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Capability of complement fixation of pemphigus antibodies in vitro (1977)

Nishikawa, Takeji ; Kurihara, Seiichi ; Harada, Takashi ; [et al.]

Springer

Archives of dermatological research 260 (1977), S. 1-6

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ISSN: 1432-069X

Keywords: Complement fixation ; Pemphigus antibodies ; Complement immunofluorescent staining ; Bullous diseases

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Description / Table of Contents: Zusammenfassung Mit Hilfe von dem kombinierten in vitro-Immunofluores-cenzkomplementfixationstest wurde in vitro-Bindung von Komplement durch Pemphigusantikörper untersucht. Drei Seren aus den 25 Seren von 22 Patienten mit Pemphigus zeigten positive Bindung von Komplement (K3), während die übrigen Seren negative Befunde zeigten. Die Spezifitätskontrolltests bestätigten, daß die positive Reaktionen spezifisch für Komplementfixation waren. Diese Komplementbindungsantikörper zeigten einen niedrigeren Titer als die korrespondierenden IgG-Antikörper und konnten nur im ausgedehnten Krankheitszustand gefunden werden. Diese Ergebnisse belegten, daß Pemphigusantikörper das Komplement in vitro fixieren. Jedoch gibt es Diskrepanzen zwischen in vivo-Komplementsvorkommen und in vitro-Komplementsbindung. Die genaue Rolle des Komplements bei der Pemphigusacantholyse muß noch weiter untersucht werden.

Notes: Summary The capability of complement fixation of pemphigus antibodies was tested using combined in vitro complement immunofluorescent (IF) staining methods. Three sera out of 25 serum samples from 22 pemphigus patients revealed positive reactions, while all other sera gave negative results. Specificity control tests confirmed the positive reactions to be specific for complement staining. Complement fixing pemphigus antibodies were titrated lower than corresponding IgG antibodies and were demonstrable only in the extensive stage of the disease. Thus, the present work supplied evidence that pemphigus antibodies fix complement in vitro. However, the discrepancy still remains between the in vivo deposition of complement in most cases of pemphigus and in vitro capability of complement fixation in only few cases. More investigations should be needed to explain the exact role of complement in pemphigus acantholysis.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00558008

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Reactive oxygen metabolite-induced toxicity to cultured bovine endothelial cells: Status of cellular iron in mediating injury (1994)

Hiraishi, Hideyuki ; Terano, Akira ; Razandi, Mahnaz ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Journal of Cellular Physiology 160 (1994), S. 132-140

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ISSN: 0021-9541

Keywords: Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: We aimed to determine the status of iron in mediating oxidant-induced damage to cultured bovine aortic endothelial cells. Chromium-51-labeled cells were exposed to reaction mixtures of xanthine oxidase/hypoxanthine and glucose oxidase/glucose; these produce superoxide and hydrogen peroxide, or hydrogen peroxide, respectively. Xanthine oxidase caused a dose dependent increase of 51Cr release. Damage was prevented by allopurinol, oxypurinol, and extracellular catalase, but not by superoxide dismutase. Prevention of xanthine oxidase-in-duced damage by catalase was blocked by an inhibitor of catalase, aminotriazole. Glucose oxidase also caused a dose-dependent increase of 51Ci release. Glucose oxidase-induced injury, which was catalase-inhibitable, was not prevented by extracellular superoxide dismutase. Both addition of and pretreatment with deferoxamine (a chelator of Fe3+) prevented glucose oxidase-induced injury. The presence of phenanthroline (a chelator of divalent Fe2+) prevented glucose oxidase-induced 51Cr release, whereas pretreatment with the agent did not. Apotransferrin (a membrane impermeable iron binding protein) failed to influence damage. Neither deferoxamine nor phenanthroline influenced cellular antioxidant defenses, or inhibited lysis by non-oxidant toxic agents. Treatment with allopurinol and oxypurinol, which inhibited cellular xanthine oxidase, failed to prevent glucose oxidase injury. We conclude that (1) among the oxygen species extracellularly generated by xanthine oxidase/hypoxanthine, hydrogen peroxide induces damage via a reaction on cellular iron; (2) deferoxamine and phenanthroline protect cells by chelating Fe3+ and Fe2+, respectively; and (3) reduction of cellular stored iron (Fe3+) to Fe2+ may be a prerequisite for mediation of oxidantinduced injury, but this occurs independently of extracellular superoxide or cellular xanthine oxidase-derived superoxide. © 1994 Wiley-Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.

Additional Material: 10 Ill.