Chemical, Biological and Medical Controversies Surrounding the Fenton Reaction

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.

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The Role of Oxidative and Nitrosative Stress of Silver Nanoparticles in Human Parasitic Helminth Brugia malayi: A Mechanistic Insight

Acta Parasitologica ◽

10.1007/s11686-021-00394-4 ◽

2021 ◽

Author(s):

Sneha Hande ◽

Vijay Sonkar ◽

Priyanka Bhoj ◽

Namdev Togre ◽

Kalyan Goswami ◽

...

Keyword(s):

Silver Nanoparticles ◽

Nitrosative Stress ◽

Brugia Malayi ◽

Oxidative And Nitrosative Stress ◽

Parasitic Helminth ◽

Mechanistic Insight

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The role of oxidative and nitrosative stress in the pathology of osteoarthritis: Novel candidate biomarkers for quantification of degenerative changes in the knee joint

Orthopedic Reviews ◽

10.4081/or.2018.7460 ◽

2018 ◽

Vol 10 (2) ◽

Cited By ~ 3

Author(s):

Alexander Franz ◽

Laura Joseph ◽

Constantin Mayer ◽

Jan-Frieder Harmsen ◽

Holger Schrumpf ◽

...

Keyword(s):

Oxidative Stress ◽

Synovial Fluid ◽

Knee Joint ◽

Human Serum ◽

Synovial Membrane ◽

Nitrosative Stress ◽

Control Groups ◽

Oxidative And Nitrosative Stress ◽

And Oxidative Stress

Osteoarthritis (OA) is the most frequently diagnosed joint disorder worldwide with increasing prevalence and crucial impact on the quality of life of affected patients through chronic pain, decreasing mobility and invalidity. Although some risk factors, such as age, obesity and previous joint injury are well established, the exact pathogenesis of OA on a cellular and molecular level remains less understood. Today, the role of nitrosative and oxidative stress has not been investigated conclusively in the pathogenesis of OA yet. Therefore, the objective of this study was to identify biological substances for oxidative and nitrosative stress, which mirror the degenerative processes in an osteoarthritic joint. 69 patients suffering from a diagnosed knee pain participated in this study. Based on the orthopedic diagnosis, patients were classified into an osteoarthritis group (OAG, n=24) or in one of two control groups (meniscopathy, CG1, n=11; anterior cruciate ligament rupture, CG2, n=34). Independently from the study protocol, all patients underwent an invasive surgical intervention which was used to collect samples from the synovial membrane, synovial fluid and human serum. Synovial biopsies were analyzed histopathologically for synovitis (Krenn-Score) and immunohistochemically for detection of end products of oxidative (8-isoprostane F2α) and nitrosative (3-nitrotyrosine) stress. Additionally, the fluid samples were analyzed for 8-isoprostane F2α and 3-nitrotyrosine by competitive ELISA method. The analyzation of inflammation in synovial biopsies revealed a slight synovitis in all three investigated groups. Detectable concentrations of 3-nitrotyrosine were reported in all three investigated groups without showing any significant differences between the synovial biopsies, fluid or human serum. In contrast, significant increased concentrations of 8-isoprostane F2α were detected in OAG compared to both control groups. Furthermore, our data showed a significant correlation between the histopathological synovitis and oxidative stress in OAG (r=0.728, P<0.01). There were no significant differences between the concentrations of 8-isoprostane F2α in synovial fluid and human serum. The findings of the current study support the hypothesis that oxidative and nitrosative stress are components of the multi-factory pathophysiological formation of OA. It seems reasonable that an inflammatory process in the synovial membrane triggers the generation of oxidative and nitrosative acting substances which can lead to a further degradation of the articular cartilage. Based on correlations between the observed degree of inflammation and investigated biomarkers, especially 8-isoprostane F2α seems to be a novel candidate biomarker for OA. However, due to the finding that also both control groups showed increased concentrations of selected biomarkers, future studies have to validate the diagnostic potential of these biomarkers in OA and in related conditions of the knee joint.

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The role of mitochondrial dysfunctions due to oxidative and nitrosative stress in the chronic pain or chronic fatigue syndromes and fibromyalgia patients: peripheral and central mechanisms as therapeutic targets?

Expert Opinion on Therapeutic Targets ◽

10.1517/14728222.2013.818657 ◽

2013 ◽

Vol 17 (9) ◽

pp. 1081-1089 ◽

Cited By ~ 42

Author(s):

Mira Meeus ◽

Jo Nijs ◽

Linda Hermans ◽

Dorien Goubert ◽

Patrick Calders

Keyword(s):

Chronic Pain ◽

Nitrosative Stress ◽

Therapeutic Targets ◽

Chronic Fatigue ◽

Oxidative And Nitrosative Stress ◽

Mitochondrial Dysfunctions

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Astrocytic Oxidative/Nitrosative Stress Contributes to Parkinson’s Disease Pathogenesis: The Dual Role of Reactive Astrocytes

Antioxidants ◽

10.3390/antiox8080265 ◽

2019 ◽

Vol 8 (8) ◽

pp. 265 ◽

Cited By ~ 17

Author(s):

Asha Rizor ◽

Edward Pajarillo ◽

James Johnson ◽

Michael Aschner ◽

Eunsook Lee

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Nitrosative Stress ◽

Critical Role ◽

Substantia Nigra Pars Compacta ◽

Environmental Toxicants ◽

Oxidative And Nitrosative Stress ◽

Reactive Astrogliosis ◽

The Impact

Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide; it is characterized by dopaminergic neurodegeneration in the substantia nigra pars compacta, but its etiology is not fully understood. Astrocytes, a class of glial cells in the central nervous system (CNS), provide critical structural and metabolic support to neurons, but growing evidence reveals that astrocytic oxidative and nitrosative stress contributes to PD pathogenesis. As astrocytes play a critical role in the production of antioxidants and the detoxification of reactive oxygen and nitrogen species (ROS/RNS), astrocytic oxidative/nitrosative stress has emerged as a critical mediator of the etiology of PD. Cellular stress and inflammation induce reactive astrogliosis, which initiates the production of astrocytic ROS/RNS and may lead to oxidative/nitrosative stress and PD pathogenesis. Although the cause of aberrant reactive astrogliosis is unknown, gene mutations and environmental toxicants may also contribute to astrocytic oxidative/nitrosative stress. In this review, we briefly discuss the physiological functions of astrocytes and the role of astrocytic oxidative/nitrosative stress in PD pathogenesis. Additionally, we examine the impact of PD-related genes such as α-synuclein, protein deglycase DJ-1( DJ-1), Parkin, and PTEN-induced kinase 1 (PINK1) on astrocytic function, and highlight the impact of environmental toxicants, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, manganese, and paraquat, on astrocytic oxidative/nitrosative stress in experimental models.

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Roles of Nitric Oxide and Prostaglandins in the Sustained Antihypertensive Effects of Acanthospermum hispidum DC. on Ovariectomized Rats with Renovascular Hypertension

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/2492483 ◽

2017 ◽

Vol 2017 ◽

pp. 1-14 ◽

Cited By ~ 2

Author(s):

Rhanany Alan Calloi Palozi ◽

Maysa Isernhagen Schaedler ◽

Cleide Adriane Signor Tirloni ◽

Aniely Oliveira Silva ◽

Francislaine Aparecida dos Reis Lívero ◽

...

Keyword(s):

Nitric Oxide ◽

Renovascular Hypertension ◽

Vascular Reactivity ◽

Nitrosative Stress ◽

Folk Medicine ◽

Thiobarbituric Acid ◽

Ovariectomized Rats ◽

Oxidative And Nitrosative Stress ◽

Antihypertensive Response

Although Acanthospermum hispidum is used in Brazilian folk medicine as an antihypertensive, no study evaluated its effects on a renovascular hypertension and ovariectomy model. So, this study investigated the mechanisms involved in the antihypertensive effects of an ethanol-soluble fraction obtained from A. hispidum (ESAH) using two-kidney-one-clip hypertension in ovariectomized rats (2K1C plus OVT). ESAH was orally administered at doses of 30, 100, and 300 mg/kg, daily, for 28 days, after 5 weeks of surgery. Enalapril (15 mg/kg) and hydrochlorothiazide (25 mg/kg) were used as standard drugs. Diuretic activity was evaluated on days 1, 7, 14, 21, and 28. Systolic, diastolic, and mean blood pressure and heart rate were recorded. Serum creatinine, urea, thiobarbituric acid reactive substances, nitrosamine, nitrite, aldosterone, vasopressin levels, and ACE activity were measured. The vascular reactivity and the role of nitric oxide (NO) and prostaglandins (PG) in the vasodilator response of ESAH on the mesenteric vascular bed (MVB) were also investigated. ESAH treatment induced an important saluretic and antihypertensive response, therefore recovering vascular reactivity in 2K1C plus OVT-rats. This effect was associated with a reduction of oxidative and nitrosative stress with a possible increase in the NO bioavailability. Additionally, a NO and PG-dependent vasodilator effect was observed on the MEV.

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