Oxidative stress: oxidants and antioxidants

Sies, Helmut

doi:10.1113/expphysiol.1997.sp004024

Cited by 3,286 publications

(2,395 citation statements)

References 12 publications

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“…In fact, the most effective antioxidant, ascorbic acid is a reducing agent and thus not only alleviate oxidative stress, but often potentiate it, by contributing to the generation of hydroxyl radicals [29, 30]. Our findings clearly demonstrate the beneficial effects of oxidizing substances that prevent damage of biological macromolecules by virtue of hydroxyl radical decomposition.…”

Section: Resultsmentioning

confidence: 62%

Oxidation Inhibits Iron-Induced Blood Coagulation

Pretorius

Bester²,

Vermeulen³

et al. 2012

CDT

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Blood coagulation under physiological conditions is activated by thrombin, which converts soluble plasma fibrinogen (FBG) into an insoluble clot. The structure of the enzymatically-generated clot is very characteristic being composed of thick fibrin fibers susceptible to the fibrinolytic degradation. However, in chronic degenerative diseases, such as atherosclerosis, diabetes mellitus, cancer, and neurological disorders, fibrin clots are very different forming dense matted deposits (DMD) that are not effectively removed and thus create a condition known as thrombosis. We have recently shown that trivalent iron (ferric ions) generates hydroxyl radicals, which subsequently convert FBG into abnormal fibrin clots in the form of DMDs. A characteristic feature of DMDs is their remarkable and permanent resistance to the enzymatic degradation. Therefore, in order to prevent thrombotic incidences in the degenerative diseases it is essential to inhibit the iron-induced generation of hydroxyl radicals. This can be achieved by the pretreatment with a direct free radical scavenger (e.g. salicylate), and as shown in this paper by the treatment with oxidizing agents such as hydrogen peroxide, methylene blue, and sodium selenite. Although the actual mechanism of this phenomenon is not yet known, it is possible that hydroxyl radicals are neutralized by their conversion to the molecular oxygen and water, thus inhibiting the formation of dense matted fibrin deposits in human blood.

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Section: Resultsmentioning

confidence: 62%

Oxidation Inhibits Iron-Induced Blood Coagulation

Pretorius

Bester²,

Vermeulen³

et al. 2012

CDT

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“…Oxidative stress refers to the imbalance with enhanced production of reactive oxygen species (ROS) and/or impaired function of the antioxidant system [33]. ROS including superoxide anion, hydroxyl radicals and hydrogen peroxide (H 2 O 2 ) are known to be important in various biological and pathological processes such as aging, http://www.cell-research.com Cell Research, 15(1):24-27, Jan 2005 | www.cell-research.com Molecular mechanism of TNF signaling and beyond inflammation, carcinogenesis, and in the pathogenesis of many human diseases such as neural degenerative diseases, AIDS, and cancer [34,35].…”

Section: A Novel Signaling Pathway Controlling Oxidative Stress-mediamentioning

confidence: 99%

Molecular mechanism of TNF signaling and beyond

2005

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Tumor necrosis factor (TNF) is a proinflammatory cytokine that plays a critical role in diverse cellular events, including cell proliferation, differentiation and apoptosis. TNF is also involved in many types of diseases. In recent years, the molecular mechanisms of TNF functions have been intensively investigated. Studies from many laboratories have demonstrated that the TNF-mediated diverse biological responses are achieved through activating multiple signaling pathways. Especially the activation of transcription factors NF-κB and AP-1 plays a critical role in mediating these cellular responses. Several proteins, including FADD, the death domain kinase RIP and the TNF receptor associated factor TRAF2 have been identified as the key effectors of TNF signaling. Recently, we found that the effector molecules of TNF signaling, such as RIP and TRAF2, are also involved in other cellular responses. These finding suggests that RIP and TRAF2 serve a broader role than as just an effector of TNF signaling.

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“…This is particularly significant in diseases such as SCA in which vascular oxidative stress is increased (Rice‐Evans et al , 1986) with accumulations of highly reactive oxygen species (ROS) including the superoxide anion, hydrogen peroxide and the hydroxyl radical (Sies, 1997; Chirico & Pialoux, 2012; Voskou et al , 2015). Myeloperoxidase released from activated neutrophils may also add to oxidant challenge in SCA, through production of hypochlorous acid (HOCl) from hydrogen peroxide (Vissers et al , 1994; Mutze et al , 2003; Zhang et al , 2013).…”

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confidence: 99%

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

et al. 2018

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SummaryPhosphatidylserine (PS) exposure increases as red cells age, and is an important signal for the removal of senescent cells from the circulation. PS exposure is elevated in red cells from sickle cell anaemia (SCA) patients and is thought to enhance haemolysis and vaso‐occlusion. Although precise conditions leading to its externalisation are unclear, high intracellular Ca2+ has been implicated. Red cells from SCA patients are also exposed to an increased oxidative challenge, and we postulated that this stimulates PS exposure, through increased Ca2+ levels. We tested four different ways of generating oxidative stress: hypoxanthine and xanthine oxidase, phenazine methosulphate, nitrite and tert‐butyl hydroperoxide, together with thiol modification with N‐ethylmaleimide (NEM), dithiothreitol and hypochlorous acid (HOCl), in red cells permeabilised to Ca2+ using bromo‐A23187. Unexpectedly, our findings showed that the four oxidants significantly reduced Ca2+‐induced PS exposure (by 40–60%) with no appreciable effect on Ca2+ affinity. By contrast, NEM markedly increased PS exposure (by about 400%) and slightly but significantly increased the affinity for Ca2+. Dithiothreitol modestly reduced PS exposure (by 25%) and HOCl had no effect. These findings emphasise the importance of thiol modification for PS exposure in sickle cells but suggest that increased oxidant stress alone is not important.

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Oxidative stress: oxidants and antioxidants

Cited by 3,286 publications

References 12 publications

Oxidation Inhibits Iron-Induced Blood Coagulation

Oxidation Inhibits Iron-Induced Blood Coagulation

Molecular mechanism of TNF signaling and beyond

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

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