scholarly journals Comparison of p53 Mutations Induced by PAHo-Quinones with Those Caused byanti-Benzo[a]pyrene Diol Epoxide in Vitro:  Role of Reactive Oxygen and Biological Selection

2006 ◽  
Vol 19 (11) ◽  
pp. 1441-1450 ◽  
Author(s):  
Yu-Min Shen ◽  
Andrea B. Troxel ◽  
Srilakshmi Vedantam ◽  
Trevor M. Penning ◽  
Jeffrey Field
Keyword(s):  
Reactive Oxygen ◽  
P53 Mutations ◽  
Diol Epoxide ◽  
Biological Selection

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.

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

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 Cdk2 and Cdk4 Activities Are Dispensable for Tumorigenesis Caused by the Loss of p53

2009 ◽  
Vol 29 (10) ◽  
pp. 2582-2593 ◽  
Author(s):  
V. C. Padmakumar ◽  
Eiman Aleem ◽  
Cyril Berthet ◽  
Mary Beth Hilton ◽  
Philipp Kaldis
Keyword(s):  
Cyclin D ◽  
P53 Mutations ◽  
Spontaneous Tumors ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Oncogenic Potential ◽  
Cyclin Dependent Kinases ◽  
Cell Cycle Inhibitors

ABSTRACT The loss of p53 induces spontaneous tumors in mice, and p53 mutations are found in approximately 50% of human tumors. These tumors are generally caused by a number of events, including genomic instability, checkpoint defects, mitotic defects, deregulation of transcriptional targets, impaired apoptosis, and G1 deregulation or a combination of these effects. In order to determine the role of proteins involved in G1 control in tumorigenesis, we focused on Cdk2 and Cdk4, two cyclin-dependent kinases that in association with cyclin E and cyclin D promote the G1/S phase transition. We analyzed the consequence of loss of Cdk2 in p53-null animals by generating Cdk2 − / − p53 − / − mice. These mice are viable and developed spontaneous tumors, predominantly lymphoblastic lymphomas, similar to p53 − / − mice. In contrast, the genotypes Cdk4 − / − p53 − / − were mostly lethal, with few exceptions, and Cdk2 − / − Cdk4 − / − p53 − / − mice die during embryogenesis at embryonic day 13.5. To study the oncogenic potential, we generated mouse embryonic fibroblasts (MEFs) and found that p53 − / −, Cdk2 − / − p53 − / −, Cdk4 − / − p53 − / −, and Cdk2 − / − Cdk4 − / − p53 − / − MEFs grew at similar rates without entering senescence. Ras-transformed MEFs of these genotypes were able to form colonies in vitro and induce tumors in nude mice. Our results suggest that tumorigenicity mediated by p53 loss does not require either Cdk2 or Cdk4, which necessitates considering the use of broad-spectrum cell cycle inhibitors as a means of effective anti-Cdk cancer therapy.

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.

scholarly journals Involvement of Reactive Oxygen Intermediates in Spontaneous and CD95(Fas/APO-1)–Mediated Apoptosis of Neutrophils

Blood ◽  
1997 ◽  
Vol 89 (5) ◽  
pp. 1748-1753 ◽  
Author(s):  
Yoshihito Kasahara ◽  
Kazuyuki Iwai ◽  
Akihiro Yachie ◽  
Kunio Ohta ◽  
Akihiro Konno ◽  
...  
Keyword(s):  
Signal Transduction Pathway ◽  
Reactive Oxygen ◽  
Reactive Oxygen Intermediates ◽  
Transduction Pathway ◽  
Spontaneous Apoptosis ◽  
Oxygen Intermediates ◽  
Hereditary Defect ◽  
Oxidative Products

Apoptosis is well known to be mediated by oxidative stress. To evaluate the functional role of reactive oxygen intermediates (ROI) produced by neutrophils, we compared the rates of apoptosis in neutrophils isolated from normal donors and from patients with chronic granulomatous disease (CGD), a hereditary defect in ROI production. Spontaneous cell death in CGD neutrophils in vitro was significantly inhibited relative to normal neutrophils. The acceleration of apoptosis induced by anti-Fas monoclonal antibody (MoAb) in CGD neutrophils was much slower than that seen in normal neutrophils. These findings suggest that the apoptosis of neutrophils may be mediated by endogenous oxidative products. This suggestion was confirmed by observation that apoptosis of normal neutrophils was markedly inhibited by reduction of intracellular levels of hydrogen peroxide (H2O2 ). The inhibition of apoptosis in normal neutrophils by adding catalase occurred regardless of the presence of anti-Fas MoAb. H2O2 increased both spontaneous apoptosis and Fas-mediated apoptosis of the CGD neutrophils in proportion to that seen in normal neutrophils. Although several factors that mediate the apoptosis of neutrophils remain to be determined, these results suggest that ROI are major mediators of the apoptosis in neutrophils and may be involved in Fas-mediated signal transduction pathway.

Sign in / Sign up

Export Citation Format

Share Document