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

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 expo...

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Published inJournal of Toxicology and Environmental Health, Part A: Strategies for Clean Air and Health Vol. 70; no. 3-4; pp. 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.
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Published England Taylor & Francis Group 01.02.2007
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Abstract 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.
AbstractList Little is known about antioxidant status, selenium status in particular, and lung response to NO2, which acts as a proinflammatory air pollutant. The effects of a low selenium diet (1.3 microg 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 NO2 (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 NO2 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 NO2 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.
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.
Author de Burbure, C. Y.
Nève, J.
Heilier, J.-F.
Borm, P. J. A.
Bernard, A. M.
Rydzynski, K.
Gromadzinska, J.
Becker, A.
Wasowicz, W.
Albrecht, C.
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Snippet 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...
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SubjectTerms 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
Title Lung Permeability, Antioxidant Status, and NO2 Inhalation: A Selenium Supplementation Study in Rats
URI https://www.tandfonline.com/doi/abs/10.1080/15287390600884875
https://www.ncbi.nlm.nih.gov/pubmed/17365591
Volume 70
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