Lung Permeability, Antioxidant Status, and NO2 Inhalation: A Selenium Supplementation Study in Rats

• Published in: Journal of Toxicology and Environmental Health, Part A: Strategies for Clean Air and Health Part A: Strategies for Clean Air and Health, 2007-02, Vol.70 (3-4), p.284-294
• Main Authors: de Burbure, C. Y., Heilier, J.-F., Nève, J., Becker, A., Albrecht, C., Borm, P. J. A., Gromadzinska, J., Wasowicz, W., Rydzynski, K., Bernard, A. M.
• Format: Article
• Language: English
• Subjects: Acid Phosphatase - metabolism; Air Pollutants - adverse effects; Alkaline Phosphatase - metabolism; Animals; Antioxidants - metabolism; Biomarkers - analysis; Biomarkers - blood; Bronchoalveolar Lavage Fluid - chemistry; Dietary Supplements; Dose-Response Relationship, Drug; Inhalation Exposure; L-Lactate Dehydrogenase - metabolism; Lung - drug effects; Male; Nitrogen Dioxide - adverse effects; Permeability - drug effects; Rats; Rats, Wistar; Selenium - pharmacology; Thiobarbituric Acid Reactive Substances - metabolism; Uteroglobin - metabolism
• ISSN: 1528-7394; 1087-2620
• DOI: 10.1080/15287390600884875

Little is known about antioxidant status, selenium status in particular, and lung response to NO 2 , which acts as a proinflammatory air pollutant. The effects of a low selenium diet (1.3 μg Se/d) with or without selenium supplementation were therefore studied in 128 Wistar rats, 2 mo old, male exposed to either acute (50 ppm, 30 min), intermittent subacute (5 ppm, 6 h/d, 5 d), intermittent long-term NO 2 (1 ppm, 10 ppm, 6 h/d, 5 d/wk, 28 d), or normal atmospheric air (controls). Following sacrifice, measurements of lipid peroxidation (thiobarbituric acid-reactive substances, chemiluminescence), antioxidative protective enzymes (glutathione peroxidase [GPx], superoxide dismutase [SOD], glutathione S-transferase [GST], ceruloplasmin), lung damage (lactate dehydrogenase, alkaline and acid phosphatases), lung permeability (total protein, albumin), and inflammation (cell populations), along with the determination of new biomarkers such as CC16 (Clara-cell protein), were performed in serum and bronchoalveolar lavage fluid (BALF). While selenium-supplemented animals had increased GPx activity in serum prior to inhalation experiments, they also had decreased BALF CC16, blood SOD, and GST levels. Nevertheless, the protective role of normal selenium status with respect to NO 2 lung toxicity was evident both for long-term and acute exposures, as the increase in BALF total proteins and corresponding decrease in serum (indicating increased lung permeability) was significantly more pronounced in selenium-deficient animals. During the various inhalation experiments, serum CC16 demonstrated its key role as an early marker of increased lung permeability. These findings corroborate the important role of selenium status in NO 2 oxidative damage modulation, but also indicate, in view of its negative impact on CC16, a natural anti-inflammatory and immunosuppressor, that caution should be used prior to advocating selenium supplementation.