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Author Nakano, Y., Asada, K. file  url
Title Hydrogen Peroxide is Scavenged by Ascorbate-specific Peroxidase in Spinach Chloroplasts Type Journal Article
Year 1981 Publication Plant and Cell Physiology Abbreviated Journal  
Volume 22 Issue 5 Pages 867-880  
Keywords Spinach; Chloroplasts; Hydrogen peroxide; Peroxidase; Ascorbate  
Abstract Intact spinach chloroplasts scavenge hydrogen peroxide with a peroxidase that uses a photoreductant as the electron donor, but the activity of ruptured chloroplasts is very low [Nakano and Asada (1980) Plant & Cell Physiol. 21 : 1295]. Ruptured spinach chloroplasts recovered their ability to photoreduce hydrogen peroxide with the concomitant evolution of oxygen after the addition of glutathione and dehydroascorbate (DHA). In ruptured chloroplasts, DHA was photoreduced to ascorbate and oxygen was evolved in the process in the presence of glutathione. DHA reductase (EC and a peroxidase whose electron donor is specific to L-ascorbate are localized in chloroplast stroma. These observations confirm that the electron donor for the scavenging of hydrogen peroxide in chloroplasts is L-ascorbate and that the L-ascorbate is regenerated from DHA by the system: photosystem I-->ferredoxin-->NADP-->glutathione. A preliminary characterization of the chloroplast peroxidase is given.  
Call Number Serial 2173  
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Author Xu, W.; Chi, L.; Xu, R.; Ke, Y.; Luo, C.; Cai, J.; Qiu, M.; Gozal, D.; Liu, R. file  url
Title Increased production of reactive oxygen species contributes to motor neuron death in a compression mouse model of spinal cord injury Type Journal Article
Year 2005 Publication Spinal Cord Abbreviated Journal Spinal Cord  
Volume 43 Issue 4 Pages 204-213  
Keywords Animals; Apoptosis/physiology; Blotting, Western/methods; Caspase 3; Caspases/metabolism; Cell Count/methods; Cytochromes c/metabolism; DNA, Single-Stranded/metabolism; Disease Models, Animal; Female; Guanine/*analogs & derivatives/metabolism; Immunohistochemistry/methods; In Situ Nick-End Labeling/methods; Lac Operon/physiology; Lipid Peroxidation/physiology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Models, Molecular; Motor Neurons/*pathology; NF-kappa B/genetics; Peroxidases; Proto-Oncogene Proteins c-fos/metabolism; Reactive Oxygen Species/*metabolism; Spinal Cord Injuries/genetics/*metabolism/*pathology/physiopathology; Staining and Labeling/methods; Superoxide Dismutase/genetics; Superoxide Dismutase-1; Time Factors  
Abstract STUDY DESIGN: Experimental laboratory investigation of the role and pathways of reactive oxygen species (ROS)-mediated motor neuron cell death in a mouse model of compression spinal cord injury. OBJECTIVES: To analyze ROS-mediated oxidative stress propagation and signal transduction leading to motor neuron apoptosis induced by compression spinal cord injury. SETTING: University of Louisville Health Science Center. METHODS: Adult C57BL/6J mice and transgenic mice overexpressing SOD1 were severely lesioned at the lumbar region by compression spinal cord injury approach. Fluorescent oxidation, oxidative response gene expression and oxidative stress damage markers were used to assay spinal cord injury-mediated ROS generation and oxidative stress propagation. Biochemical and immunohistochemical analyses were applied to define the ROS-mediated motor neuron apoptosis resulted from compression spinal cord injury. RESULTS: ROS production was shown to be elevated in the lesioned spinal cord as detected by fluorescent oxidation assays. The early oxidative stress response markers, NF-kappaB transcriptional activation and c-Fos gene expression, were significantly increased after spinal cord injury. Lipid peroxidation and nucleic acid oxidation were also elevated in the lesioned spinal cord and motor neurons. Cytochrome c release, caspase-3 activation and apoptotic cell death were increased in the spinal cord motor neuron cells after spinal cord injury. On the other hand, transgenic mice overexpressing SOD1 showed lower levels of steady-state ROS production and reduction of motor neuron apoptosis compared to that of control mice after spinal cord injury. CONCLUSION: These data together provide direct evidence to demonstrate that the increased production of ROS is an early and likely causal event that contributes to the spinal cord motor neuron death following spinal cord injury. Thus, antioxidants/antioxidant enzyme intervention combined with other therapy may provide an effective approach to alleviate spinal cord injury-induced motor neuron damage and motor dysfunction.  
Call Number Serial 2145  
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Author Peng, Y.; Yang, P.-H.; Guo, Y.; Ng, S.S.M.; Liu, J.; Fung, P.C.W.; Tay, D.; Ge, J.; He, M.-L.; Kung, H.-F.; Lin, M.C. file  url
Title Catalase and peroxiredoxin 5 protect Xenopus embryos against alcohol-induced ocular anomalies Type Journal Article
Year 2004 Publication Investigative Ophthalmology & Visual Science Abbreviated Journal Invest Ophthalmol Vis Sci  
Volume 45 Issue 1 Pages 23-29  
Keywords Abnormalities, Drug-Induced/etiology/metabolism/*prevention & control; Animals; Biomarkers/analysis; Blotting, Western; Catalase/*physiology; Choroid/abnormalities; Dose-Response Relationship, Drug; Embryo, Nonmammalian/drug effects; Ethanol/*toxicity; Eye Abnormalities/chemically induced/metabolism/*prevention & control; Eye Proteins; Homeodomain Proteins/genetics/metabolism; Microphthalmos/chemically induced/metabolism/prevention & control; Oxidative Stress; Paired Box Transcription Factors; Peroxidases/*physiology; Peroxiredoxins; Reactive Nitrogen Species/antagonists & inhibitors/metabolism; Reactive Oxygen Species/antagonists & inhibitors/metabolism; Repressor Proteins; Retina/abnormalities; Reverse Transcriptase Polymerase Chain Reaction; T-Box Domain Proteins/genetics/metabolism; *Xenopus Proteins; Xenopus laevis/*embryology  
Abstract PURPOSE: To study the molecular mechanisms underlying alcohol-induced ocular anomalies in Xenopus embryos. METHODS: Xenopus embryos were exposed to various concentrations (0.1%-0.5%) of alcohol, and the subsequent effects in eye development and in eye marker gene expression were determined. To investigate the role of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in fetal alcohol syndrome (FAS)-associated ocular injury, two antioxidant enzymes, catalase and peroxiredoxin 5, were overexpressed in the two blastomeres of the two-cell stage Xenopus embryos. RESULTS: Exposure of Xenopus embryos to alcohol during eye development produced marked gross ocular anomalies, including microphthalmia, incomplete closure of the choroid fissure, and malformation of the retina in 40% of the eyes examined. In parallel, alcohol (0.1%-0.5%) dose dependently and significantly reduced the expression of several eye marker genes, of which TBX5, VAX2, and Pax6 were the most vulnerable. Overexpression of catalase and of cytosolic and mitochondrial peroxiredoxin 5 restored the expression of these alcohol-sensitive eye markers and significantly decreased the frequency of ocular malformation from 39% to 21%, 19%, and 13% respectively. All these enzymes reduced alcohol-induced ROS production, but only peroxiredoxin 5 inhibited RNS formation in the alcohol-treated embryos. CONCLUSIONS: The results suggest that oxidative and nitrosative stresses both contribute to alcohol-induced fetal ocular injury.  
Call Number Serial 1475  
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Author Peng, Y.; Yang, P.-H.; Ng, S.S.M.; Lum, C.T.; Kung, H.-F.; Lin, M.C. file  url
Title Protection of Xenopus laevis embryos against alcohol-induced delayed gut maturation and growth retardation by peroxiredoxin 5 and catalase Type Journal Article
Year 2004 Publication Journal of Molecular Biology Abbreviated Journal J Mol Biol  
Volume 340 Issue 4 Pages 819-827  
Keywords Animals; Antioxidants/metabolism; Biomarkers; Catalase/*metabolism; Culture Techniques/methods; Digestive System/drug effects/embryology/*growth & development; Embryo, Nonmammalian/anatomy & histology/*drug effects; Ethanol/*toxicity; Female; Gene Expression Regulation, Developmental/drug effects; Microinjections; Peroxidases/*metabolism; Peroxiredoxins; Reactive Nitrogen Species/analysis/antagonists & inhibitors/metabolism; Reactive Oxygen Species/analysis/antagonists & inhibitors/metabolism; Reverse Transcriptase Polymerase Chain Reaction; Xenopus laevis/*embryology  
Abstract Accumulated evidence indicates that maternal alcohol consumption causes fetal enteric damage and growth retardation. In this study, we investigated the underlying molecular mechanisms in a Xenopus model of fetal alcohol exposure. We established a condition of transient alcohol exposure that produces tadpoles with delayed gut maturation and decreased body length. We then investigated the roles of reactive oxygen species (ROS) and reactive nitrogen species (RNS) by microinjecting plasmids expressing catalase and peroxiredoxin 5 (PRDX5) into two-cell stage embryos. Finally, the effects of these enzymes on the expression of key gut developmental genes were determined by animal cap explant assay. We showed that exposure of Xenopus embryos to 0.5% alcohol from stage 13 to stage 22 produced tadpoles with delayed gut maturation, reduced growth, and down-regulation in several gut developmental genes, with VegT, Pax6 and Sox17 most vulnerable. We further demonstrated that microinjection of catalase attenuated alcohol-induced ROS production and restored the expression of VegT and Pax6, but protected the embryos from delayed gut development and retarded growth only partially. By contrast, microinjection of PRDX5 reduced both ROS and RNS production, and prevented the gut and growth defects, and restored VegT, Pax6 and Sox17 gene expression. A positive correlation was found between delayed gut maturation and reduced body length. These results indicate the crucial roles of both the ROS-Pax6 and RNS-Sox17 signaling axes in alcohol-induced fetal gut defects and growth retardation. In addition, they suggest strongly a cause-and-effect relationship between alcohol-induced delayed gut maturation and growth retardation.  
Call Number Serial 1474  
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Author Semchyshyn, H.; Bagnyukova, T.; Lushchak, V. file  url
Title Involvement of soxRS regulon in response of Escherichia coli to oxidative stress induced by hydrogen peroxide Type Journal Article
Year 2005 Publication Biochemistry. Biokhimiia Abbreviated Journal Biochemistry (Mosc)  
Volume 70 Issue 11 Pages 1238-1244  
Keywords Bacterial Proteins/*genetics; Escherichia coli/enzymology/*genetics/*physiology; Escherichia coli Proteins/*genetics; Glucosephosphate Dehydrogenase/metabolism; Glutathione Peroxidase/metabolism; Hydrogen Peroxide/*pharmacology; *Oxidative Stress; *Regulon; Superoxide Dismutase/metabolism; Trans-Activators/*genetics; Transcription Factors/*genetics  
Abstract The effect of hydrogen peroxide on the activity of soxRS and oxyR regulon enzymes in different strains of Escherichia coli has been studied. Treatment of bacteria with 20 microM H2O2 caused an increase in catalase and peroxidase activities (oxyR regulon) in all strains investigated. It is shown for the first time that oxidative stress induced by hydrogen peroxide causes in some E. coli strains a small increase in activity of superoxide dismutase and glucose-6-phosphate dehydrogenase (soxRS regulon). This effect is cancelled by chloramphenicol, an inhibitor of protein synthesis in prokaryotes. The increase in soxRS regulon enzyme activities was not found in the strain lacking the soxR gene. These results provide evidence for the involvement of the soxRS regulon in the adaptive response of E. coli to oxidative stress induced by hydrogen peroxide.  
Call Number Serial 348  
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