A Novel pH-responsive Fe-MOF System for Enhanced Cancer Treatment Mediated by Fenton Reaction

2021 ◽  
Author(s):  
Senlin Wang ◽  
Hong-Shuai Wu ◽  
Kai Sun ◽  
Jinzhong Hu ◽  
Fanghui Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Hydroxyl Radical ◽  
Cancer Treatment ◽  
Cell Apoptosis ◽  
Fenton Reaction ◽  
Reactive Oxygen ◽  
Cationic Polymer ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Ph Responsive

Recently, the toxic hydroxyl radical (·OH) has received wide interest in inducing cell apoptosis by increasing the intracellular reactive oxygen species (ROS) levels. Herein, a cationic polymer (MV-PAH) was rationally...

scholarly journals Iron Fenton oxidation of 2′-deoxyguanosine in physiological bicarbonate buffer yields products consistent with the reactive oxygen species carbonate radical anion not the hydroxyl radical

2020 ◽  
Vol 56 (68) ◽  
pp. 9779-9782 ◽  
Author(s):  
Aaron M. Fleming ◽  
Cynthia J. Burrows
Keyword(s):  
Reactive Oxygen Species ◽  
Hydroxyl Radical ◽  
Fenton Reaction ◽  
Radical Anion ◽  
Reactive Oxygen ◽  
Fenton Oxidation ◽  
Oxygen Species ◽  
Bicarbonate Buffer ◽  
Carbonate Radical ◽  
Carbonate Radical Anion

Fe(ii)-Fenton reaction in bicarbonate buffer yields CO3˙−, not HO˙, oxidizing 2′-deoxyguanosine to yield 8-oxo-7,8-dihydro-2′-deoxyguanosine with no ribose damage.

scholarly journals Reactive Oxygen Species Contribute to the Bactericidal Effects of the Fluoroquinolone Moxifloxacin in Streptococcus pneumoniae

2015 ◽  
Vol 60 (1) ◽  
pp. 409-417 ◽  
Author(s):  
M. J. Ferrándiz ◽  
A. J. Martín-Galiano ◽  
C. Arnanz ◽  
T. Zimmerman ◽  
A. G. de la Campa
Keyword(s):  
Reactive Oxygen Species ◽  
Streptococcus Pneumoniae ◽  
Hydroxyl Radical ◽  
Fenton Reaction ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Oxygen Species ◽  
Acetyl Coa ◽  
Transcriptomic Response ◽  
Content Type

ABSTRACTWe studied the transcriptomic response ofStreptococcus pneumoniaeto the fluoroquinolone moxifloxacin at a concentration that inhibits DNA gyrase. Treatment of the wild-type strain R6, at a concentration of 10× the MIC, triggered a response involving 132 genes after 30 min of treatment. Genes from several metabolic pathways involved in the production of pyruvate were upregulated. These included 3 glycolytic enzymes, which ultimately convert fructose 6-phosphate to pyruvate, and 2 enzymes that funnel phosphate sugars into the glycolytic pathway. In addition, acetyl coenzyme A (acetyl-CoA) carboxylase was downregulated, likely leading to an increase in acetyl-CoA. When coupled with an upregulation in formate acetyltransferase, an increase in acetyl-CoA would raise the production of pyruvate. Since pyruvate is converted by pyruvate oxidase (SpxB) into hydrogen peroxide (H2O2), an increase in pyruvate would augment intracellular H2O2. Here, we confirm a 21-fold increase in the production of H2O2and a 55-fold increase in the amount of hydroxyl radical in cultures treated during 4 h with moxifloxacin. This increase in hydroxyl radical through the Fenton reaction would damage DNA, lipids, and proteins. These reactive oxygen species contributed to the lethality of the drug, a conclusion supported by the observed protective effects of an SpxB deletion. These results support the model whereby fluoroquinolones cause redox alterations. The transcriptional response ofS. pneumoniaeto moxifloxacin is compared with the response to levofloxacin, an inhibitor of topoisomerase IV. Levofloxacin triggers the transcriptional activation of iron transport genes and also enhances the Fenton reaction.

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