scholarly journals Radiation Induces Endothelial Dysfunction in Murine Intestinal Arterioles via Enhanced Production of Reactive Oxygen Species

2006 ◽  
Vol 26 (2) ◽  
pp. 287-294 ◽  
Author(s):  
Ossama A. Hatoum ◽  
Mary F. Otterson ◽  
Doron Kopelman ◽  
Hiroto Miura ◽  
Igor Sukhotnik ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Enhanced Production

scholarly journals Arginase and vascular aging

2008 ◽  
Vol 105 (5) ◽  
pp. 1632-1642 ◽  
Author(s):  
Lakshmi Santhanam ◽  
David W. Christianson ◽  
Daniel Nyhan ◽  
Dan E. Berkowitz
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Reactive Oxygen ◽  
No Production ◽  
Oxygen Species ◽  
Vascular Aging ◽  
Enhanced Production ◽  
Age Related ◽  
Cardiovascular Morbidity And Mortality ◽  
Aging Models

Vascular and associated ventricular stiffness is one of the hallmarks of the aging cardiovascular system. Both an increase in reactive oxygen species production and a decrease in nitric oxide (NO) bioavailability contribute to the endothelial dysfunction that underlies this vascular stiffness, independent of other age-related vascular pathologies such as atherosclerosis. The activation/upregulation of arginase appears to be an important contributor to age-related endothelial dysfunction by a mechanism that involves substrate (l-arginine) limitation for NO synthase (NOS) 3 and therefore NO synthesis. Not only does this lead to impaired NO production but also it contributes to the enhanced production of reactive oxygen species by NOS. Although arginase abundance is increased in vascular aging models, it appears that posttranslational modification by S-nitrosylation of the enzyme enhances its activity as well. The S-nitrosylation is mediated by the induction of NOS2 in the endothelium. Furthermore, arginase activation contributes to aging-related vascular changes by mechanisms that are not directly related to changes in NO signaling, including polyamine-dependent vascular smooth muscle proliferation and collagen synthesis. Taken together, arginase may represent an as yet elusive target for the modification of age-related vascular and ventricular stiffness contributing to cardiovascular morbidity and mortality.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

scholarly journals TiO2-Capped Gold Nanorods for Plasmon-Enhanced Production of Reactive Oxygen Species and Photothermal Delivery of Chemotherapeutic Agents

2018 ◽  
Vol 10 (33) ◽  
pp. 27965-27971 ◽  
Author(s):  
Liangcan He ◽  
Chenchen Mao ◽  
Michael Brasino ◽  
Albert Harguindey ◽  
Wounjhang Park ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Gold Nanorods ◽  
Reactive Oxygen ◽  
Chemotherapeutic Agents ◽  
Oxygen Species ◽  
Enhanced Production

scholarly journals Chemical Mechanisms of Nanoparticle Radiosensitization and Radioprotection: A Review of Structure-Function Relationships Influencing Reactive Oxygen Species

2020 ◽  
Vol 21 (2) ◽  
pp. 579 ◽  
Author(s):  
Douglas Howard ◽  
Sonia Sebastian ◽  
Quy Van-Chanh Le ◽  
Benjamin Thierry ◽  
Ivan Kempson
Keyword(s):  
Reactive Oxygen Species ◽  
Structure Function ◽  
Reactive Oxygen ◽  
Metal Nanoparticle ◽  
Ros Generation ◽  
Oxygen Species ◽  
X Rays ◽  
Chemical Mechanisms ◽  
Enhanced Production ◽  
Physico Chemical

Metal nanoparticles are of increasing interest with respect to radiosensitization. The physical mechanisms of dose enhancement from X-rays interacting with nanoparticles has been well described theoretically, however have been insufficient in adequately explaining radiobiological response. Further confounding experimental observations is examples of radioprotection. Consequently, other mechanisms have gained increasing attention, especially via enhanced production of reactive oxygen species (ROS) leading to chemical-based mechanisms. Despite the large number of variables differing between published studies, a consensus identifies ROS-related mechanisms as being of significant importance. Understanding the structure-function relationship in enhancing ROS generation will guide optimization of metal nanoparticle radiosensitisers with respect to maximizing oxidative damage to cancer cells. This review highlights the physico-chemical mechanisms involved in enhancing ROS, commonly used assays and experimental considerations, variables involved in enhancing ROS generation and damage to cells and identifies current gaps in the literature that deserve attention. ROS generation and the radiobiological effects are shown to be highly complex with respect to nanoparticle physico-chemical properties and their fate within cells. There are a number of potential biological targets impacted by enhancing, or scavenging, ROS which add significant complexity to directly linking specific nanoparticle properties to a macroscale radiobiological result.

scholarly journals Hyperuricemia induces endothelial dysfunction by increasing reactive oxygen species

2013 ◽  
Vol 34 (suppl 1) ◽  
pp. P601-P601 ◽  
Author(s):  
A. H. P. Linke ◽  
A. Oberbach ◽  
N. Jehmlich ◽  
N. Schlichting ◽  
G. Schuler ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Role of TNF-α-induced reactive oxygen species in endothelial dysfunction during reperfusion injury

2008 ◽  
Vol 295 (6) ◽  
pp. H2242-H2249 ◽  
Author(s):  
Xue Gao ◽  
Hanrui Zhang ◽  
Souad Belmadani ◽  
Junxi Wu ◽  
Xiangbin Xu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Myocardial Ischemia ◽  
Endothelial Function ◽  
Xanthine Oxidase ◽  
Reactive Oxygen ◽  
Neutrophil Activation ◽  
Superoxide Production ◽  
Oxygen Species ◽  
Tnf Α

We hypothesized that neutralization of TNF-α at the time of reperfusion exerts a salubrious role on endothelial function and reduces the production of reactive oxygen species. We employed a mouse model of myocardial ischemia-reperfusion (I/R, 30 min/90 min) and administered TNF-α neutralizing antibodies at the time of reperfusion. I/R elevated TNF-α expression (mRNA and protein), whereas administration of anti-TNF-α before reperfusion attenuated TNF-α expression. We detected TNF-α expression in vascular smooth muscle cells, mast cells, and macrophages, but not in the endothelial cells. I/R induced endothelial dysfunction and superoxide production. Administration of anti-TNF-α at the onset of reperfusion partially restored nitric oxide-mediated coronary arteriolar dilation and reduced superoxide production. I/R increased the activity of NAD(P)H oxidase and of xanthine oxidase and enhanced the formation of nitrotyrosine residues in untreated mice compared with shams. Administration of anti-TNF-α before reperfusion blocked the increase in activity of these enzymes. Inhibition of xanthine oxidase (allopurinol) or NAD(P)H oxidase (apocynin) improved endothelium-dependent dilation and reduced superoxide production in isolated coronary arterioles following I/R. Interestingly, I/R enhanced superoxide generation and reduced endothelial function in neutropenic animals and in mice treated with a neutrophil NAD(P)H oxidase inhibitor, indicating that the effects of TNF-α are not through neutrophil activation. We conclude that myocardial ischemia initiates TNF-α expression, which induces vascular oxidative stress, independent of neutrophil activation, and leads to coronary endothelial dysfunction.

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