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  • 1
    Online Resource
    Online Resource
    New York, NY :Springer,
    Keywords: Active oxygen--Pathophysiology. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (392 pages)
    Edition: 1st ed.
    ISBN: 9781461510871
    Series Statement: Developments in Molecular and Cellular Biochemistry Series ; v.37
    Language: English
    Note: MOLECULAR AND CELLULAR BIOCHEMISTRY -- Editor's page -- Copyright -- CONTENTS VOLUME 234/235, Nos. 1 & -- 2, May/June 2002 -- Preface -- Cyclic oxidation and reduction of protein methionine residues is an important antioxidant mechanism -- Signal transduction by nitric oxide in cellular stress responses -- Effects of antioxidants against atherosclerosis -- Molecular pathology of dityrosine cross-links in proteins: Structural and functional analysis offour proteins -- The role of nitric oxide in lung innate immunity: Modulation by surfactant protein-A -- Redox signaling -- Control of mitochondrial membrane potential and ROS formation by reversible phosphorylation of cytochrome c oxidase -- Molecular mechanisms of nitrogen dioxide induced epithelial injury in the lung -- Differential role of hydrogen peroxide in UV-induced signal transduction -- Upregulation of phosphoinositide 3-kinase and protein kinase B in alveolar macrophages following ozone inhalation. Role of NF-KB and STAT-1 in ozone-induced nitric oxide production and toxicity -- Phospholipase D/phosphatidic acid signal transduction: Role and physiological significance in lung -- Role of mitogen-activated protein kinases (MAPK) in cell injury and proliferation by environmental particulates -- Doxorubicin-induced apoptosis: Implications in cardiotoxicity -- Depletion of Bcl-2 by an antisense oligonucleotide induces apoptosis accompanied by oxidation and externalization of phosphatidylserine in NCI-H226 lung carcinoma cells -- Interactions of copper with glycated proteins: Possible involvement in the etiology of diabetic neuropathy -- Mechanisms of neutrophil-induced DNA damage in respiratory tract epithelial cells -- Asbestos-induced alveolar epithelial cell apoptosis: Role of mitochondrial dysfunction caused by ironderived free radicals. , Involvement of hydrogen peroxide in asbestos-induced NFAT activation -- NF-KB, a pivotal transcription factor in silica-induced diseases -- Effect of inhaled crystalline silica in a rat model: Time course of pulmonary reactions -- The role of AP-l, NF-KB and ROS/ NOS in skin carcinogenesis: The JB6 model is predictive -- Reactive oxygen species in choline deficiency induced carcinogenesis and nitrone inhibition -- Tumor necrosis factor-a gene promoter polymorphism in coal workers' pneumoconiosis -- Nitric oxide decreases the sensitivity of pulmonary endothelial cells to LPS-induced apoptosis in azinc-dependent fashion -- Cytokine polymorphisms in silicosis and other pneumoconioses -- Endogenous regulation of the acute inflammatory response -- Role of nitric oxide in liver ischemia and reperfusion injury -- Oxidative stress and TNF-a induce histone acetylation and NF-KB/AP-1 activation in alveolar epithelial cells: Potential mechanism in gene transcription in lung inflammation -- Heme oxygenase/carbon monoxide signaling pathways: Regulation and functional significance -- The role of oxidative stress in nickel and chromate genotoxicity -- Arsenic carcinogenicity: Relevance ofc-Src activation -- Roles of ferritin and iron in ischemic preconditioning of the heart -- Molecular mechanisms of Cr (VI)-induced carcinogenesis -- Arsenic induces oxidative DNA damage in mammalian cells -- Generation of reactive oxygen species in the enzymatic reduction of PbCrO4 and related DNA damage -- Soluble metals as well as the insoluble particle fraction are involved in cellular DNA damage induced by particulate matter -- Nitroxides as antioxidants: Tempol protects against EO9 cytotoxicity -- Reversal of fluoride induced cell injury through elimination of fluoride and consumption of diet rich in essential nutrients and antioxidants. , Measurements in vivo of parameters pertinent to ROS/RNS using EPR spectroscopy -- In vivo imaging of free radicals: Applications from mouse to man -- In vivo bioassays of acute asbestosis and its correlation with ESR spectroscopy and imaging in redox status -- On the application of 4-hydroxybenzoic acid as a trapping agent to study hydroxyl radical generation during cerebral ischemia and reperfusion -- In vivo detection of nitric oxide distribution in mice -- In vivo measurement of tumor redox environment using EPR spectroscopy -- Index to Volume 234/235.
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  • 2
    Online Resource
    Online Resource
    New York, NY :Springer,
    Keywords: Metals--Carcinogenicity--Congresses. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (231 pages)
    Edition: 1st ed.
    ISBN: 9781461507932
    Series Statement: Developments in Molecular and Cellular Biochemistry Series ; v.34
    Language: English
    Note: MOLECULAR MECHANISMS OF METAL TOXICITY AND CARCINOGENESIS -- Editor's page -- Copyright -- CONTENTS VOLUME 222, Nos. 1 & -- 2, June 2001 -- Preface -- Molecular mechanisms of metal toxicity and carcinogenesis -- Cadmium-induced apoptosis and phenotypic changes in mouse thymocytes -- Cytotoxicity and transcriptional activation of stress genes in human liver carcinoma cells (HepG2) exposed to cadmium chloride -- Arsenic-induced NFKB transactivation through Erks- and JNKs-dependent pathways in mouse epidermal JB6 cells -- Lead-related effects on rat fibroblasts -- In vivo reduction of chromium (VI) and its related free radical generation -- Atrazine potentiation of arsenic trioxide-induced cytotoxicity and gene expression in human liver carcinoma cells (HepG2) -- Combining Drosophila melanogaster somatic-mutation-recombination and electron-spin-resonance-spectroscopy data to interpret epidemiologic observations on chromium carcinogenicity -- Carcinogenic potential and genomic instability of beryllium sulphate in BALB/c-3T3 cells -- Cr (VI) induces cell growth arrest through hydrogen peroxide-mediated reactions -- Comparison of roles of three mitogen-activated protein kinases induced by chromium(VI) and cadmium in non-small-cell lung carcinoma cells -- Differential zinc and DNA binding by partial peptides of human protamine HP2 -- Reduction of Cr (VI) by cysteine: Significance in human lymphocytes and formation of DNA damage in reactions with variable reduction rates -- Transactivation of RARE and GRE in the cellular response to arsenic -- Orthopaedic implant related metal toxicity in terms of human lymphocyte reactivity to metal-protein complexes produced from cobalt-base and titanium-base implant alloy degradation -- Arsenic contamination of groundwater and prevalence of arsenical dermatosis in the Hetao plain area, Inner Mongolia, China. , Involvement of Erks activation in cadmium-induced AP-1 transactivation in vitro and in vivo -- Chromium (VI)-induced oxidative stress, apoptotic cell death and modulation of p53 tumor suppressor gene -- Carcinogenic metals and NF-KB activation -- Effects of glutathione on chromium-induced DNA crosslinking and DNA polymerase arrest -- Cell apoptosis induced by carcinogenic metals -- Gene expression profile in response to chromium-induced cell stress in A549 cells -- Cr (VI) increases tyrosine phosphorylation through reactive oxygen species-mediated reactions -- Molecular biology of nickel carcinogenesis -- Model reactions of Cr (VI) with DNA mediated by thiol species -- On the mechanism of Cr (VI)-induced carcinogenesis: Dose dependence of uptake and cellular responses -- Index to Volume 222.
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  • 3
    ISSN: 1573-4919
    Keywords: hydroxyl radical ; messenger ; NF-κB activation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Although it is generally believed that reactive oxygen species activate NF-κB, a primary oxidative stress-responsive transcription factor, it is unclear which one among these species causes NF-κB activation. Our hypothesis is that hydroxyl radical (·OH) functions as a messenger for the activation of NF-κB. Jurkat cells, macrophages and JB6 cells were used to test this hypothesis. Cr(VI), silica and ZnO were used as sources of ·OH radicals. None of these ·OH generating systems involves exogenous H2O2. Cr(VI) expressed enhanced activity in induction of NF-κB in Jurkat cells. This activation of NF-κB was decreased by a metal chelator, diethylene triaminepentaacetic acid or a H2O2 scavenger, catalase, but was increased by superoxide dismutase. Mn(II), which reacts with Cr(IV) to inhibit this metal ion-mediated ·OH generation, decreased the NF-κB activation. Sodium formate, an ·OH radical scavenger, also inhibited the NF-κB activation. Electron spin resonance measurements show that Cr(VI) was reduced by Jurket cells to Cr(IV) and Cr(V). During the reduction process, molecular oxygen was reduced to O2- and then to H2O2, which reacted with Cr(IV) and Cr(V) to generate ·OH radical. The ·OH generation correlated with the Cr(VI)-induced NF-κB activation. Similarly, silica caused NF-κB activation in macrophages via the ·OH radical-mediated reaction. This radical was generated via metal mediated reaction from H2O2, which was generated by the reduction of molecular oxygen via O2- as an intermediate during the silica-stimulated ‘respirable burst’. Silica particles did not cause ·OH generation either in Jurket or in JB6 cells and thus did not cause any observable NF-κB activation in these cells. ZnO induced NF-κB activation in JB6 cells through the generation of ·OH resulting from light irradiation of ZnO which was measured by electron spin resonance. The results thus show that ·OH radical functions as a messenger for NF-κB activation. Antioxidants, which scavenge ·OH radical or its precursors, inhibit NF-κB activation. Metal chelators, which make metal ions incapable of generating ·OH from H2O2, inhibit activation of this transcription factor.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-4919
    Keywords: cellular apoptosis ; vanadium ; hydrogen peroxide ; reactive oxygen species
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Apoptosis is a physiological mechanism for the control of DNA integrity in mammalian cells. Vanadium induces both DNA damage and apoptosis. It is suggested that vanadium-induced apoptosis serves to eliminate DNA-damaged cells. This study is designed to clarify a role of reactive oxygen species in the mechanism of apoptosis induced by vanadium. We established apoptosis model with murine epidermal JB6 P+ cells in the response to vanadium stimulation. Apoptosis was detected by a cell death ELISA assay and morphological analysis. The result shows that apoptosis induced by vanadate is dose-dependent, reaching its saturation level at a concentration of 100 μM vanadate. Vanadyl (IV) can also induce apoptosis albeit with lesser potency. A role of reactive oxygen species was analyzed by multiple reagents including specific scavengers of different reactive oxygen species. The result shows that vanadate-induced apoptosis is enhanced by NADPH, superoxide dismutase and sodium formate, but was inhibited by catalase and deferoxamine. Cells exposed to vanadium consume more molecular oxygen and at the same time, produce more H2O2 as measured by the change in fluorescence of scopoletin in the presence of horseradish peroxidase. This change in oxygen consumption and H2O2 production is enhanced by NADPH. Taken together, these results show that vanadate induces apoptosis in epidermal cells and H2O2 induced by vanadate plays a major role in this process.
    Type of Medium: Electronic Resource
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