Selenium deficiency-induced redox imbalance leads to metabolic reprogramming and inflammation in the liver

Tang, Chaohua; Li, Shuang; Zhang, Kai; Li, Jing; Han, Yunsheng; Zhan, Tengfei; Zhao, Qingyu; Guo, Xiaoqing; Zhang, Junmin

doi:10.1016/j.redox.2020.101519

Cited by 84 publications

(51 citation statements)

References 54 publications

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“…The production performance including feed intake, weight, and feed utilization rate showed that there was a significant difference between the control group and the Se-deficient group. The production performance of the Se-deficient group was significantly lower than that in the control group ( Tang et al., 2020 ). The clinical manifestations of the Se-deficient group were normal body temperature, but mental retardation, gray skin, muscle weakness, mild edema in abdomen and buttocks, swing of hind limbs during the walking, tremor, and mild diarrhea during forced exercise.…”

Section: Discussionmentioning

confidence: 63%

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

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Selenium (Se) deficiency can seriously affect the small intestine of swine, and cause diarrhea in swine. However, the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported. Here, to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal Se deficiency were established. Twenty-four pure line castrated male Yorkshire pigs (45 d old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into 2 equal groups and fed Se-deficient diet (0.007 mg Se/kg) as the Se-deficiency group, or fed Se-adequate diet (0.3 mg Se/kg) as the control group for 16 weeks. The intestinal porcine enterocyte cell line (IPEC-J2) was divided into 2 groups, and cultured by Se-deficient medium as the Se-deficient group, or cultured by normal medium as the control group. Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. Autophagy staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. According to the reactive oxygen species (ROS) staining results, the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1 , microtubule-associated proteins 1A ( LC3-1 ), microtubule-associated proteins 1B ( LC3-2 ), autophagy-related protein 5 ( ATG5 ), autophagy-related protein 12 ( ATG12 ), autophagy-related protein 16 ( ATG16 ), mammalian target of rapamycin ( mTOR ), calmodulin-dependent protein kinase kinase β ( CAMKK-β ), adenosine 5′-monophosphate-activated protein kinase ( AMPK ), sarco(endo)plasmic reticulum Ca 2+ -ATPase ( SERCA ), and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro ( P < 0.05). Altogether, our results indicated that Se deficiency could destroy the calcium homeostasis of the swine small intestine to trigger cell autophagy and oxidative stress, which was helpful to explain the mechanism of Se deficiency-induced diarrhea in swine.

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Section: Discussionmentioning

confidence: 63%

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

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“…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: 65%

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.

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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.

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“…EEFSEC is the translation factor responsible for incorporation of selenocysteines into selenoproteins [ 67 ]. Selenium depletion leads to global decrease in expression of selenoproteins [ [68] , [69] , [70] ] while selenium supplementation prior to AF treatment at low doses was shown to attenuate cell lethality [ 71 ]. EEFSEC was specifically downregulated with a ranking of 4126 out of 4377 proteins in OPLS-DA of AF against TRi-1 and TRi-2 ( Supplementary Table 4 ).…”

Section: Resultsmentioning

confidence: 99%

Comprehensive chemical proteomics analyses reveal that the new TRi-1 and TRi-2 compounds are more specific thioredoxin reductase 1 inhibitors than auranofin

et al. 2021

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Selenium deficiency-induced redox imbalance leads to metabolic reprogramming and inflammation in the liver

Cited by 84 publications

References 54 publications

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

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

Comprehensive chemical proteomics analyses reveal that the new TRi-1 and TRi-2 compounds are more specific thioredoxin reductase 1 inhibitors than auranofin

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