Abstract
Abstract Both selenium, as an effector and regulator of antioxidative enzymes activity, and thyroid hormones are potent immunomodulators. Besides, selenium incorporated into iodothyronine deiodinases is involved in the thyroid function and thus indirectly regulates the immune response. Studies of the mutual influence of selenium and thyroid hormones on the immune response are scarce, hence we analyzed the effects of an iodothyronine deiodinases blocker, propylthiouracil (PTU), and selenium deficiency on the function of peritoneal macrophages, and titer of naturally occurring anti-sheep red blood cells (SRBC) IgM antibodies in juvenile rats. The experiment was carried out on 64 Wistar male rats allotted to 4 groups: controlselenium adequate PTU- group; selenium adequate, PTU+ group; selenium defi cient, PTU- group; and selenium defi cient, PTU+. The selenium adequate and selenium defi cient groups were fed a diet containing 0.334 and 0.031 mg Se/kg, respectively. PTU+ groups received PTU (150 mg/L) in drinking water. After 3 weeks, thyroxine (T4), triiodothyronine (T3), and thyroid stimulating hormone (TSH) were determined. The animals having “intermediate” concentrations of T3 (1.56-1.69 nmol/L) and T4 (41-50 nmol/L) were excluded from further analysis. Thus, PTU+ groups included hypothyroid animals (T3≤1.55 nmol/L; T4≤40 nmol/L), while PTU- groups included euthyroid rats (T3≥1.70 nmol/L; T4≥50 nmol/L). Both groups of selenium deficient rats had, when compared to the control group, a significantly lower activity of glutathione peroxidase GPx1 and GPx3. Neither selenium deficiency nor PTU influenced the adherence of peritoneal macrophages. Selenium deficiency significantly decreased the peroxide synthesis in macrophages and significantly increased the titer of anti-SRBC IgM. Hypotyroidism alone or in combination with selenium deficiency had no influence on these parameters.
Highlights
Selenium is an essential microelement which achieves its biological effects in the form of selenocysteine incorporated into selenoproteins
In this study selenium status was determined on the basis of blood selenium concentration and activity of plasma glutathione peroxidase 3 activity (GPx3) and erythrocyte GPx1
Based on the measured values of these biomarkers it was estimated that the minimal selenium requirements are 0.06 mg Se/kg feed and 0.08 mg/kg feed [32]
Summary
Selenium is an essential microelement which achieves its biological effects in the form of selenocysteine incorporated into selenoproteins. Most of its immunomodulatory effects have been explained by its role in antioxidant protection, i.e. in controlling the activities of reactive oxygen species (ROS)-mediated glutathione peroxidases (Gpx) and thioredoxin reductase. Selenium deficiency results in an inadequate activity of reactive oxygen species (ROS), controlling selenoproteins, and oxidative stress mediated cells damage or, in the case of selenium excess, reduced microbicidal effect of neutrophils, monocytes/macrophages and NK cells [2,7,8,9,10]. Selenium influences cells of adaptive immunity and its deficiency is accompanied by a reduced number of T lymphocytes [11] and their decreased proliferation and differentiation [12,13,14]. Selenium deficiency reduces the number of B lymphocytes but its effect on antibody synthesis is antigen dependent [10]
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