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Human & Experimental Toxicology
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Toxic effects of selenium inhalation: acute damage of the respiratory system of mice

Duangrudee Cherdwongchareonsuk

Department of Anatomy, Abel Salazar Institute for Biomedical Sciences, University of Porto, Largo Prof. Abel Salazar, 2, 4099-003 Porto, Portugal; Department of Medical Science, Faculty of Science, Burapha University, Thailand; duangrud{at}yahoo.comorduangrud@hotmail.com

Artur P Águas

ICBAS, Department of Anatomy, Abel Salazar Institute for Biomedical Sciences, UMIB, University of Porto, Largo Prof. Abel Salazar, 2, 4099-003 Porto, Portugal

Rui Henrique

Department of Pathology, Portuguese Oncology Institute, Porto, Portugal

Suchart Upatham

Department of Medical Science, Faculty of Science, Burapha University, Thailand

Antonio Sousa Pereira

ICBAS, Department of Anatomy, Abel Salazar Institute for Biomedical Sciences, UMIB, University of Porto, Largo Prof. Abel Salazar, 2, 4099-003 Porto, Portugal

Accidental inhalation of selenium by humans has been associated with damage of respiratory tissues that is lacking a detailed histological definition. We have investigated the natural history of injury to the tracheal epithelium and lungs induced by a single intratracheal instillation of CD-1 mice with two different doses of dimethyl selenide (0.05 and 0.1 mg Se/kg of body weight). The animals were sacrificed 1, 7, 14, and 28 days after the single selenium treatment. Samples of the trachea and lungs were studied by light microscopy. The tracheal epithelium showed loss of cilia and acute necrosis that was followed by metaplastic transformation. Edema and diffuse alveolar damage was observed in the lungs. Our data suggest that: i) severity of respiratory lesions caused by selenium is dose dependent; ii) selenium causes transient metaplastic transformation of the tracheal epithelium; iii) chronic inflammation and increased thickness of alveolar septa occur in the lungs; iv) 4 weeks after selenium treatment, mice recover from the tracheal injury, whereas no amelioration of pulmonary lesions was observed.

Key Words: inflammation • lung alveoli • lung edema • metaplasia

Human & Experimental Toxicology, Vol. 22, No. 10, 551-557 (2003)
DOI: 10.1191/0960327103ht396oa


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This article has been cited by other articles:


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