Zusammenfassung
Zu hohe Sonnen- bzw. UV-Belastung führt zu akuten und chronischen Lichtschäden der Haut. Auf molekularer Ebene entstehen durch die UV-Strahlung Veränderungen an der DNA, vor allem sog. Zyklobutanpyrimidindimere und 6-4-Photoprodukte [3]. Unter der Einwirkung von UV-Strahlung entstehen in der Haut auch freie Radikale wie der Singulettsauerstoff (1O2), das Hydroxylradikal (HO*), das Superoxidanion (02 -) und Peroxiradikale (ROO*) [14]. Diese Radikale schädigen die Zellmembranen und auch die Zellkern-DNA. Die durch die UV-Strahlung verursachten DNA-Schäden führen zur Freisetzung löslicher Faktoren - Zytokine wie Interleukin-10 und Tumornekrosefaktor -, die zur akuten Sonnenbrandreaktion und immunsuppressiven Wirkung der UV-Strahlung beitragen [15]. Bei mangelhafter Wiederherstellung durch endogene Reparaturmechanismen entstehen aus DNA-Schäden spezifische, für die UV-Strahlung typische Mutationen (C→T, CC→TT Transitionen), u.a. am p-53-Tumor-supressorgen [2]. Die UV-Strahlung des Sonnenspektrums ist ein vollstaändiges karzinogen, das als Tumorinitiator und -promotor workt. Die kausale Rolle hoher kumulativer UV-Dosen bei der Enstehung von Basaliomen und Plattenepithelkarzinomen der Haut ist durch epidemiologische Studien eindeutig belegt [21]. Die durch die UV-Strahlung verursachte Immunsuppression, die sowohl lokaler als auch systemischer Natur sein kann, sowie die Schädigung immunkompetenter Langerhans-Zellen in der Haut tragen zur UV-Karzinogenese bei.
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Wolf, P. (1997). Photoprotektion. In: Krutmann, J., Hönigsmann, H. (eds) Handbuch der dermatologischen Phototherapie und Photodiagnostik. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60425-6_16
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