Oxidative and Nitrosative Stress Induced in Myofibrillar Proteins by a Hydroxyl-Radical-Generating System: Impact of Nitrite and Ascorbate

2014 ◽  
Vol 62 (10) ◽  
pp. 2158-2164 ◽  
Author(s):  
Adriana Villaverde ◽  
Vita Parra ◽  
Mario Estévez
2019 ◽  
Vol 297 ◽  
pp. 124941 ◽  
Author(s):  
Bhoke Marwa Nyaisaba ◽  
Shaimaa Hatab ◽  
Xinxin Liu ◽  
Yu Chen ◽  
Xuhuan Chen ◽  
...  

2003 ◽  
Vol 28 (1) ◽  
pp. 75-104 ◽  
Author(s):  
Mark J. Burkitt

A critical evaluation is made of the role of the Fenton reaction (Fe2+ + H2O2 → Fe3+ + •OH + OH-) in the promotion of oxidative damage in mammalian systems. Following a brief, historical overview of the Fenton reaction, including the formulation of the Haber–Weiss cycle as a mechanism for the catalysis of hydroxyl radical production, an appraisal is made of the biological relevance of the reaction today, following recognition of the important role played by nitric oxide and its congers in the promotion of biomolecular damage. In depth coverage is then given of the evidence (largely from EPR studies) for and against the hydroxyl radical as the active oxidant produced in the Fenton reaction and the role of metal chelating agents (including those of biological importance) and ascorbic acid in the modulation of its generation. This is followed by a description of the important developments that have occurred recently in the molecular and cellular biology of iron, including evidence for the presence of ‘free’ iron that is available in vivo for the Fenton reaction. Particular attention here is given to the role of the iron-regulatory proteins in the modulation of cellular iron status and how their functioning may become dysregulated during oxidative and nitrosative stress, as well as in hereditary haemochromatosis, a common disorder of iron metabolism. Finally, an assessment is made of the biological relevance of ascorbic acid in the promotion of hydroxyl radical generation by the Fenton reaction in health and disease.


2004 ◽  
Vol 4 (1) ◽  
Author(s):  
José Pedraza-Chaverrí ◽  
Diana Barrera ◽  
Perla D Maldonado ◽  
Yolanda I Chirino ◽  
Norma A Macías-Ruvalcaba ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Aderville Cabassi ◽  
Simone Maurizio Binno ◽  
Stefano Tedeschi ◽  
Gallia Graiani ◽  
Cinzia Galizia ◽  
...  

Rationale. Heart failure (HF) is accompanied by the development of an imbalance between oxygen- and nitric oxide-derived free radical production leading to protein nitration. Both chlorinating and peroxidase cycle of Myeloperoxidase (MPO) contribute to oxidative and nitrosative stress and are involved in tyrosine nitration of protein. Ceruloplasmin (Cp) has antioxidant function through its ferroxidase I (FeOxI) activity and has recently been proposed as a physiological defense mechanism against MPO inappropriate actions.Objective. We investigated the relationship between plasma MPO-related chlorinating activity, Cp and FeOxI, and nitrosative stress, inflammatory, neurohormonal, and nutritional biomarkers in HF patients.Methods and Results. In chronic HF patients (n=81, 76±9 years, NYHA Class II (26); Class III (29); Class IV (26)) and age-matched controls (n=17, 75±11 years, CTR), plasma MPO chlorinating activity, Cp, FeOxI, nitrated protein, free Malondialdehyde, BNP, norepinephrine, hsCRP, albumin, and prealbumin were measured. Plasma MPO chlorinating activity, Cp, BNP, norepinephrine, and hsCRP were increased in HF versus CTR. FeOxI, albumin, and prealbumin were decreased in HF. MPO-related chlorinating activity was positively related to Cp (r= 0.363,P<0.001), nitrated protein, hsCRP, and BNP and inversely to albumin.Conclusions. Plasma MPO chlorinated activity is increased in elderly chronic HF patients and positively associated with Cp, inflammatory, neurohormonal, and nitrosative parameters suggesting a role in HF progression.


Author(s):  
Marietta Zita Poles ◽  
László Juhász ◽  
Mihály Boros

AbstractMammalian methanogenesis is regarded as an indicator of carbohydrate fermentation by anaerobic gastrointestinal flora. Once generated by microbes or released by a non-bacterial process, methane is generally considered to be biologically inactive. However, recent studies have provided evidence for methane bioactivity in various in vivo settings. The administration of methane either in gas form or solutions has been shown to have anti-inflammatory and neuroprotective effects in an array of experimental conditions, such as ischemia/reperfusion, endotoxemia and sepsis. It has also been demonstrated that exogenous methane influences the key regulatory mechanisms and cellular signalling pathways involved in oxidative and nitrosative stress responses. This review offers an insight into the latest findings on the multi-faceted organ protective activity of exogenous methane treatments with special emphasis on its versatile effects demonstrated in sepsis models.


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