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      A review of the molecular mechanisms of hyperglycemia-induced free radical generation leading to oxidative stress : YARIBEYGIet al.

      1 , 2 , 3 , 4 , 5
      Journal of Cellular Physiology
      Wiley

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          Abstract

          The prevalence of diabetes is growing worldwide with an increasing morbidity and mortality associated with the development of diabetes complications. Free radical production is a normal biological process that is strictly controlled and has been shown to be important in normal cellular homeostasis, and in the bodies response to pathogens. However, there are several mechanisms leading to excessive free radical production that overcome the normal protective quenching mechanisms. Studies have shown that many of the diabetes complications result from excessive free radical generation and oxidative stress, and it has been shown that chronic hyperglycemia is a potent inducer for free radical production, generated through several pathways and triggering multiple molecular mechanisms. An understanding of these processes may help us to improving our preventive or therapeutic strategies. In this review, the major molecular pathways involved in free radical generation induced by hyperglycemia are described.

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          The sites and topology of mitochondrial superoxide production.

          Mitochondrial superoxide production is an important source of reactive oxygen species in cells, and may cause or contribute to ageing and the diseases of ageing. Seven major sites of superoxide production in mammalian mitochondria are known and widely accepted. In descending order of maximum capacity they are the ubiquinone-binding sites in complex I (site IQ) and complex III (site IIIQo), glycerol 3-phosphate dehydrogenase, the flavin in complex I (site IF), the electron transferring flavoprotein:Q oxidoreductase (ETFQOR) of fatty acid beta-oxidation, and pyruvate and 2-oxoglutarate dehydrogenases. None of these sites is fully characterized and for some we only have sketchy information. The topology of the sites is important because it determines whether or not a site will produce superoxide in the mitochondrial matrix and be able to damage mitochondrial DNA. All sites produce superoxide in the matrix; site IIIQo and glycerol 3-phosphate dehydrogenase also produce superoxide to the intermembrane space. The relative contribution of each site to mitochondrial reactive oxygen species generation in the absence of electron transport inhibitors is unknown in isolated mitochondria, in cells or in vivo, and may vary considerably with species, tissue, substrate, energy demand and oxygen tension. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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            High protonic potential actuates a mechanism of production of reactive oxygen species in mitochondria.

            Formation of H2O2 has been studied in rat heart mitochondria, pretreated with H2O2 and aminotriazole to lower their antioxidant capacity. It is shown that the rate of H2O2 formation by mitochondria oxidizing 6 mM succinate is inhibited by a protonophorous uncoupler, ADP and phosphate, malonate, rotenone and myxothiazol, and is stimulated by antimycin A. The effect of ADP is abolished by carboxyatractylate and oligomycin. Addition of uncoupler after rotenone induces further inhibition of H2O2 production. Inhibition of H2O2 formation by uncoupler, malonate and ADP+Pi is shown to be proportional to the delta psi decrease by these compounds. A threshold delta psi value is found, above which a very strong increase in H2O2 production takes place. This threshold slightly exceeds the state 3 delta psi level. The data obtained are in line with the concept [Skulachev, V.P., Q. Rev. Biophys. 29 (1996), 169-2021 that a high proton motive force in state 4 is potentially dangerous for the cell due to an increase in the probability of superoxide formation.
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              NADPH oxidase: an update.

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                Author and article information

                Journal
                Journal of Cellular Physiology
                J Cell Physiol
                Wiley
                00219541
                February 2019
                February 2019
                August 26 2018
                : 234
                : 2
                : 1300-1312
                Affiliations
                [1 ]Chronic Kidney Disease Research Center; Shahid Beheshti University of Medical Sciences; Tehran Iran
                [2 ]Weill Cornell Medicine College; Doha Qatar
                [3 ]Biotechnology Research Center, Pharmaceutical Technology Institute; Mashhad University of Medical Sciences; Mashhad Iran
                [4 ]Neurogenic Inflammation Research Center; Mashhad University of Medical Sciences; Mashhad Iran
                [5 ]School of Pharmacy, Mashhad University of Medical Sciences; Mashhad Iran
                Article
                10.1002/jcp.27164
                30146696
                1172c9c6-8e42-4373-a2ae-97bf89c89690
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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