The role of necroptosis and apoptosis through the oxidative stress pathway in the liver of selenium-deficient swine

Zhang, Yuan; Yu, Dahai; Zhang, Jiuli; Bao, Jun; Tang, Chaohua; Zhang, Ziwei

doi:10.1039/c9mt00295b

Cited by 29 publications

(18 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Numerous studies have shown that Se‐deficient diets in different animals cause different symptoms, and the clinical symptoms of the majority of animals include varying degrees of diarrhea. Moreover, Se‐deficient swine have diarrhea associated with weight loss (Y. Zhang et al, 2020). Baldwin and Wiley's (2002) research showed that Se reduced damage to the intestinal epithelium.…”

Section: Introductionmentioning

confidence: 99%

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Zhang

Bao

et al. 2020

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

Selenium (Se) deficiency has a significant impact on the swine breeding industry by inducing digestive system damage and diarrhea. However, the molecular mechanism remains unclear. Our objectives were to investigate if different amounts of necroptosis, inflammatory responses, and T helper cell 1/T helper cell 2 (Th1/Th2) imbalances were induced by Se deficiency in intestinal porcine jejunal epithelial cells (IPEC-J2) and swine ileum tissue. Therefore, Se-deficient models were successfully established both in vitro and in vivo. In the current study, the cell morphological observation results showed that Se deficiency seriously affected the growth and differentiation of IPEC-J2 cells. Moreover, the necroptosis staining and histomorphology observation results showed that the number of necroptotic cells increased significantly, and the ileal tissue exhibited abnormal structures, including necroptotic features and inflammatory cell infiltration, in the Se-deficient group. Furthermore, Se deficiency resulted in accelerated cell necroptosis by increasing (p < .05) the expression of genes related to the tumor necrosis factor-α pathway at both the protein and messenger RNA (mRNA) levels compared to the control group. Moreover, the relative mRNA and protein expression of the inflammatory genes and their responses to dietary Se deficiency were consistent with the resultant Th1/Th2 imbalances in vitro and in vivo. Taken together, the results suggested that Se deficiency caused necroptosis, inflammatory responses, and abnormal expression of cytokines in swine ileum tissue. These findings might help us to explain the damage induced by Se deficiency to the digestive system of swine.

show abstract

Section: Introductionmentioning

confidence: 99%

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Zhang

Bao

et al. 2020

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The recognized sign of selenium (Se) deficiency, liver necrosis, was mostly discovered in rats (Burk et al, 2010;Schwarz and Foltz, 2010; and swines (Tang et al, 2020;Zhang Y. et al, 2020). However, in our previous report (Huang et al, 2011(Huang et al, , 2015, we also found liver necrosis induced by Se and vitamin E (VE) deficiency in chicks.…”

Section: Introductionmentioning

confidence: 66%

“…And six common genes (Gpx1, Gpx4, Selenok, Selenoo, Selenop, and Selenow) were downregulated by dietary Se deficiency in liver and muscle at weeks 2 and 6 (Huang et al, 2015;Sun et al, 2018). In addition to the analogous response of these selenoprotein genes in other animals (Huang et al, 2015;Sunde et al, 2016;Sun et al, 2018;Chen et al, 2019;Zhang Y. et al, 2020), these (a, b, c, d).…”

Section: Discussionmentioning

confidence: 92%

“…Generally, apoptosis and necrosis are considered to be separate entities, but an alternate view is emerging that both are frequently a result of the same initiating factors and signaling pathways. Furthermore, apoptosis and necrosis in their pure form may represent extremes of a continuum of cell death rather than being separate entities (Zhang Y. et al, 2020). However, the protection of VE against the incidence of liver necrosis in the Se-deficient chicks was seemingly independent of muscle GPX and SOD activities.…”

Section: Discussionmentioning

confidence: 98%

“…The lack of Se and VE in chicks leads to hepatic necrosis and increased peroxidation (Guillermo et al, 2018). Lipid peroxidation may cause membrane destruction and cell death, thereby triggering the process of necrosis (Burk et al, 1980;Zhang Y. et al, 2020). Although the mechanistic basis of mitochondrial injury may vary in different settings, mitochondrial permeability and dysfunction are common events that lead to cell apoptosis and necrosis (Guicciardi et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Selenoproteins Protect Against Avian Liver Necrosis by Metabolizing Peroxides and Regulating Receptor Interacting Serine Threonine Kinase 1/Receptor Interacting Serine Threonine Kinase 3/Mixed Lineage Kinase Domain-Like and Mitogen-Activated Protein Kinase Signaling

Zhang

Wang

et al. 2021

Front. Physiol.

View full text Add to dashboard Cite

Liver necroptosis of chicks is induced by selenium (Se)/vitamin E (VE) deficiencies and may be associated with oxidative cell damage. To reveal the underlying mechanisms of liver necrosis, a pool of the corn–soy basal diet (10 μg Se/kg; no VE added), a basal diet plus all-rac-α-tocopheryl acetate (50 mg/kg), Se (sodium selenite at 0.3 mg/kg), or both of these nutrients were provided to day-old broiler chicks (n = 40/group) for 6 weeks. High incidences of liver necrosis (30%) of chicks were induced by –SE–VE, starting at day 16. The Se concentration in liver and glutathione peroxidase (GPX) activity were decreased (P < 0.05) by dietary Se deficiency. Meanwhile, Se deficiency elevated malondialdehyde content and decreased superoxide dismutase (SOD) activity in the liver at weeks 2 and 4. Chicks fed with the two Se-deficient diets showed lower (P < 0.05) hepatic mRNA expression of Gpx1, Gpx3, Gpx4, Selenof, Selenoh, Selenok, Selenom, Selenon, Selenoo, Selenop, Selenot, Selenou, Selenow, and Dio1 than those fed with the two Se-supplemented diets. Dietary Se deficiency had elevated (P < 0.05) the expression of SELENOP, but decreased the downregulation (P < 0.05) of GPX1, GPX4, SELENON, and SELENOW in the liver of chicks at two time points. Meanwhile, dietary Se deficiency upregulated (P < 0.05) the abundance of hepatic proteins of p38 mitogen-activated protein kinase, phospho-p38 mitogen-activated protein kinase, c-Jun N-terminal kinase, phospho-c-Jun N-terminal kinase, extracellular signal-regulated kinase, phospho-mitogen-activated protein kinase, receptor-interacting serine-threonine kinase 1 (RIPK1), receptor-interacting serine-threonine kinase 3 (RIPK3), and mixed lineage kinase domain-like (MLKL) at two time points. In conclusion, our data confirmed the differential regulation of dietary Se deficiency on several key selenoproteins, the RIPK1/RIPK3/MLKL, and mitogen-activated protein kinase signaling pathway in chicks and identified new molecular clues for understanding the etiology of nutritional liver necrosis.

show abstract

Selenium deficiency causes apoptosis through endoplasmic reticulum stress in swine small intestine

Zheng

Zhang²,

Guan

et al. 2021

BioFactors

Self Cite

View full text Add to dashboard Cite

Selenium (Se) plays a crucial role in intestinal health. However, the specific mechanism by which deficiency of Se causes intestinal damage remains unclear. This study was to explore whether Se deficiency can cause ER stress and induce apoptosis in swine small intestine. We established the Se deficiency swine model in vivo and the intestinal epithelial (IPEC-J2) cell Se deficiency model in vitro. The results of morphological observation showed that Se deficiency caused structural damage in intestinal villi and the decrease of goblet cell structure. The apoptotic characteristics such as nucleolar condensation, mitochondrial swelling, and apoptotic bodies were observed in the IPEC-J2 cells. The results of acridine orange/ethidium bromide and mitochondrial membrane potential fluorescence staining in vitro showed that there were more apoptotic cells in the Se-deficiency group than that in the control group. The protein and/or mRNA expression levels of Bax, Bcl-2, caspase 3, caspase 8, caspase 9, cytc, PERK, ATF6, IRE, XBP1, CHOP, GRP78, which are related to ER stress-apoptosis pathway, were significantly increased in the Se-deficient group which compared with the control group in vivo and in vitro were consistent. These results indicated that Se deficiency induced ER stress and increased the apoptosis in swine small intestine and IPEC-J2 cells and then caused the damage in swine small intestinal tissue. Besides, the results of gene expressions in our experiment proved that ER stress induced by Se deficiency promoted

show abstract

The role of necroptosis and apoptosis through the oxidative stress pathway in the liver of selenium-deficient swine

Abstract: Necroptosis is regarded as a new paradigm of cell death that plays a key role in the liver damage observed with selenium (Se) deficiency.

Cited by 29 publications

References 49 publications

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Selenium deficiency induced necroptosis, Th1/Th2 imbalance, and inflammatory responses in swine ileum

Selenoproteins Protect Against Avian Liver Necrosis by Metabolizing Peroxides and Regulating Receptor Interacting Serine Threonine Kinase 1/Receptor Interacting Serine Threonine Kinase 3/Mixed Lineage Kinase Domain-Like and Mitogen-Activated Protein Kinase Signaling

Selenium deficiency causes apoptosis through endoplasmic reticulum stress in swine small intestine

Contact Info

Product

Resources

About