Onderzoeker Fattman en collega’s vonden in een experiment dat het anti-oxidant enzym extracellular superoxide dismutase (EC-SOD) de longen van muizen beschermde tegen injecties met crocidoliet, de meest gevaarlijke blauwe asbestvezels (crocidoliet). Anti-oxidanten zijn vitamines, minieralen of enzymen die bepaalde schadelijke stoffen in het lichaam, de zgn. vrije radicalen, tegengaan. Het bekendste anti-oxidant enzym is het superoxide-dismutase (SOD)-enzym. Bron: Fattman CL, Tan RJ, Tobolewski JM & Oury TD (2006). Increased sensitivity to asbestos-induced lung injury in mice lacking extracellular superoxide dismutase. Free Radical Biology & Medicine 40 Feb 15.40(4):601-7.
Fattman CL, Tan RJ, Tobolewski JM & Oury TD (2006). Increased sensitivity to asbestos-induced lung injury in mice lacking extracellular superoxide dismutase. Free Radical Biology & Medicine 40 Feb 15.40(4):601-7.
Abstract
Asbestosis is a chronic form of interstitial lung disease characterized by inflammation and fibrosis that results from the inhalation of asbestos fibers. Although the pathogenesis of asbestosis is poorly understood, reactive oxygen species may mediate the progression of this disease. The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) can protect the lung against a variety of insults. however, its role in asbestosis is unknown. To determine if EC-SOD plays a direct role in protecting the lung from asbestos-induced injury, intratracheal injections of crocidolite were given to wild-type and ec-sod-null mice. Bronchoalveolar lavage fluid (BALF) from asbestos-treated ec-sod-null mice at 24 h, 14 days, or 28 days posttreatment showed increased inflammation and total BALF protein content compared to that of wild-type mice. In addition, lungs from ec-sod-null mice showed increased hydroxyproline content compared to those of wild-type mice, indicating a greater fibrotic response. Finally, lungs from ec-sod-null mice showed greater oxidative damage, as assessed by nitrotyrosine content compared to those of their wild-type counterparts. These results indicate that depletion of EC-SOD from the lung increases oxidative stress and injury in response to asbestos.