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Am J Physiol Lung Cell Mol Physiol 278: L719-L725, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 4, L719-L725, April 2000

Increased production of nitrotyrosine in lung tissue of rats with radiation-induced acute lung injury

Chizuko Tsuji1, Sumie Shioya2, Yuki Hirota3, Naoto Fukuyama1, Daisaku Kurita2, Toshimori Tanigaki2, Yasuyo Ohta2, and Hiroe Nakazawa1

Departments of 1 Physiology and 2 Internal Medicine, Tokai University School of Medicine, Isehara, Kanagawa 259-11; and 3 Electro-Chemical and Cancer Institute, Chofu, Tokyo 182-0022, Japan

The purposes of this study were 1) to identify the nitric oxide (NO) synthase (NOS) isoform responsible for NO-mediated radiation-induced lung injury, 2) to examine the formation of nitrotyrosine, and 3) to see whether nitrotyrosine formation and lung injury are reduced by an inducible NOS (iNOS) inhibitor, aminoguanidine. The left hemithorax of rats was irradiated (20 Gy), and the degree of lung injury, the expression of NOS isoforms, and the formation of nitrotyrosine and superoxide were examined after 2 wk. iNOS mRNA was induced, and endothelial NOS mRNA was markedly increased in the irradiated lung. Nitrotyrosine was detected biochemically and immunohistochemically. Aminoguanidine prevented acute lung injury as indicated by decreased protein concentration and lactate dehydrogenase activity in bronchoalveolar lavage fluid and improved NMR parameters and histology. Furthermore, the formation of nitrotyrosine was significantly reduced in the aminoguanidine group. We conclude that iNOS induction is a major factor in radiation-induced lung injury and that nitrotyrosine formation may participate in the NO-induced pathogenesis.

nitric oxide; nitric oxide synthase; aminoguanidine


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