Dietary Selenium Deficiency Facilitated Reduced Stomatin and Phosphatidylserine Externalization, Increasing Erythrocyte Osmotic Fragility in Mice

Duan, Shiyu; Chen, Sijie; Liang, Wan; Chen, Miaoyu; Chen, Yu; Guo, Mengyao

doi:10.1007/s12011-020-02162-3

Cited by 7 publications

(1 citation statement)

References 42 publications

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“…Osmotic fragility tests revealed that the erythrocytes from the Se-D group were more prone to hemolysis than those in Se-A group under hypotonic stress, possibly because of oxidative stress-mediated changes in erythrocyte membranes [ 33 , 34 ]. The results are similar to those from previous studies on mice and chickens fed a Se-deficient diet [ 30 , 34 , 35 ]. Se deficiency did not significantly affect the spleen index in pigs, in agreement with results obtained in chickens with Se deficiency for 3 weeks [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

Selenium deficiency induces spleen pathological changes in pigs by decreasing selenoprotein expression, evoking oxidative stress, and activating inflammation and apoptosis

Sun

Zhang

et al. 2021

J Animal Sci Biotechnol

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Background The immune system is one aspect of health that is affected by dietary selenium (Se) levels and selenoprotein expression. Spleen is an important immune organ of the body, which is directly involved in cellular immunity. However, there are limited reports on Se levels and spleen health. Therefore, this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis. Methods Twenty-four pure line castrated male Yorkshire pigs (45 days old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into two equal groups and fed Se-deficient diet (0.007 mg Se/kg) or Se-adequate diet (0.3 mg Se/kg) for 16 weeks. At the end of the trial, blood and spleen were collected to assay for erythroid parameters, the osmotic fragility of erythrocytes, the spleen index, histology, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining, Se concentrations, the selenogenome, redox status, and signaling related inflammation and apoptosis. Results Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes (P < 0.05). The spleen index did not change, but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased, the red pulp increased, and splenocyte apoptosis occurred in the Se deficient group. Se deficiency decreased the Se concentration and selenoprotein expression in the spleen (P < 0.05), blocked the glutathione and thioredoxin antioxidant systems, and led to redox imbalance. Se deficiency activated the NF-κB and HIF-1α transcription factors, thus increasing pro-inflammatory cytokines (IL-1β, IL-6, IL-8, IL-17, and TNF-α), decreasing anti-inflammatory cytokines (IL-10, IL-13, and TGF-β) and increasing expression of the downstream genes COX-2 and iNOS (P < 0.05), which in turn induced inflammation. In addition, Se-deficiency induced apoptosis through the mitochondrial pathway, upregulated apoptotic genes (Caspase3, Caspase8, and Bak), and downregulated antiapoptotic genes (Bcl-2) (P < 0.05) at the mRNA level, thus verifying the results of TUNEL staining. Conclusions These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins, oxidative stress, inflammation and apoptosis.

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