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Träfflista för sökning "L773:1523 0864 OR L773:1557 7716 srt2:(2000-2004)"

Sökning: L773:1523 0864 OR L773:1557 7716 > (2000-2004)

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2.
  • Abdiu, Avni, 1963-, et al. (författare)
  • Thioredoxin blood level increases after severe burn injury
  • 2000
  • Ingår i: Antioxidants and Redox Signaling. - 1523-0864 .- 1557-7716. ; 2:4, s. 707-716
  • Tidskriftsartikel (refereegranskat)abstract
    • We have investigated the thioredoxin (TRX) levels in severely burned patients and the possible origin of TRX, based on the recent understanding that TRX is a potent antioxidant with cytoprotective functions. Serum and plasma samples from burns patients and healthy blood donors were collected during the first 10 post-bum days and analyzed in a sandwich TRX enzyme-linked immunosorbent assay (ELISA). The TRX levels found were correlated to a panel of blood tests. The presence of TRX in platelets was investigated by immunoelectron microscopy and Western blotting. TRX serum levels of the severely burned patients showed a significant increase, with a mean serum TRX concentration on the day of injury of 76.5 ▒ 19.5 ng/ml (mean ▒ SD) and on post-burn day one 122.6 ▒ 66.9 ng/ml, compared to control blood donor levels of 22.7 ▒ 12.2 ng/ml (p = 0.0041 and 0.0117, respectively). A second peak of increase was found on post-burn days 7 to 9 with a four- to five-fold rise in concentration compared to controls. TRX elevation correlated well with increased platelet (p = 0.007) and leukocyte counts (p = 0.002). We also demonstrated by immunoelectron microscopy and Western blotting the presence of TRX in platelets. In conclusion, our demonstration of TRX release in burn injuries indicates that the TRX system is involved in a rapid antioxidant defense, coagulation processes, cell growth, and control of the extracellular peroxide tone intimately linked to cytoprotection and wound healing in burns. One of the cell types that delivers TRX promptly and efficiently into the blood may be the platelet.
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3.
  • Allen, John (författare)
  • Superoxide as an obligatory, catalytic intermediate in photosynthetic reduction of oxygen by adrenaline and dopamine.
  • 2003
  • Ingår i: Antioxidants & Redox Signaling. - : Mary Ann Liebert Inc. - 1557-7716 .- 1523-0864. ; 5:1, s. 7-14
  • Tidskriftsartikel (refereegranskat)abstract
    • The superoxide anion radical is known to be the first product of photosynthetic reduction of oxygen mediated by a variety of electron carriers. The effectiveness of many of these electron carriers as herbicides, and the toxicity of the superoxide they produce, have been suggested to rule out oxygen reduction as a physiological component of normal photosynthesis. Here results with isolated spinach chloroplasts are presented that demonstrate that the related catecholamines adrenaline and dopamine mediate photosynthetic reduction of oxygen. Complete inhibition by added superoxide dismutase of light-dependent oxygen uptake by isolated chloroplasts and of the electron transport it supports indicates that superoxide is an obligatory catalytic intermediate, not a product, in adrenaline- and dopamine-mediated oxygen reduction. These compounds might function as chemical analogues of a proposed natural mediator, or oxygen-reducing factor, that allows oxygen reduction to participate in energy transduction in photosynthesis. The identity of the putative natural mediator and the role of oxygen reduction in photosynthesis are discussed. The fully oxidized form of adrenaline, adrenochrome, also acts as a mediator of photosynthetic oxygen uptake, but only by reducing oxygen to superoxide.
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4.
  • Chlichlia, K., et al. (författare)
  • Redox events in HTLV-1 tax-induced apoptotic T-cell death
  • 2002
  • Ingår i: Antioxidants and Redox Signaling. - : Mary Ann Liebert, Inc. publishers. - 1523-0864 .- 1557-7716. ; 4:3, s. 471-477
  • Tidskriftsartikel (refereegranskat)abstract
    • A number of studies implicate reactive oxygen intermediates in the induction of DNA damage and apoptosis. Recent studies suggest that the human T-cell leukemia virus type I (HTLV-1) Tax protein induces oxidative stress and apoptotic T-cell death. Activation of the T-cell receptor/CD3 pathway enhances the Tax-mediated oxidative and apoptotic effects. Tax-mediated apoptosis and oxidative stress as well as activation of nuclear factor-kappaB can be potently suppressed by antioxidants. This review focuses on Tax-dependent changes in the intracellular redox status and their role in Tax-mediated DNA damage and apoptosis. The relevance of these observations to HTLV-1 virus-mediated T-cell transformation and leukemogenesis are discussed.
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5.
  • Dahlgren, Claes, 1949, et al. (författare)
  • Ionomycin-induced neutrophil NADPH oxidase activity is selectively inhibited by the serine protease inhibitor diisopropyl fluorophosphate.
  • 2002
  • Ingår i: Antioxidants & redox signaling. - : Mary Ann Liebert Inc. - 1523-0864 .- 1557-7716. ; 4:1, s. 17-25
  • Tidskriftsartikel (refereegranskat)abstract
    • The calcium-specific ionophore ionomycin triggers neutrophils to activate their NADPH oxidase and generate reactive oxygen species. This activation is restricted to intracellular sites and involves the neutrophil granules. Cells that have experienced an ionomycin-induced rise in intracellular calcium will also mobilize their intracellular granules and are primed to subsequent challenge with the chemoattractant formylmethionyl-leucyl-phenylalanine (fMLF), but have lost their ability to become desensitized to the same agonist. We have investigated the involvement of serine proteases in the calcium-induced effector functions using the inhibitor diisopropyl fluorophosphate (DFP). The ionomycin-induced NADPH oxidase activity was abrogated by the protease inhibitor, whereas the activity induced by fMLF was unaffected. The DFP-dependent inhibition was restricted to the NADPH oxidase activity, as all other ionomycin-induced cellular activities were largely unaffected. We thus suggest that a serine protease is of importance for the calcium ionophore-induced signal(s) to reach and activate the dormant NADPH oxidase in the neutrophil granules.
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8.
  • Foyer, C H, et al. (författare)
  • Lessons from redox signaling in plants.
  • 2003
  • Ingår i: Antioxidants & Redox Signaling. - : Mary Ann Liebert Inc. - 1557-7716 .- 1523-0864. ; 5:1, s. 3-5
  • Tidskriftsartikel (refereegranskat)
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10.
  • Karlsson, Anna, 1967, et al. (författare)
  • Assembly and activation of the neutrophil NADPH oxidase in granule membranes.
  • 2002
  • Ingår i: Antioxidants & redox signaling. - : Mary Ann Liebert Inc. - 1523-0864 .- 1557-7716. ; 4:1, s. 49-60
  • Forskningsöversikt (refereegranskat)abstract
    • Phagocyte activation is accompanied by assembly of an NADPH oxidase that reduces oxygen to form a number of reactive species. These oxygen radicals can eradicate invading microorganisms, regulate the function of other immune reactive cells, and cause damage to "innocent bystander" cells. It is generally assumed that the NADPH oxidase is activated exclusively in the plasma membrane. In neutrophils, this assumption does not fit with the subcellular localization of the membrane component of the oxidase, which is stored in granule compartments. It has now become increasingly evident that oxidants are also produced in an intracellular compartment that we identify as the specific granules. Myeloperoxidase is stored in another granule subset, the azurophil granules, and participates in the processing of the oxidative metabolites. We suggest that neutrophil activation is accompanied by fusion between azurophil and specific granules, allowing these peroxidase-dependent reactions to take place. The presented data suggest a requisite role for neutrophil oxidants complementing their function as microbial killing agents. Signaling capabilities of the oxidants, affecting for example, the state of protein phosphorylation, regulation of transcription factors, and induction of apoptosis, are discussed.
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