Selenium supplementation modulates apoptotic processes in thyroid follicular cells

Abstract

Selenium (Se) is an essential micronutrient modulating several physiopathological processes in the human body. The aim of the study is to characterize the molecular effects determined by Sesupplementation in thyroid follicular cells, using as model the well-differentiated rat thyroid follicular cell line FRTL5. Experiments have been performed to evaluate the effects of Se on cell growth, mortality and proliferation and on modulation of pro-and antiapoptotic pathways. The results indicate that Sesupplementation improves FRTL5 growth rate. Furthermore, Se reduces the proportion of cell death and modulates both proapoptotic (p53 and Bim) and antiapoptotic (NF-kB and Bcl2) mRNA levels. In addition, incubation with high doses of Na-Se might prevent the ER-stress apoptosis induced by tunicamycin, as assessed by membrane integrity maintenance, reduction in caspase 3/7 activities, and reduction in Casp-3 and PARP cleavage. Taken together, these results provide molecular evidences indicating the role of Se supplementation on cell death and apoptosis modulation in thyroid follicular cells. These observations may be useful to understand the effects of this micronutrient on the physiopathology of the thyroid gland.

Effect of selenium on thyroid autoimmunity and regulatory T cells in patients with Hashimoto’s thyroiditis: A prospective randomized‐controlled trial

“…A possible mechanism for the beneficial effect of Se in HT is associated with the role of selenoenzymes in immunoregulatory processes, involving T cells activity and cytokine production. In line with this explanation, sodium selenite dose‐dependently inhibited HLA‐DR molecule expression of thyrocytes induced by IFN‐γ, and prevented apoptosis of thyroid follicular cells by TNF antagonism 40,41 . In a Polish study, the addition of selenomethionine (SeMet) to levothyroxine treatment inhibited lymphocyte release of IL‐2, IFN‐γ, and TNF, which was accompanied by a reduction of CRP 31 .…”

“…In line with this explanation, sodium selenite dose‐dependently inhibited HLA‐DR molecule expression of thyrocytes induced by IFN‐γ, and prevented apoptosis of thyroid follicular cells by TNF antagonism. 40 , 41 In a Polish study, the addition of selenomethionine (SeMet) to levothyroxine treatment inhibited lymphocyte release of IL‐2, IFN‐γ, and TNF, which was accompanied by a reduction of CRP. 31 Another Italian trial showed that supplementation with SeMet downregulated the IFN‐γ‐inducible chemokines (CXCL9 and CXCL10).…”

Selenium supplementation through Se-rich dietary matrices can upregulate the anti-inflammatory responses in lipopolysaccharide-stimulated murine macrophages

“…Increased expression of selenoproteins, including GPx1 is known to mitigate inflammation and bolster immunity that involves down-regulation of COX-2 and mPGES-1, while upregulating H-PGDS to effect a process called “eicosanoid class switching mechanism” in Se stimulated RAW264.7 cells (Yui, Imataka, Nakamura, Ohara, & Naito, 2015; Duntas, 2009; Vunta et al, 2007). Higher Se supplementation up to 2 µM in the form of sodium selenite is also reported to inhibit NFκB-dependent transcription (Nettore et al, 2017; Meplan et al, 2016; Youn et al, 2008; Maehira, Mivagi, & Eguchi, 2003). Se deficient conditions, there is increased ROS generation that is closely associated with increased inflammatory genes, which results in augmentation of oxidative stress in cells.…”

Nutritional and Environmental Factors in Thyroid Carcinogenesis

“…Its anticancer role has been recently demonstrated [60], as well as the ability to act as antiapoptotic factor in thyroid follicular cells [61]. Its natural source is soil, plants, microorganisms, animals, and sea salt, but sulfur emitted by volcanoes competes with selenium compounds for uptake by plants, causing a decrease in available selenium [22].…”