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Eur Respir J 1993; 6: 1317-1323
Copyright © ERS Journals Ltd 1993


Original Articles

Selenium deficiency augments the pulmonary toxic effects of oxygen exposure in the rat

FH Hawker, HE Ward, PM Stewart, LA Wynne, and PJ Snitch

Selenium (Se) is a component of the antioxidant enzyme glutathione peroxidase (GSHPx). We wanted to determined whether Se deficiency predisposes to pulmonary O2 toxicity. Sixteen weanling rats were fed a Se-free diet (Se-). Sixteen rats fed the same diet had drinking water supplemented with 400 micrograms.l-1 sodium selenite (Se+). After 5 weeks, rats were killed after exposure to either 95% O2 or air for 36 h. Se concentration in blood, lung, liver, heart, muscle and spleen, and blood GSHPx activity were higher in Se+ than in Se- groups. Pulmonary oedema developed in both O2-exposed groups, but was more severe in Se-O2 group than in the Se+O2 group, as judged by the presence of pleural effusions (7 out of 8 versus 0 out of 8), elevated lavage protein concentration (173 +/- 17 versus 120 +/- 14 micrograms.ml-1), and higher wet/dry weight ratio (W:D) (5.8 +/- 0.07 versus 5.4 +/- 0.07). W:D correlated inversely with lung Se content in O2-exposed rats. Both O2-exposed groups had a reduction in the amount of less aggregated lavage phospholipid (PL) compared with the Se+air group. However, the Se-O2 group had increased total PL, because of an increase in more aggregated PL. We conclude that Se deficiency exacerbates pulmonary injury in O2-exposed rats, and that O2 toxicity is associated with an altered physical form of alveolar surfactant.


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