period. No changes in body weight were observed in the hyperthyroid groups (T3, T3 + DBP) compared with controls. There were significantly higher serum T3 levels observed in the hyperthyroid rats than in the control, but the serum thyroid stimulating hormone levels were markedly lower in the hyperthyroid rats. DBP significantly decreased the weight of the testes in the normal (DBP) and hyperthyroid (T3 + DBP) groups. The serum testosterone concentrations were significantly lower in only DBP group. DBP significantly increased the 8-hydroxy-2-deoxyguanosine (8-OHdG) level in the testes, whereas the DBP-induced 8-OHdG levels were slightly higher in T3 + DBP group. Superoxide dismutase and glutathione peroxidase activities were significantly higher in the testes of the DBP or T3 + DBP groups. Catalase (CAT) activity was significantly higher in the DBP treatment group, but the T3 + DBP group showed slightly lower DBP-induced CAT activity. The testicular expression of thyroid hormone receptor ,-1 (TR,-1) was significantly higher in the DBP groups, and androgen receptor (AR) expression was not detected in the DBP treatment group. In addition, DBP significantly increased the peroxisome proliferator-activated receptor-r (PPAR-r) levels in the testis. These results suggest that hyperthyroidism can cause a change in the expression level of PPAR-r in testes, and may increase the levels of oxidative damage induced by the metabolic activation of DBP. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 245,255, 2007. [source] Bioaccumulation and ROS generation in liver of freshwater fish, goldfish Carassius auratus under HC Orange No. 1 exposureENVIRONMENTAL TOXICOLOGY, Issue 3 2007Yuanyuan Sun Abstract HC Orange No. 1 (CAS No. 54381-08-7, 2-nitro-4,-hydroxydiphenylamine) is used as a color additive in hair dyes. In this study, laboratory experiment was carried out to determine HC Orange No. 1 bioaccumulation and oxidative stress in the liver of freshwater fish, goldfish Carassius auratus. Fish were exposed to different concentrations (0.05, 0.1, 0.2, 0.5, and 1.0 mg/L) of HC Orange No. 1 for 10 days, with one group assigned as control. The accumulation of HC Orange No. 1 in liver increased with the exposure concentration (R2 = 0.94). A secondary spin trapping technique was used followed by electron paramagnetic resonance (EPR) analysis to study the reactive oxygen species (ROS) production. On the basis of the hyperfine splitting constants and shape of the EPR spectrum, the ROS generated in fish liver after exposure was identified as hydroxyl radical (,OH). There is a good correlation between the exposure concentrations and ,OH generation (R2 = 0.92). The ,OH signal intensity of the EPR spectrum showed a significant increase (P < 0.05) when the HC Orange No. 1 concentration was 1.0 mg/L, compared with that of the control. A good positive relationship (R2 = 0.95) was found between the ,OH formation and accumulation level of HC Orange No. 1 in liver. The changes of the activities of catalase (CAT), superoxide dismutase (SOD), glutathione S -transferase (GST), and contents of reduced glutathione (GSH) were also detected. These observations indicated a possible mechanism of oxidative stress induced by HC Orange No. 1 on fish. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 256,263, 2007. [source] Mechanism of DNA damage by cadmium and interplay of antioxidant enzymes and agentsENVIRONMENTAL TOXICOLOGY, Issue 2 2007Veera L. D. Badisa Abstract Cadmium is an environmental toxicant, which causes cancer in different organs. It was found that it damages DNA in the various tissues and cultured cell lines. To investigate the mechanism of DNA damage, we have studied the effect of cadmium-induced DNA damage in plasmid pBR322 DNA, and the possible ameliorative effects of antioxidative agents under in vitro conditions. It was observed that cadmium alone did not cause DNA damage. However, it caused DNA damage in the presence of hydrogen peroxide, in a dose dependent manner, because of production of hydroxyl radicals. Findings from this study show the conversion of covalently closed circular double-stranded pBR 322 DNA to the open circular and linear forms of DNA when treated with 10 ,M cadmium and various concentrations of H2O2. The conversion was due to nicking in DNA strands. The observed rate of DNA strand breakage was dependent on H2O2 concentration, temperature, and time. Metallothionein I failed to prevent cadmium-induced DNA nicking in the presence of H2O2. Of the two antioxidant enzymes (catalase and superoxide dismutase) studied, only catalase conferred significant (50,60%) protection. EDTA and DMSO exhibited protection similar to catalase, while mannitol showed only about 20% protection against DNA damage. Ethyl alcohol failed to ameliorate cadmium-induced DNA strands break. From this study, it is plausible to infer that cadmium in the presence of hydrogen peroxide causes DNA damage probably by the formation of hydroxyl ions. These results may indicate that cadmium in vivo could play a major role in the DNA damage induced by oxidative stress. © 2007 Wiley Periodicals, Inc. Environ Toxicol 22: 144,151, 2007. [source] Effects of dietary N -acetylcysteine on the oxidative stress induced in tilapia (Oreochromis Niloticus) exposed to a microcystin-producing cyanobacterial water bloom,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 8 2009María Puerto Abstract Fish can be exposed to toxic cyanobacterial cells in natural waters and fish farms and suffer from oxidative damage. The present study investigates the effects of N-acetylcysteine (NAC), a glutathione (GSH) precursor, on the oxidative stress induced by Microcystis cyanobacterial cells containing microcystins (MCs) in tilapia fish (Oreochromis niloticus). Variation in lipid peroxidation (LPO) levels, carbonyl group content, reduced glutathione to oxidized glutathione ratio (GSH: GSSG), and catalase (Enzyme Commission [EC] 1.11.1.6), superoxide dismutase (SOD; EC 1.15.1.1), glutathione reductase (GR; EC 1.8.1.7), glutathione peroxidase (GPx; EC 1.11.1.9), and glutathione S-transferase (EC 2.5.1.18) activities in liver and kidney of tilapia exposed to a single oral dose of 120 ,g MC-LR (with leucine [L] and arginine [R])/fish and killed in 24 h were investigated in the absence and presence of 20.0, 44.0, and 96.8 mg NAC/fish/d. Results showed a protective role of NAC, depending on the dose and the biomarker considered. The increase in LPO (1.9-and 1.4-fold in liver and kidney, respectively) and the decreased protein content and GSH:GSSG in the liver induced by MCs were recovered mainly by the lower doses of NAC employed. Antioxidant enzyme activities increased (range, 1.4-to 1.7-fold) by MCs also were ameliorated by NAC, although the highest level used induced significant alteration of some enzymatic activities, such as SOD, GPx, and GR. Thus, NAC can be considered to be a useful chemoprotectant that reduces hepatic and renal oxidative stress in the prophylaxis and treatment of MC-related intoxications in fish when careful attention is given to its application dose because of its own pro-oxidant activity, as shown in the present study at 96.8 mg NAC/ fish/d. [source] Oxidative stress, defense response, and early biomarkers for lead-contaminated soil in Vicia faba seedlings,ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 4 2008Cheng-Run Wang Abstract Chemical analyses and biological measurements were investigated in leaves of Vicia faba seedlings exposed to extraneous lead (Pb) at 0 to 2,000 mg/kg of soil for a month. The results showed that superoxide radical (O,,2) production, increased along with total Pb in leaves and available Pb in soil, resulted in enhancement of malondialdehyde and carbonyl groups. Antioxidant enzymes, including corresponding isoenzymes and heat shock protein 70 (hsp 70), were also enhanced to some extent. Significant changes were detected in the patterns and intensities of guaiacol peroxidase isoenzymes, while superoxide dismutase, catalase, and ascorbate peroxidase isoenzymes only changed intensities. Superoxide dismutase activities increased with the increase of extraneous Pb at 0 to 500 mg/kg of soil and tended to decline thereafter, which might be responsible for the decrease of hydrogen peroxide and accumulation of O,,2. Guaiacol peroxidase and ascorbate peroxidase enzymes were upregulated to become major scavengers of excess hydrogen peroxide on the condition of decreased catalase activities. Levels of hsp 70 were well correlated with Pb contents in leaves (r = 0.777), O,,2 accumulation (r = 0.985, p < 0.01), and carbonyl groups (r = 0.920, p < 0.01) under extraneous Pb at 0 to 250 mg/kg of soil, suggesting that hsp 70 induced by O,,2 was possibly involved in disposal of denatured proteins. The results showed that O,,2, hsp 70, and guaiacol peroxidase isoenzymes had the most sensitive responses in the seedlings and these parameters could be potential early biomarkers of soil Pb contamination. [source] Laminar xanthine oxidase, superoxide dismutase and catalase activities in the prodromal stage of black-walnut induced equine laminitisEQUINE VETERINARY JOURNAL, Issue 1 2007J. P. LOFTUS Summary Reasons for study: Xanthine oxidase (XO)-dependent production of superoxide anion and hydrogen peroxide, a characteristic of ischaemia-reperfusion injury, may contribute to the development of equine laminitis. Objective: To determine the levels of XO and antioxidant enzymes (catalase, superoxide dismutase [SOD]) in the digital laminae of normal horses (CON) and horses in the developmental stage of laminitis using the black walnut extract (BWE) model. Methods: Healthy horses (n = 12) were administered BWE (BWE group, n = 6), or water (CON group, n = 6) through a nasogastric tube. At the onset of leucopenia in the BWE-treated animals, all horses were anaesthetised, digital laminae and other samples collected rapidly and flash frozen, and the animals subjected to euthanasia. Extracts of the frozen tissues were assayed for the 2 conformational forms of xanthine: oxygen oxidoreductase (XOR), namely, xanthine dehydrogenase (XDH) and xanthine oxidase (XO), as well as the antioxidant enzymes, SOD and catalase. Results: Extracts of liver, lungs and skin, but not digital laminae, from either CON or BWE-treated horses had endogenous SOD, whereas all had endogenous XO and catalase. The levels of XDH, XO and catalase were similar in extracts of laminae from CON and BWE-treated horses as was the ratio of XDH to XO in extracts. Conclusions and potential relevance: The absence of increased XO activity suggest against the involvement of this reactive oxygen intermediate-generating system in the development of laminar pathology in BWE-treated horses. Conversely, the absence of SOD from extracts of equine digital laminae, but not other tissues, suggests that the equine digital laminae are highly susceptible to damage by superoxide anion, produced, for example, by emigrant inflammatory leucocytes. [source] BRIEF REPORT: Increased blood oxidative stress in amphetamine usersADDICTION BIOLOGY, Issue 1 2010Piyarat Govitrapong ABSTRACT Amphetamine derivatives have been shown to be a potential brain neurotoxin based on the production of free radicals that occurs after administration. The purpose of this study was to examine the lipid peroxidation and antioxidant enzymes in the blood of amphetamine users. The plasma lipid peroxidation was determined and reported as thiobarbituric acid reactive substance and was significantly increased (+21%), whereas the activities of the erythrocyte antioxidant enzymes glutathione peroxidase, catalase, and superoxide dismutase were significantly decreased (,32%, ,14% and ,31%, respectively) in amphetamine users. These results implicated the potential role of oxidative stress in amphetamine-induced neurotoxicity. [source] Adaptative response of antioxidant enzymes in different areas of rat brain after repeated d -amphetamine administrationADDICTION BIOLOGY, Issue 3 2001Félix Carvalho d-Amphetamine has been shown to be a potential brain neurotoxic agent, particularly to dopaminergic neurones. Reactive oxygen species indirectly generated by this drug have been indicated as an important factor in the appearance of neuronal damage but little is known about the adaptations of brain antioxidant systems to its chronic administration. In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD). When compared to a pair-fed control group, d-amphetamine treatment enhanced the activity of GST in hypothalamus to 167%, GPx in striatum to 127%, in nucleus accumbens to 192%, and in medial prefrontal cortex to 139%, GRed in hypothalamus to 139%, as well as catalase in medial prefrontal cortex to 153%. However, the same comparison revealed a decrease in the activity of GRed in medial pre-frontal cortex by 35%. Food restriction itself reduced GRed activity by 49% and enhanced catalase activity to 271% in nucleus accumbens. The modifications observed for the measured antioxidant enzymes reveal that oxidative stress probably plays a role in the deleterious effects of this drug in CNS and that, in general, the brain areas studied underwent adaptations which provided protection against the continuous administration of the drug. [source] Altered sensorimotor development in a transgenic mouse model of amyotrophic lateral sclerosisEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2004Julien Amendola Abstract Most neurodegenerative diseases become manifest at an adult age but abnormalities or pathological symptoms appear earlier. It is important to identify the initial mechanisms underlying such progressive neurodegenerative disease in both humans and animals. Transgenic mice expressing the familial amyotrophic lateral sclerosis (ALS)-linked mutation (G85R) in the enzyme superoxide dismutase 1 (SOD1) develop motor neuron disease at 8,10 months of age. We address the question of whether the mutation has an early impact on spinal motor networks in postnatal mutant mice. Behavioural tests showed a significant delay in righting and hind-paw grasping responses in mutant SOD1G85R mice during the first postnatal week, suggesting a transient motor deficit compared to wild-type mice. In addition, extracellular recordings from spinal ventral roots in an in vitro brainstem,spinal cord preparation demonstrated different pharmacologically induced motor activities between the two strains. Rhythmic motor activity was difficult to evoke with N -methyl- dl -aspartate and serotonin at the lumbar levels in SOD1G85R mice. In contrast to lumbar segments, rhythmic activity was similar in the sacral roots from the two strains. These results strongly support the fact that the G85R mutation may have altered lumbar spinal motor systems much earlier than previously recognized. [source] Stabilization of mutant Cu/Zn superoxide dismutase (SOD1) protein by coexpressed wild SOD1 protein accelerates the disease progression in familial amyotrophic lateral sclerosis miceEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2001Kei Fukada Abstract Transgenic mice carrying familial amyotrophic lateral sclerosis (FALS)-linked mutant Cu/Zn superoxide dismutase (SOD1) genes such as G93A (G93A-mice) and G85R (G85R-mice) genes develop limb paresis. Introduction of human wild type SOD1 (hWT-SOD1) gene, which does not cause motor impairment by itself, into different FALS mice resulted in different effects on their clinical courses, from no effect in G85R-mice to acceleration of disease progression in G93A-mice. However, the molecular mechanism which causes the observed difference, has not been clarified. We hypothesized that the difference might be caused by the stability of mutant SOD1 proteins. Using a combination of mass spectrometry and enzyme-linked immunosorbent assay, we found that the concentration of G93A-SOD1 protein was markedly elevated in tissues of transgenic mice carrying both G93A - and hWT-SOD1 genes (G93A/hWT-mice) compared to that in G93A-mice, and also found that the concentration of G93A-SOD1 protein had a close relation to the disease duration. The concentration of metallothionein-I/II in the spinal cord, reflecting the degree of copper-mediated oxidative stress, was highest in G93A/hWT-mice, second in G93A-mice, and normal in the mice carrying hWT-SOD1 gene. These results indicated that the increase of G93A-SOD1 protein was responsible for the increase of oxidative stress and disease acceleration in G93A/hWT-mice. We speculate that coexpression of hWT-SOD1 protein is deleterious to transgenic mice carrying a stable mutant such as G93A-SOD1, because this mutant protein is stabilized by hWT-SOD1 protein, but not to transgenic mice carrying an unstable mutant such as G85R-SOD1, because this mutant protein is not stabilized by hWT-SOD1. [source] | ||||||||||||||||||||||