Effects of Iron Oxide Nanoparticles on Pulmonary Morphology, Redox System, Production of Immunoglobulins and Chemokines in Rats: In Vivo and in Vitro Studies

Brigitta Szalay1, Zuzana Kováciková2, Márta Brózik3, Tamás Pándics1, and Erzsébet Tátrai1

1 National Institute of Environmental Health, Budapest, Hungary
2 Slovak Medical University, Bratislava, Slovakia
3 National Institute of Rheumatology and Physiotherapy, Budapest, Hungary

Corresponding author: Brigitta Szalay
    National Institute of Environmental Health
    1097, Gyáli út 2-6
    Budapest H-1437, PO Box 839, Hungary
    Telephone: +36-1-476-1100
    Fax number: 36-1-215-0148
    E-mail: brszalay@gmail.com

CEJOEM 2008, Vol.14. No.2.: 149-164

Key words:
iron oxide, nanoparticles, EC-SOD, immunoglobulins, lungs, MCP-1; MIP-1 alpha, pulmonary morphology, rats, total glutathione

Abstract:
Nano-sized iron oxide has recently been hypothesized to change pulmonary morphology, metabolism, and immunological reactions. The aim of our study was the determination of the effect of iron oxide nanoparticles on pulmonary morphology, redox system, production of immunoglobulins and chemokines based on single intratracheal instillation in male SPRD rats. Histology of the lungs and their regional lymph nodes was examined after iron  (III) oxide exposure. IgA, IgG and IgM were determined in bronchoalveolar lavage (BAL) and the whole blood by enzyme-linked immunosorbent assay (ELISA). Total glutathione (GSH) and extracellular superoxide dismutase (EC-SOD) were measured after one week and one month of exposure. In addition, the primary culture of alveolar macrophages and type II alveolar epithelial cells was exposed with iron oxide (average particle size: 29 nm) for determination of LC50. The cell membranes were studied by lectin histochemistry. The expression of macrophage inhibitory protein-1α (MIP-1α) and macrophage chemoattractant protein-1 (MCP-1) was determined from the supernatant of primary culture of these cells. Iron oxide caused interstitial pulmonary inflammation with moderate fibrosis by the end of the 4th postexposure week. IgA decreased significantly in the whole blood, but not in bronchoalveolar lavage. IgG and IgM significantly decreased in BAL, whereas they were unchanged in blood. The expression of MCP-1 and MIP-1α in alveolar macrophages and pneumocytes type II increased significantly. These results show that iron oxide nanoparticles caused mild pulmonary toxicity: they induced moderate interstitial inflammation and fibrosis furthermore immunosuppression of immunoglobulins examined.

Received: 6 October 2008
Accepted: 28 November 2008
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