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Author Nakano, Y., Asada, K. file  url
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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 1.8.5.1) 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 Schoenfeld, J.D.; Sibenaller, Z.A.; Mapuskar, K.A.; Wagner, B.A.; Cramer-Morales, K.L.; Furqan, M.; Sandhu, S.; Carlisle, T.L.; Smith, M.C.; Abu Hejleh, T.; Berg, D.J.; Zhang, J.; Keech, J.; Parekh, K.R.; Bhatia, S.; Monga, V.; Bodeker, K.L.; Ahmann, L.; Vollstedt, S.; Brown, H.; Shanahan Kauffman, E.P.; Schall, M.E.; Hohl, R.J.; Clamon, G.H.; Greenlee, J.D.; Howard, M.A.; Schultz, M.K.; Smith, B.J.; Riley, D.P.; Domann, F.E.; Cullen, J.J.; Buettner, G.R.; Buatti, J.M.; Spitz, D.R.; Allen, B.G. file  url
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Title O2(-) and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate Type Journal Article
Year 2017 Publication Cancer Cell Abbreviated Journal Cancer Cell  
Volume 31 Issue 4 Pages 487-500.e8  
Keywords Animals; Antineoplastic Combined Chemotherapy Protocols/therapeutic use; Ascorbic Acid/administration & dosage/adverse effects/*pharmacology; Brain Neoplasms/*drug therapy; Carcinoma, Non-Small-Cell Lung/*drug therapy/metabolism/mortality/radiotherapy; Cell Line, Tumor; Chemoradiotherapy/methods; Female; Glioblastoma/*drug therapy/metabolism; Humans; Hydrogen Peroxide/pharmacology; Iron/*metabolism; Lung Neoplasms/*drug therapy/metabolism/mortality/radiotherapy; Male; Mice, Nude; Oxygen/metabolism; Radiation-Sensitizing Agents/pharmacology; Xenograft Model Antitumor Assays; ferritin; glioblastoma multiforme; hydrogen peroxide; labile iron metabolism; non-small cell lung cancer; oxidative stress; pharmacological ascorbate; superoxide; superoxide dismutase; transferrin receptor  
Abstract Pharmacological ascorbate has been proposed as a potential anti-cancer agent when combined with radiation and chemotherapy. The anti-cancer effects of ascorbate are hypothesized to involve the autoxidation of ascorbate leading to increased steady-state levels of H2O2; however, the mechanism(s) for cancer cell-selective toxicity remain unknown. The current study shows that alterations in cancer cell mitochondrial oxidative metabolism resulting in increased levels of O2(-) and H2O2 are capable of disrupting intracellular iron metabolism, thereby selectively sensitizing non-small-cell lung cancer (NSCLC) and glioblastoma (GBM) cells to ascorbate through pro-oxidant chemistry involving redox-active labile iron and H2O2. In addition, preclinical studies and clinical trials demonstrate the feasibility, selective toxicity, tolerability, and potential efficacy of pharmacological ascorbate in GBM and NSCLC therapy.  
Call Number Serial 2122  
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