Influence of Selenium on Mast Cell Mediator Release Reza Safaralizadeh & Maryam Nourizadeh & Ahad Zare & Gholam Ali Kardar & Zahra Pourpak Received: 15 February 2013 / Accepted: 20 May 2013 / Published online: 20 June 2013 # Springer Science+Business Media New York 2013 Abstract Selenium supplementation still enhanced the im- mune response even in individuals who, according to cur- rent standards, would be considered as not being overtly selenium deficient. Mast cells are granulated cells that play a pivotal role in allergic reactions. In this study, we inves- tigated the modulatory effect of sodium selenite on medi- ator release and degranulation of murine mast cell line (MC/9). Cells were pre-treated with selenium selenite (1, 2, 3 μg/ml) for 24 h and controls left untreated. Then, cells were sensitized overnight with anti-dinitrophenyl (DNP) IgE and challenged with DNP/HSA for degranulation in- duction. The histamine and prostaglandin D2 (PGD2) were measured by ELISA, and β-hexosaminidase was measured by spectrophotometery method. Selenium-treated cells re- vealed significant decrease in concentration of PGD2 (P=0.019) and β-hexosaminidase (P=0.009). In addition, a slight reduction of histamine release by the selenium- treated cells was observed, based on our intracellular and extracellular assessments. The most inhibitory effect of sele- nium supplementation on mediator release of MC/9 cells was obtained in the presence of 3 μg/ml of sodium selenite. The results of the present study demonstrate beneficial effects of supplemental selenium in attenuating clinical manifestations of allergy and asthma. Keywords Murine mast cell line . Selenium . Histamine . Prostaglandin D2 . β-Hexosaminidase Introduction Previous studies demonstrated that selenium reduces the severity of the inflammatory responses, including the mod- ulation of the important mediators of acute asthmatic re- actions and of pro-inflammatory leukotrienes, as well as sustaining the inflammatory process that reduces the late allergic reaction metabolism. Moreover, selenium deficien- cy diminishes the effectiveness of the immune cells [1–3]. Mast cells play a central role in inflammatory and imme- diate allergic reactions upon FcεRI crosslinking [4]. Con- stant mast cell activation in asthma appears to be a charac- teristic of the chronic inflammatory nature of the disease such as tissue remodeling, smooth muscle hypertrophy, and mucus hypersecretion [5, 6]. These mediators such as hista- mine, proteases, chemotactic factors, cytokines, and metab- olites of arachidonic acid may affect the vasculature, smooth muscle, connective tissue, mucous glands, and inflammato- ry cells. Thus, it is necessary to investigate different anti- inflammatory reagents for preventing uncontrolled release of these mediators which can result in severe allergic reactions [7, 8]. Observational studies have reported the associations be- tween asthma and dietary antioxidants (vitamin E, vitamin C, carotenoids, selenium, polyphenols, and vitamin D) [9, 10]. Anti-inflammatory effect of selenium on the LPS-induced ex- pression of two important pro-inflammatory genes (TNF-α and cyclooxygenase-2) in murine macrophages has been reported [11]. Thus, manipulating the function and mediator release of mast cells might be a promising strategy in controlling the outcome of allergic and inflammatory responses [5, 12]. In the present study, we therefore investigated the effects of supplemental selenium on the release of mast cell medi- ators including histamine, prostaglandin D2, and β- hexosaminidase in a murine mast cell line (MC/9). R. Safaralizadeh Department of Animal Biology, Faculty of Natural Science, University of Tabriz, 29 bahman Blvd, Tabriz, Iran M. Nourizadeh : A. Zare : G. A. Kardar : Z. Pourpak (*) Immunology Asthma and Allergy Research Institute, Tehran University of Medical Sciences, Tehran, Iran e-mail: zpourpak@hbi.ir Z. Pourpak Departmen of Immunology and Allergy, Children Medical Center, Tehran University of Medical Sciences, Tehran, Iran Biol Trace Elem Res (2013) 154:299–303 DOI 10.1007/s12011-013-9712-x