Abstract
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.
Highlights
The recognized sign of selenium (Se) deficiency, liver necrosis, was mostly discovered in rats (Burk et al, 2010; Schwarz and Foltz, 2010; Wang H. et al, 2020) and swines (Tang et al, 2020; Zhang Y. et al, 2020)
We have investigated the expression profiles of 14 selenoprotein genes (i.e., Gpx1, Gpx4, Selenof, Selenoi, Selenok, Selenon, Selenoo, Selenop, Selenos, Selenot, Selenow, Msrb1, Txnrd1, and Txnrd2) in the liver and muscles of chicks fed with Se-deficient (0.01 mg/kg) and adequate (0.3 mg/kg) diets at week 6 (Huang et al, 2011, 2015)
24–25 selenoprotein genes were postulated in avians (Mariotti et al, 2012; Li et al, 2018), so this study followed to investigate the changes of 25 selenoproteins in the liver of chicks responded to dietary Se and vitamin E (VE) deficiencies
Summary
The recognized sign of selenium (Se) deficiency, liver necrosis, was mostly discovered in rats (Burk et al, 2010; Schwarz and Foltz, 2010; Wang H. et al, 2020) and swines (Tang et al, 2020; Zhang Y. et al, 2020). We have investigated the expression profiles of 14 selenoprotein genes (i.e., Gpx, Gpx, Selenof, Selenoi, Selenok, Selenon, Selenoo, Selenop, Selenos, Selenot, Selenow, Msrb, Txnrd, and Txnrd2) in the liver and muscles of chicks fed with Se-deficient (0.01 mg/kg) and adequate (0.3 mg/kg) diets at week 6 (Huang et al, 2011, 2015). Dietary Se deficiency decreased (P < 0.05) mRNA levels of seven common selenoprotein genes (i.e., Gpx, Gpx, Selenok, Selenon, Selenoo, Selenop, and Selenow) in liver and muscle. The activities and mRNA levels of two abundant selenoprotein (GPX1 and GPX4) genes are highly regulated by Se status in chicks (Huang et al, 2011; Li et al, 2018; Ren et al, 2018). Other five selenoprotein genes code for glutathione peroxidase 3 (GPX3) (Zhu et al, 2018), selenoprotein P (SELENOP) (Short et al, 2020; GülKlein et al, 2021), selenoprotein W (SELENOW) (Shin et al, 2019), selenoprotein N (SELENON) (Silwal et al, 2020), and methionine sulfoxide reductase B1 (MsrB1) were regulated by Se status in chicks
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