In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy

2011 ◽  
Vol 462 (5) ◽  
pp. 733-743 ◽  
Author(s):  
Oscar H. Cingolani ◽  
Néstor G. Pérez ◽  
Irene L. Ennis ◽  
María C. Álvarez ◽  
Susana M. Mosca ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Hypertrophy ◽  
Reactive Oxygen ◽  
Oxygen Species

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.

Nitrate tolerance does not increase production of peroxynitrite in the heart

2002 ◽  
Vol 283 (1) ◽  
pp. H69-H76 ◽  
Author(s):  
Tamás Csont ◽  
Csaba Csonka ◽  
Annamária Ónody ◽  
Anikó Görbe ◽  
László Dux ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Dysfunction ◽  
Reactive Oxygen ◽  
Nitrate Tolerance ◽  
Oxygen Species ◽  
Mechanical Function ◽  
Nitrate Treatment

Clinical studies have suggested that long-term nitrate treatment does not improve and may even worsen cardiovascular mortality, and the possible role of nitrate tolerance has been suspected. Nitrate tolerance has been recently shown to increase vascular superoxide and peroxynitrite production leading to vascular dysfunction. Nevertheless, nitrates exert direct cardiac effects independent from their vascular actions. Therefore, we investigated whether in vivo nitroglycerin treatment leading to vascular nitrate tolerance increases cardiac formation of nitric oxide (NO), reactive oxygen species, and peroxynitrite, thereby leading to cardiac dysfunction. Nitrate tolerance increased bioavailability of NO in the heart without increasing formation of reactive oxygen species. Despite elevated myocardial NO, neither cardiac markers of peroxynitrite formation nor cardiac mechanical function were affected by nitroglycerin treatment. However, serum free nitrotyrosine, a marker for systemic peroxynitrite formation, was significantly elevated in nitroglycerin-treated animals. This is the first demonstration that, although the systemic effects of nitroglycerin may be deleterious due to enhancement of extracardiac peroxynitrite formation, nitroglycerin does not result in oxidative damage in the heart.

scholarly journals Attenuation of Ischemia-Induced Mouse Brain Injury by SAG, a Redox-Inducible Antioxidant Protein

2001 ◽  
Vol 21 (6) ◽  
pp. 722-733 ◽  
Author(s):  
Guo-Yuan Yang ◽  
Li Pang ◽  
Hai-Liang Ge ◽  
Mingjia Tan ◽  
Wen Ye ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Brain Injury ◽  
Mouse Brain ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Model Systems ◽  
Oxygen Species ◽  
Antioxidant Protein

Cerebral ischemia resulting from a disruption of blood flow to the brain initiates a cascade of events that causes neuron death and leads to neurologic dysfunction. Reactive oxygen species are thought, at least in part, to mediate this disease process. The authors recently cloned and characterized an antioxidant protein, SAG (sensitive to apoptosis gene), that is redox inducible and protects cells from apoptosis induced by redox agents in a number of in vitro cell model systems. This study reports a neuroprotective role of SAG in ischemia/reperfusion-induced brain injury in an in vivo mouse model. SAG was expressed at a low level in brain tissue and was inducible after middle cerebral artery occlusion with peak expression at 6 to 12 hours. At the cellular level, SAG was mainly expressed in the cytoplasm of neurons and astrocytes, revealed by double immunofluorescence. An injection of recombinant adenoviral vector carrying human SAG into mouse brain produced an overexpression of SAG protein in the injected areas. Transduction of AdCMVSAG (wild-type), but not AdCMVmSAG (mutant), nor the AdCMVlacZ control, protected brain cells from ischemic brain injury, as evidenced by significant reduction of the infarct areas where SAG was highly expressed. The result suggests a rather specific protective role of SAG in the current in vivo model. Mechanistically, SAG overexpression decreased reactive oxygen species production and reduced the number of apoptotic cells in the ischemic areas. Thus, antioxidant SAG appears to protect against reactive oxygen species–induced brain damage in mice. Identification of SAG as a neuroprotective molecule could lead to potential stroke therapies.

scholarly journals Cytotoxic and Antitumor Activity of Sulforaphane: The Role of Reactive Oxygen Species

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Piero Sestili ◽  
Carmela Fimognari
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Target Cells ◽  
Cancer Therapies ◽  
Oxygen Species ◽  
Reactive Oxygen Species Formation ◽  
Species Formation

According to recent estimates, cancer continues to remain the second leading cause of death and is becoming the leading one in old age. Failure and high systemic toxicity of conventional cancer therapies have accelerated the identification and development of innovative preventive as well as therapeutic strategies to contrast cancer-associated morbidity and mortality. In recent years, increasing body ofin vitroandin vivostudies has underscored the cancer preventive and therapeutic efficacy of the isothiocyanate sulforaphane. In this review article, we highlight that sulforaphane cytotoxicity derives from complex, concurring, and multiple mechanisms, among which the generation of reactive oxygen species has been identified as playing a central role in promoting apoptosis and autophagy of target cells. We also discuss the site and the mechanism of reactive oxygen species’ formation by sulforaphane, the toxicological relevance of sulforaphane-formed reactive oxygen species, and the death pathways triggered by sulforaphane-derived reactive oxygen species.

scholarly journals Damage-Induced Calcium Signaling and Reactive Oxygen Species Mediate Macrophage Activation in Zebrafish

2021 ◽  
Vol 12 ◽  
Author(s):  
Tamara Sipka ◽  
Romain Peroceschi ◽  
Rahma Hassan-Abdi ◽  
Martin Groß ◽  
Felix Ellett ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Calcium Signaling ◽  
Macrophage Activation ◽  
Macrophage Polarization ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Macrophage Recruitment ◽  
Early Wound

Immediately after a wound, macrophages are activated and change their phenotypes in reaction to danger signals released from the damaged tissues. The cues that contribute to macrophage activation after wounding in vivo are still poorly understood. Calcium signaling and Reactive Oxygen Species (ROS), mainly hydrogen peroxide, are conserved early wound signals that emanate from the wound and guide neutrophils within tissues up to the wound. However, the role of these signals in the recruitment and the activation of macrophages is elusive. Here we used the transparent zebrafish larva as a tractable vertebrate system to decipher the signaling cascade necessary for macrophage recruitment and activation after the injury of the caudal fin fold. By using transgenic reporter lines to track pro-inflammatory activated macrophages combined with high-resolutive microscopy, we tested the role of Ca²⁺ and ROS signaling in macrophage activation. By inhibiting intracellular Ca²⁺ released from the ER stores, we showed that macrophage recruitment and activation towards pro-inflammatory phenotypes are impaired. By contrast, ROS are only necessary for macrophage activation independently on calcium. Using genetic depletion of neutrophils, we showed that neutrophils are not essential for macrophage recruitment and activation. Finally, we identified Src family kinases, Lyn and Yrk and NF-κB as key regulators of macrophage activation in vivo, with Lyn and ROS presumably acting in the same signaling pathway. This study describes a molecular mechanism by which early wound signals drive macrophage polarization and suggests unique therapeutic targets to control macrophage activity during diseases.

Phthalates Rapidly Increase Production of Reactive Oxygen Species in Vivo: Role of Kupffer Cells

2001 ◽  
Vol 59 (4) ◽  
pp. 744-750 ◽  
Author(s):  
Ivan Rusyn ◽  
Maria B. Kadiiska ◽  
Anna Dikalova ◽  
Hiroshi Kono ◽  
Ming Yin ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Kupffer Cells ◽  
Reactive Oxygen ◽  
Oxygen Species
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