Reactive Oxygen Species Generated from the Reaction of Copper(II) Complexes with Biological Reductants Cause DNA Strand Scission

1998 ◽  
Vol 357 (2) ◽  
pp. 231-239 ◽  
Author(s):  
Jun-ichi Ueda ◽  
Mamiko Takai ◽  
Yoshie Shimazu ◽  
Toshihiko Ozawa
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Strand Scission ◽  
Dna Strand

scholarly journals Ginger Oleoresin Alleviated γ-Ray Irradiation-Induced Reactive Oxygen Species via the Nrf2 Protective Response in Human Mesenchymal Stem Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Kaihua Ji ◽  
Lianying Fang ◽  
Hui Zhao ◽  
Qing Li ◽  
Yang Shi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Ros Scavenging ◽  
Genes Encoding ◽  
Dna Strand

Unplanned exposure to radiation can cause side effects on high-risk individuals; meanwhile, radiotherapies can also cause injury on normal cells and tissues surrounding the tumor. Besides the direct radiation damage, most of the ionizing radiation- (IR-) induced injuries were caused by generation of reactive oxygen species (ROS). Human mesenchymal stem cells (hMSCs), which possess self-renew and multilineage differentiation capabilities, are a critical population of cells to participate in the regeneration of IR-damaged tissues. Therefore, it is imperative to search effective radioprotectors for hMSCs. This study was to demonstrate whether natural source ginger oleoresin would mitigate IR-induced injuries in human mesenchymal stem cells (hMSCs). We demonstrated that ginger oleoresin could significantly reduce IR-induced cytotoxicity, ROS generation, and DNA strand breaks. In addition, the ROS-scavenging mechanism of ginger oleoresin was also investigated. The results showed that ginger oleoresin could induce the translocation of Nrf2 to cell nucleus and activate the expression of cytoprotective genes encoding for HO-1 and NQO-1. It suggests that ginger oleoresin has a potential role of being an effective antioxidant and radioprotective agent.

scholarly journals Lipocalin produced by myelofibrosis cells affects the fate of both hematopoietic and marrow microenvironmental cells

Blood ◽  
2015 ◽  
Vol 126 (8) ◽  
pp. 972-982 ◽  
Author(s):  
Min Lu ◽  
Lijuan Xia ◽  
Yen-Chun Liu ◽  
Tsivia Hochman ◽  
Laetizia Bizzari ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Dna Strand Breaks ◽  
Oxygen Species ◽  
Strand Breaks ◽  
Cd34 Cells ◽  
Key Points ◽  
Dna Strand

Key Points LCN2 acts to generate reactive oxygen species, leading to increased DNA strand breaks and apoptosis in normal CD34+ cells. LCN2 promotes the generation of osteoblasts but diminishes adipogenesis, resembling the composition of the MF marrow microenvironment.

scholarly journals Stimulation of NADH-dependent microsomal DNA strand cleavage by rifamycin SV

1995 ◽  
Vol 307 (2) ◽  
pp. 361-367 ◽  
Author(s):  
E Kukiełka ◽  
A I Cederbaum
Keyword(s):  
Reactive Oxygen Species ◽  
Hydroxyl Radical ◽  
Radical Scavenging ◽  
Reactive Oxygen ◽  
Redox Cycling ◽  
Rat Liver Microsomes ◽  
Oxygen Species ◽  
Rifamycin Sv ◽  
Dna Strand ◽  
Stimulation Of

Rifamycin SV is an antibiotic anti-bacterial agent used in the treatment of tuberculosis. This drug can autoxidize, especially in the presence of metals, and generate reactive oxygen species. A previous study indicated that rifamycin SV can increase NADH-dependent microsomal production of reactive oxygen species. The current study evaluated the ability of rifamycin SV to interact with iron and increase microsomal production of hydroxyl radical, as detected by conversion of supercoiled plasmid DNA into the relaxed open circular state. The plasmid used was pBluescript II KS(-), and the forms of DNA were separated by agarose-gel electrophoresis. Incubation of rat liver microsomes with plasmid plus NADH plus ferric-ATP caused DNA strand cleavage. The addition of rifamycin SV produced a time- and concentration-dependent increase in DNA-strand cleavage. No stimulation by rifamycin SV occurred in the absence of microsomes, NADH or ferric-ATP. Stimulation occurred with other ferric complexes besides ferric-ATP, e.g. ferric-histidine, ferric-citrate, ferric-EDTA, and ferric-(NH4)2SO4. Rifamycin SV did not significantly increase the high rates of DNA strand cleavage found with NADPH as the microsomal reductant. The stimulation of NADH-dependent microsomal DNA strand cleavage was completely blocked by catalase, superoxide dismutase, GSH and a variety of hydroxyl-radical-scavenging agents, but not by anti-oxidants that prevent microsomal lipid peroxidation. Redox cycling agents, such as menadione and paraquat, in contrast with rifamycin SV, stimulated the NADPH-dependent reaction; menadione and rifamycin SV were superior to paraquat in stimulating the NADH-dependent reaction. These results indicate that rifamycin SV can, in the presence of an iron catalyst, increase microsomal production of reactive oxygen species which can cause DNA-strand cleavage. In contrast with other redox cycling agents, the stimulation by rifamycin SV is more pronounced with NADH than with NADPH as the microsomal reductant. Interactions between rifamycin SV, iron and NADH generating hydroxyl-radical-like species may play a role in some of the hepatotoxic effects associated with the use of this antibacterial antibiotic.

Reactive oxygen species controllable non-thermal helium plasmas for evaluation of plasmid DNA strand breaks

2012 ◽  
Vol 101 (22) ◽  
pp. 224101 ◽  
Author(s):  
Jae Young Kim ◽  
Dong-Hoon Lee ◽  
John Ballato ◽  
Weiguo Cao ◽  
Sung-O Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Plasmid Dna ◽  
Reactive Oxygen ◽  
Dna Strand Breaks ◽  
Oxygen Species ◽  
Strand Breaks ◽  
Dna Strand
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