Reactive Oxygen and Nitrogen Species, Oxidative and Nitrosative Stress, and Their Role in the Pathogenesis of Acute Kidney Injury

2010 ◽  
pp. 161-177 ◽  
Author(s):  
Eisei Noiri ◽  
Francesco Addabbo ◽  
Michael S. Goligorsky
Small ◽  
2021 ◽  
Vol 17 (8) ◽  
pp. 2005113
Author(s):  
Dong‐Yang Zhang ◽  
Hengke Liu ◽  
Ting He ◽  
Muhammad Rizwan Younis ◽  
Tianhui Tu ◽  
...  

Biomaterials ◽  
2021 ◽  
Vol 271 ◽  
pp. 120706 ◽  
Author(s):  
Dong-Yang Zhang ◽  
Muhammad Rizwan Younis ◽  
Hengke Liu ◽  
Shan Lei ◽  
Yilin Wan ◽  
...  

Small ◽  
2021 ◽  
Vol 17 (8) ◽  
pp. 2170033
Author(s):  
Dong‐Yang Zhang ◽  
Hengke Liu ◽  
Ting He ◽  
Muhammad Rizwan Younis ◽  
Tianhui Tu ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Micol Falabella ◽  
Elena Forte ◽  
Maria Chiara Magnifico ◽  
Paolo Santini ◽  
Marzia Arese ◽  
...  

Here we have collected evidence suggesting that chronic changes in the NO homeostasis and the rise of reactive oxygen species bioavailability can contribute to cell dysfunction in Leber’s hereditary optic neuropathy (LHON) patients. We report that peripheral blood mononuclear cells (PBMCs), derived from a female LHON patient with bilateral reduced vision and carrying the pathogenic mutation 11778/ND4, display increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS), as revealed by flow cytometry, fluorometric measurements of nitrite/nitrate, and 3-nitrotyrosine immunodetection. Moreover, viability assays with the tetrazolium dye MTT showed that lymphoblasts from the same patient are more sensitive to prolonged NO exposure, leading to cell death. Taken together these findings suggest that oxidative and nitrosative stress cooperatively play an important role in driving LHON pathology when excess NO remains available over time in the cell environment.


Open Medicine ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. 704-712
Author(s):  
Raducu Popescu ◽  
Walther Bild ◽  
Alin Ciobica ◽  
Veronica Bild

AbstractAccumulating evidence suggests that the nongenomic cardiovascular actions of aldosterone are produced by varied cellular pathways and mediated by a multitude of messenger systems including the reactive oxygen and nitrogen species. Considering the involvement of the oxidative and nitrosative stress in the pathways leading to the activation of the angiotensin — aldosterone system, in the current study we tried to evaluate the functional interactions between aldosterone, angiotensin II and antioxidants in isolated vascular smooth muscle of aortic rings from rats. Our data provide additional arguments that the nongenomic actions of aldosterone on aortic smooth muscle cells of rats are a question of cross-talk and balance between its rapid vasoconstrictor and vasodilator effects, as result of the activation of reactive oxygen species in the first case and of nitrogen species in the second. In this way, it seems that at low ambient oxidative stress, aldosterone promotes nitric oxide (NO) production and vasodilatation, while in situations with increased oxidative stress the endothelial dysfunction and detrimental effects induced by vasoconstriction will prevail. Thus, aldosterone could be considered both “friend and foe”. This could be relevant for the ways in which aldosterone damages cardiovascular functions and could lead to significant therapeutic improvements.


2006 ◽  
Vol 34 (1) ◽  
pp. 197-199 ◽  
Author(s):  
K. Dyet ◽  
J. Moir

Reactive oxygen and nitrogen species are produced by the human immune system in response to infection. Methods to detoxify these reactive species are vital to the survival of human pathogens, such as Neisseria meningitidis, which is the major aetiological agent of bacterial meningitis. Following activation, macrophages produce superoxide (O2−), hydrogen peroxide (H2O2) and nitric oxide (NO). The toxicity of O2−, generated using X/Xo (xanthine/xanthine oxidase), and H2O2 was investigated in the presence and absence of the NO donor DEA-NONOate [2-(N,N-diethylamino)-diazenolate-2-oxide diethylammonium salt]. Most of the toxicity from X/Xo was due to H2O2. In N. meningitidis, NO decreased the toxicity of the H2O2. In contrast, in the enteric bacterium Escherichia coli, NO increased the toxicity of the H2O2.


2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Peter Mittwede ◽  
Lusha Xiang ◽  
Silu Lu ◽  
John Clemmer ◽  
Robert Hester

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