Role of reactive oxygen species in organophosphate insecticide phosalone toxicity in erythrocytes in vitro

2003 ◽  
Vol 17 (2) ◽  
pp. 153-157 ◽  
Author(s):  
I Altuntas ◽  
N Delibas ◽  
D.K Doguc ◽  
S Ozmen ◽  
F Gultekin
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Organophosphate Insecticide

scholarly journals A Novel Tetrapeptide Derivative Exhibits In Vitro Inhibition of Neutrophil-Derived Reactive Oxygen Species and Lysosomal Enzymes Release

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Sumitra Miriyala ◽  
Manikandan Panchatcharam ◽  
Meera Ramanujam ◽  
Rengarajulu Puvanakrishnan
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Anion ◽  
Lysosomal Enzymes ◽  
Reactive Oxygen ◽  
Peptide Sequence ◽  
Ros Generation ◽  
Oxygen Species ◽  
Complement Factors

Neutrophil infiltration plays a major role in the pathogenesis of myocardial injury. Oxidative injury is suggested to be a central mechanism of the cellular damage after acute myocardial infarction. This study is pertained to the prognostic role of a tetrapeptide derivative PEP1261 (BOC-Lys(BOC)-Arg-Asp-Ser(tBu)-OtBU), a peptide sequence (39–42) of lactoferrin, studied in the modulation of neutrophil functions in vitro by measuring the reactive oxygen species (ROS) generation, lysosomal enzymes release, and enhanced expression of C proteins. The groundwork experimentation was concerned with the isolation of neutrophils from the normal and acute myocardial infarct rats to find out the efficacy of PEP1261 in the presence of a powerful neutrophil stimulant, phorbol 12-myristate 13 acetate (PMA). Stimulation of neutrophils with PMA resulted in an oxidative burst of superoxide anion and enhanced release of lysosomal enzymes and expression of complement proteins. The present study further demonstrated that the free radicals increase the complement factors in the neutrophils confirming the role of ROS. PEP1261 treatment significantly reduced the levels of superoxide anion and inhibited the release of lysosomal enzymes in the stimulated control and infarct rat neutrophils. This study demonstrated that PEP1261 significantly inhibited the effect on the ROS generation as well as the mRNA synthesis and expression of the complement factors in neutrophils isolated from infarct heart.

Acetylation of H4K12 in porcine oocytes during in vitro aging: potential role of ooplasmic reactive oxygen species

2011 ◽  
Vol 75 (4) ◽  
pp. 638-646 ◽  
Author(s):  
Mao-Sheng Cui ◽  
Xian-Long Wang ◽  
Da-Wei Tang ◽  
Jing Zhang ◽  
Yan Liu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Potential Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
In Vitro Aging

The Role of Reactive Oxygen Species in the Light-Induced Deformation of DNA

1984 ◽  
Vol 39 (9) ◽  
pp. 1276-1280 ◽  
Author(s):  
R. Baumann ◽  
M. Herrmann ◽  
H. Parlar
Keyword(s):  
Reactive Oxygen Species ◽  
Excited States ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
In Vivo Experiments ◽  
Pyrimidine Bases ◽  
Effect Of Oxygen

Dimerizations and reactions with water of pyrimidine bases are the primary steps held respon­sible for the deformation of DNA at short wavelengths in vitro and in vivo experiments. However the influence of oxygen in combination with water on the UV deformation at wavelengths rep­resentative for troposphere is evident from the observed data and both together are needed to change the DNA structure. The only plausible explanation for the effect of oxygen is the forma­tion of reactive oxygen species during the UV irradiation of DNA. In the present work the deformation of DNA by different oxygen species like singlet oxygen (1O2), superoxideanion (O2-), hydroxyradical (·OH), ozone (O3) and hydrogenperoxide (H2O2) is excluded with the help of chemical-trapping experiments. The photo-induced transformation proceeds via excited states of DNA. which react with groundstate oxygen to afford peroxide.

scholarly journals The Role of Reactive Oxygen Species in In Vitro Cardiac Maturation

2019 ◽  
Vol 25 (6) ◽  
pp. 482-493 ◽  
Author(s):  
Nima Momtahan ◽  
Cody O. Crosby ◽  
Janet Zoldan
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cardiac Maturation

scholarly journals Mitochondria-Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ilya A. Demyanenko ◽  
Vlada V. Zakharova ◽  
Olga P. Ilyinskaya ◽  
Tamara V. Vasilieva ◽  
Artem V. Fedorov ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Wound Healing ◽  
Smooth Muscle Actin ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Diabetic Mice ◽  
Mitochondrial Reactive Oxygen Species ◽  
Genetically Diabetic Mice

Oxidative stress is widely recognized as an important factor in the delayed wound healing in diabetes. However, the role of mitochondrial reactive oxygen species in this process is unknown. It was assumed that mitochondrial reactive oxygen species are involved in many wound-healing processes in both diabetic humans and animals. We have applied the mitochondria-targeted antioxidant 10-(6′-plastoquinonyl)decyltriphenylphosphonium (SkQ1) to explore the role of mitochondrial reactive oxygen species in the wound healing of genetically diabetic mice. Healing of full-thickness excisional dermal wounds in diabetic C57BL/KsJ-db−/db− mice was significantly enhanced after long-term (12 weeks) administration of SkQ1. SkQ1 accelerated wound closure and stimulated epithelization, granulation tissue formation, and vascularization. On the 7th day after wounding, SkQ1 treatment increased the number of α-smooth muscle actin-positive cells (myofibroblasts), reduced the number of neutrophils, and increased macrophage infiltration. SkQ1 lowered lipid peroxidation level but did not change the level of the circulatory IL-6 and TNF. SkQ1 pretreatment also stimulated cell migration in a scratch-wound assay in vitro under hyperglycemic condition. Thus, a mitochondria-targeted antioxidant normalized both inflammatory and regenerative phases of wound healing in diabetic mice. Our results pointed to nearly all the major steps of wound healing as the target of excessive mitochondrial reactive oxygen species production in type II diabetes.

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