title: [Redox sensitive behavior of selenite in the presence of reactive oxygen species. Are there nonenzymatic direct reaction pathways].
abstract: From extensive research over the last decade it has been known that selenium is essential as necessary component of selenoaminoacids and of specific enzymes. Among others, the redoxpair GSH/GSSG is closely connected with antioxidative processes. Moreover it inhibits and/or activates molecular key reactions with the involvement of various small reactive O- and N-species. We investigated the direct interaction of selenite with components of the respiratory burst of human blood cells, considering the redoxamphoterie of alkali-selenite. Selenite tend to redox-disproportation depending on the pH-value. Whether selenite leads to oxidation or reductation is dependent not only on the pH-value, but also on the redox-potential of the reaction partners. In in-vivo adapted in-vitro conditions (ph = 7.4; mumolar concentrations of reaction partners) we observed the following results: 1. SeO3(2-) is not oxidized by H2O2/NO or triplet-oxygen, when the oxidatives are applied alone; 2. SeO3(2-) is quantitatively oxidized from SeO4(2-) by the combination H2O2/NO2- or O2-/NO; 3. SeO3(2-) is semiquantitatively oxidized by singlett oxygen to SeO4(2-). The composition of reaction products was measured by 77Se-NMR-spectroscopy. The reactive intermediate product for the 2. reaction should be peroxynitrite (HOONO). One cannot rule out the possibility that HOONO reacts on a large scale with H2O2 to singlett oxygen. Subsequently singlett oxygen oxidizes selenite. The pathophysiological impact of singlett oxygen in processes like arteriosclerosis is now being investigated. It has been supposed, that singlett oxygen is participating in processes of lipidperoxidation invivo. Further investigations have to show, to what extent selenite is effective as direct 1O2-scavanger.
authors.affiliation: Klinik und Poliklinik für Frauenheilkunde und Geburtshilfe, Universitätsklinikum, Technischen Universität Dresden. zialblcl@res.urz.tu-dresden.de
authors.forename: S
authors.initials: S
authors.lastname: Albrecht
authors.forename: T
authors.initials: T
authors.lastname: Zimmermann
authors.forename: R
authors.initials: R
authors.lastname: Grützmann
authors.forename: D
authors.initials: D
authors.lastname: Scheller
authors.forename: H D
authors.initials: HD
authors.lastname: Saeger
authors.forename: W
authors.initials: W
authors.lastname: Distler
mesh_terms: D001161:Arteriosclerosis / Q000503:physiopathology; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology; D009682:Magnetic Resonance Spectroscopy; D009566:Nitrates / Q000502:physiology; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000378:metabolism*; D016897:Respiratory Burst / Q000502:physiology; D012643:Selenium / Q000502:physiology*
chemical_list: D009566:Nitrates; D017382:Reactive Oxygen Species; C039642:peroxynitric acid; D012643:Selenium