Therapeutic iminoboronate-based polymersomes with a Cu(ii)-mediated Fenton reaction-enhanced ROS-response

2020 ◽  
Vol 56 (81) ◽  
pp. 12246-12249
Author(s):  
Ruidong Cheng ◽  
Guo Li ◽  
Li Fan ◽  
Jinqiang Jiang ◽  
Yue Zhao

The iminoboronate-terminalized starlike prodrug, N3-(OEG-IBCAPE)4, is prepared to investigate the Cu(ii)-mediated Fenton reaction-enhanced response to reactive oxygen species.

2021 ◽  
Author(s):  
Senlin Wang ◽  
Hong-Shuai Wu ◽  
Kai Sun ◽  
Jinzhong Hu ◽  
Fanghui Chen ◽  
...  

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...


2020 ◽  
Vol 56 (68) ◽  
pp. 9779-9782 ◽  
Author(s):  
Aaron M. Fleming ◽  
Cynthia J. Burrows

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.


2001 ◽  
Vol 117 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Anna Yu Bogdanova ◽  
Mikko Nikinmaa

In the present study, we have investigated if reactive oxygen species are involved in the oxygen-dependent regulation of potassium-chloride cotransport activity in trout erythrocyte membrane. An increase in the oxygen level caused an increase in chloride-sensitive potassium transport (K+-Cl− cotransport). 5 mM hydrogen peroxide caused an increase in K+-Cl− cotransport at 5% oxygen. The increase in flux could be inhibited by adding extracellular catalase in the incubation. Pretreatment of the cells with mercaptopropionyl glycine (MPG), a scavenger of reactive oxygen species showing preference for hydroxyl radicals, abolished the activation of the K+-Cl− cotransporter by increased oxygen levels. The inhibition by MPG was reversible, and MPG could not inhibit the activation of transporter by the sulfhydryl reagent, N-ethylmaleimide, indicating that the effect of MPG was due to the scavenging of reactive oxygen species and not to the reaction of MPG with the cotransporter. Copper ions, which catalyze the production of hydroxyl radicals in the Fenton reaction, activated K+-Cl− cotransport significantly at hypoxic conditions (1% O2). These data suggest that hydroxyl radicals, formed from O2 in close vicinity to the cell membrane, play an important role in the oxygen-dependent activation of the K+-Cl− cotransporter.


2019 ◽  
Vol 7 (2) ◽  
pp. 314-323 ◽  
Author(s):  
Chaoqun You ◽  
Zhiguo Gao ◽  
Hongshuai Wu ◽  
Kai Sun ◽  
Like Ning ◽  
...  

A succinic peroxide-filled Fenton reaction activable Pt/Fe3O4@SP-PLGA lipo-polymersome displays ROS mediated chemodynamic therapy (CDT).


2007 ◽  
Vol 73 (23) ◽  
pp. 7740-7743 ◽  
Author(s):  
Gaëtan Gogniat ◽  
Sam Dukan

ABSTRACT Here, we show that resistance of Escherichia coli to TiO2 photocatalysis involves defenses against reactive oxygen species. Results support the idea that TiO2 photocatalysis generates damage which later becomes deleterious during recovery. We found this to be partly due to DNA attack via hydroxyl radicals generated by the Fenton reaction during recovery.


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

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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