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      Oxidative stress: a concept in redox biology and medicine

      review-article
      Redox Biology
      Elsevier
      Oxidative stress, Redox balance, Oxidants, Antioxidants, Redox signaling, Adaptive response

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          Abstract

          “Oxidative stress” as a concept in redox biology and medicine has been formulated in 1985; at the beginning of 2015, approx. 138,000 PubMed entries show for this term. This concept has its merits and its pitfalls. Among the merits is the notion, elicited by the combined two terms of (i) aerobic metabolism as a steady-state redox balance and (ii) the associated potential strains in the balance as denoted by the term, stress, evoking biological stress responses. Current research on molecular redox switches governing oxidative stress responses is in full bloom. The fundamental importance of linking redox shifts to phosphorylation/dephosphorylation signaling is being more fully appreciated, thanks to major advances in methodology. Among the pitfalls is the fact that the underlying molecular details are to be worked out in each particular case, which is bvious for a global concept, but which is sometimes overlooked. This can lead to indiscriminate use of the term, oxidative stress, without clear relation to redox chemistry. The major role in antioxidant defense is fulfilled by antioxidant enzymes, not by small-molecule antioxidant compounds. The field of oxidative stress research embraces chemistry, biochemistry, cell biology, physiology and pathophysiology, all the way to medicine and health and disease research.

          Graphical abstract

          Highlights

          • Oxidative stress denotes deviation from redox steady state.

          • Oxidative stress is an attribute of aerobic metabolism.

          • Oxidative stress evokes stress responses.

          • Oxidative stress activates molecular redox switches.

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          Most cited references21

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          Hydroperoxide metabolism in mammalian organs.

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            Strategies of antioxidant defense.

            H Sies (1993)
            Cellular protection against the deleterious effects of reactive oxidants generated in aerobic metabolism, called oxidative stress, is organized at multiple levels. Defense strategies include three levels of protection; prevention, interception, and repair. Regulation of the antioxidant capacity includes the maintenance of adequate levels of antioxidant and the localization of antioxidant compounds and enzymes. Short-term and long-term adaptation and cell specialisation in these functions are new areas of interest. Control over the activity of prooxidant enzymes, such as NADPH oxidase and NO synthases, is crucial. Synthetic antioxidants mimic biological strategies.
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              Activation of the OxyR transcription factor by reversible disulfide bond formation.

              The OxyR transcription factor is sensitive to oxidation and activates the expression of antioxidant genes in response to hydrogen peroxide in Escherichia coli. Genetic and biochemical studies revealed that OxyR is activated through the formation of a disulfide bond and is deactivated by enzymatic reduction with glutaredoxin 1 (Grx1). The gene encoding Grx1 is regulated by OxyR, thus providing a mechanism for autoregulation. The redox potential of OxyR was determined to be -185 millivolts, ensuring that OxyR is reduced in the absence of stress. These results represent an example of redox signaling through disulfide bond formation and reduction.
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                Author and article information

                Contributors
                Journal
                Redox Biol
                Redox Biol
                Redox Biology
                Elsevier
                2213-2317
                02 January 2015
                April 2015
                02 January 2015
                : 4
                : 180-183
                Affiliations
                [0005]Institute of Biochemistry and Molecular Biology I, and Leibniz Research Institute for Environmental Medicine, Heinrich-Heine-University Düsseldorf, Building 22.03, University Street 1, D-40225 Düsseldorf, Germany
                Article
                S2213-2317(15)00003-8
                10.1016/j.redox.2015.01.002
                4309861
                25588755
                26c7c84e-7e47-4967-8ab9-ee4d53026b2a
                © 2015 Published by Elsevier B.V.
                Categories
                Mini Review

                oxidative stress,redox balance,oxidants,antioxidants,redox signaling,adaptive response

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