Zusammenfassung
Niedrige Dosen ionisierender γ-Strahlung von 137-Cäsium wirken im menschlichen Blut als unphysiologisches Stimulanz von Entzündungsreaktionen. Strahlung erhöht die Aktivierung des “oxidative burst” nach Behandlung des Blutes mit Aktivatoren, wie Ca2+ Ionophor A23187 oder Phorbolester. Diese Reaktion wird durch Amplifizierung der zellulären Chemilumineszenz mit Luminol gemessen. Die erhöhte Lumineszenz kann einige Minuten nach der Bestrahlung beobachtet werden, dauert mindestens 1 h, ist durch die interzelluläre Verbreitung eines Vermittlermoleküls gekennzeichnet und ist γ-dosisabhängig (5–50 μSv, in vitro). Eine ähnliche Reaktion konnte bei Patienten nach einer routinemäßigen Röntgenaufnahme der Lunge festgestellt werden. Die Reaktion ist gehemmt durch EGTA und Adenosin (zwei Zeichen ihrer Ca2+-Abhängigkeit) und durch den Phospho-lipase A2-Blocker p-Bromphenacylbromid. Der Cyclo-oxygenase-Blocker Aspirin ist dagegen nur teilweise effektiv. Diese Reaktionen auf niedrige Dosen implizieren die Wirkung von zweiten Boten-Systemen, insbesondere Metaboliten von Arachidonsäure und sind von molekularer „Beschädigung- & Reparatur-“ Reaktionen unabhängig. Die Ergebnisse zeigen einen Mechanismus der niedrigen Strahlendosen mit Konsequenzen für die Homöeostasis von Entzündungs- und zweiten Boten-Reaktionen.
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Vicker, M.G., Bultmann, H., Glade, U., Häfker, T. (1990). The Biological Mechanism of Low Dose Ionizing Radiation: Induction of Inflammatory Reactions in Human Blood. In: Köhnlein, W., Kuni, H., Schmitz-Feuerhake, I. (eds) Niedrigdosisstrahlung und Gesundheit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-93475-9_7
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