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Author (up) Diaz-Acosta, A.; Sandoval, M.L.; Delgado-Olivares, L.; Membrillo-Hernandez, J. file  url
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  Title Effect of anaerobic and stationary phase growth conditions on the heat shock and oxidative stress responses in Escherichia coli K-12 Type Journal Article
  Year 2006 Publication Archives of Microbiology Abbreviated Journal Arch Microbiol  
  Volume 185 Issue 6 Pages 429-438  
  Keywords Aerobiosis/physiology; Anaerobiosis/physiology; Bacterial Proteins/genetics; Electrophoresis, Polyacrylamide Gel; Escherichia coli K12/genetics/*growth & development/metabolism; Escherichia coli Proteins/genetics/*metabolism; Heat-Shock Proteins/genetics/metabolism; *Hot Temperature; Hydrogen Peroxide/pharmacology; Kinetics; Microbial Viability/drug effects; Mutation/genetics; Oxidation-Reduction; Oxidative Stress/*physiology; Oxygen/pharmacology; Protein Biosynthesis/drug effects; Sigma Factor/genetics  
  Abstract The natural living style of Escherichia coli occurs in the gastrointestinal tract, where most of its existence is spent under anaerobic conditions and in stationary phase of growth. Here we report on the heat shock response of E. coli K-12 cells growing in the presence or absence of oxygen. An rpoH mutant (impaired in the synthesis of the sigma(32) transcriptional factor) exhibited an increased sensitivity to heat shock but only in the exponential phase of aerobic growth, suggesting that in anaerobic growth conditions, and in aerobic stationary phase, sigma(32)-independent mechanisms are playing a prime role in protecting cells from heat stress. Our results demonstrated that sigma(S) is not involved in this protection system. Studies on the kinetics of synthesis of Heat shock proteins (Hsp) after an abrupt rise in temperature demonstrated that in the absence of oxygen, the synthesis of Hsp is triggered faster and is sustained for a longer period of time compared to aerobic growth conditions. Finally, the heated cells in the exponential phase of aerobic growth displayed a high concentration of oxidatively damaged proteins in the presence of 4 mM H(2)O(2), in sharp contrast to cultures of stationary phase or anaerobic growth.  
  Call Number Serial 298  
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Author (up) 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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