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The levels of hydrogen sulfide in chicken livers. The asterisk indicates that there were significant differences (p < 0.05) between the control group and the lab group. Each value represented the means ± SD of 20 individuals
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Selenium (Se) is an indispensable trace mineral that was associated with liver injuries in animal models. Hydrogen sulfide (H2S) is involved in many liver diseases, and autophagy can maintain liver homeostasis with a stress stimulation. However, little is known about the correlation between H2S and autophagy in the liver injury chicken models induc...
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Sleep deprivation (SD) is widespread in society causing serious damage to cognitive function. Hydrogen sulfide (H2S), the third gas signal molecule, plays important regulatory role in learning and memory functions. Inhibition of excessive autophagy and upregulation of silent information regulator 1 (Sirt-1) have been reported to prevent cognitive d...
Citations
... In some in vitro studies, 3-MST is also recognized as a potential selenium transporter which carries selenium in the form of selenodiglutathione in metabolic pathways, where selenophosphate synthesis is required to produce Secys-tRNA, a precursor of selenocysteine present in selenoenzymes in bacteria and mammals [120]. Contrarily, supplementation of selenium deficient diets with chicken resulted in abnormal increases in the levels of H 2 S released by 3-MST, CSE, and CBE, inducing liver injury [121,122]. These studies highlight the importance of achieving proper balance between selenium supply and the H 2 S-producing role of 3-MST for desired pharmacological effect. ...
3-mercaptopyruvate sulfurtransferase (3-MST) plays the important role of producing hydrogen sulfide. Conserved from bacteria to Mammalia, this enzyme is localized in mitochondria as well as the cytoplasm. 3-MST mediates the reaction of 3-mercaptopyruvate with dihydrolipoic acid and thioredoxin to produce hydrogen sulfide. Hydrogen sulfide is also produced through cystathionine beta-synthase and cystathionine gamma-lyase, along with 3-MST, and is known to alleviate a variety of illnesses such as cancer, heart disease, and neurological conditions. The importance of cystathionine beta-synthase and cystathionine gamma-lyase in hydrogen sulfide biogenesis is well-described, but documentation of the 3-MST pathway is limited. This account compiles the current state of knowledge about the role of 3-MST in physiology and pathology. Attempts at targeting the 3-MST pathway for therapeutic benefit are discussed, highlighting the potential of 3-MST as a therapeutic target.
... The liver is an affected organ when selenium deficiency occurs. 28 Selenium prevents apoptosis, necrosis, and other damage as a result of oxidative stress. It suppresses the upregulation of metal-induced autophagy. ...
Selenium (Se) deficiency is associated with certain abnormalities, such as Keshan disease, cancer, cardiovascular disease (CVD), viral infections, infertility, immune system abnormalities, metabolic diseases, neurological disorders, and growth retardation. Its antioxidant properties are integrated into various selenoenzymes, mainly glutathione peroxidase (GPx) and thioredoxin reductase (Trx). These selenoenzymes act as a protective mechanism to prevent oxidative stress-induced cellular injury, regulate DNA transcription, and cell proliferation. Decreased levels of antioxidants induce reactive oxygen species (ROS) accumulation resulting in loss of mitochondrial structure and function. The antioxidant properties of selenium could depress ROS and modulates autophagy by interfering initiation of autophagy and phagophore formation. Inhibition at the initiation stage not only involves mTOR and AMPK, an autophagy-related regulators, but also autophagy markers, including Beclin 1, Atg5, LC3, and p62; thus, phagophore and autophagosome are not formed. This review will discuss the role of selenium in modulating autophagy in various organs.
... Adding appropriate Se could inhibit the crosstalk between cadmium-induced endoplasmic reticulum stress and autophagy, thereby alleviating the toxicity of cadmium to liver cancer cells [64]. Se deficiency caused an increase in the expression of autophagy-related genes (ATG5, LC3-I, LC3-II, Beclin1, and Dynein) in the liver, and autophagy participated in the liver injury model of Se-deficient chickens [65]. Our findings were in good agreement with these studies and indicated that the ChTLR4/MyD88/NF-κB signaling pathway mediated the occurrence of autophagy in the Se-deficient bursa of Fabricius. ...
To explore the role of ChTLR4/MyD88/NF-κB signaling pathway on autophagy induced by selenium (Se) deficiency in the chicken bursa of Fabricius, autophagosome formation in the bursa of Fabricius was observed by transmission electron microscopy. Quantitative real-time PCR (qRT-PCR) and Western blot were used to detect the expression of ChTLR4 and its signaling pathway molecules (MyD88, TRIF, and NF-κB), inflammatory factors (IL-1β, IL-8, and TNF-α), and autophagy-related factors (ATG5, Beclin1, and LC3-II) in the Se-deficient chicken bursa of Fabricius at different ages. The results showed that ChTLR4/MyD88/NF-κB signaling pathway was activated in the chicken bursa of Fabricius and autophagy was induced at the same time by Se deficiency. In order to verify the relationship between the autophagy and ChTLR4/MyD88/NF-κB signaling pathway, HD11 cells were used to establish the normal C group, low Se group, and low Se + TLR4 inhibitor (TAK242) group. The results demonstrated that autophagy could be hindered when the TLR4 signaling pathway was inhibited under Se deficiency. Furthermore, autophagy double-labeled adenovirus was utilized to verify the integrity of autophagy flow induced by Se deficiency in HD11 cells. The results showed that it appeared to form a complete autophagy flow under the condition of Se deficiency and could be blocked by TAK242. In summary, we found that Se deficiency was involved in the chicken bursa of Fabricius autophagy occurring by activating the ChTLR4/MyD88/NF-κB pathway.
... Typical mitophagy with many mitochondrial malformations, impaired mitochondrial structure, and blurred mitochondrial cristae morphology was observed in hepatocytes of the low-selenium group compared to the normal group, in keeping with the previous study [41]. Notably, in addition to the liver, selenium deficiency is also closely associated with autophagy in spleen and heart tissues [42,43]. ...
... The activation of ULK1 proteins induces activation of hepatic mitophagy activity [45], which in turn attenuated isoproterenol-induced myocardial fibrosis in mice [46]. On the contrary, the expression of mTOR and p-mTOR proteins gradually increased, and mitophagy was reduced in nano-selenium supplement groups, consistent with the other studies [27,45,47], suggesting that selenium can increase mTOR and p-mTOR protein expression and effectively reduce oxidative stress as well as autophagy [41]. Furthermore, the expression of ULK1 and p-ULK1 proteins decreased after nano-selenium supplement interventions. ...
Background:
As a central organ of energy metabolism, the liver is closely related to selenium for its normal function and disease development. However, the underlying roles of mitochondrial energy metabolism and mitophagy in liver fibrosis associated with selenium remain unclear.
Methods:
28 rats were randomly divided into normal, low-selenium, nano-selenium supplement-1, and supplement-2 groups for a 12-week intervention. We observed pathological and ultrastructural changes in the liver and analyzed the effects of selenium deficiency and nano-selenium supplementation on liver metabolic activities and crucial proteins expression of mammalian target of the rapamycin (mTOR) signaling pathway.
Results:
Selenium deficiency caused liver pathological damage and fibrosis with the occurrence of mitophagy by disrupting normal metabolic activities; meanwhile, the mTOR signaling pathway was up-regulated to enhance mitophagy to clear damaged mitochondria. Furthermore, nano-selenium supplements could reduce the severity of pathological damage and fibrosis in livers and maintain normal energy metabolic activity. With the increased concentrations of nano-selenium supplement, swelling mitochondria and mitophagy gradually decreased, accompanied by the higher expression of mTOR and phosphorylation-modified mTOR proteins and lower expression of unc-51 like autophagy activating kinase 1 (ULK1) and phosphorylation-modified ULK1 proteins.
Conclusions:
Mitophagy regulated by the mTOR signaling pathway plays a dual protective role on low-selenium inducing liver fibrosis and nano-selenium supplements preventing liver fibrosis. Mitochondrial energy metabolism plays an important role in these processes as well.
... Also, Se deficiency improved autophagy, H 2 S production and expression of CBS, CSE, and 3-MST genes in the liver, all of which are involved in liver injury [7]. Dietary supplementation of 3 mg/kg arsenic blocked chicken liver growth and development; decreased liver protein contents, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, nitric oxide (NO) content, activities of total nitric oxide synthase (TNOs), and inducible nitric oxide synthase (iNOS); and increased the content of MDA, activities of alanine transaminase (ALT) and aspartate aminotransferase (AST) and apoptosis rates of liver cells [8]. ...
Selenium-enriched yeast (SeY) plays an important role in the liver health and metabolism of the broiler. However, the mechanism by which it regulates liver metabolism and the health of broilers is largely unknown. Therefore, this study was conducted to elucidate the key genes and signaling pathways involved in regulating SeY in liver metabolism and bird’s health. Thus, the mRNA expression microarray, GSE25151, was downloaded from Gene Expression Omnibus (GEO) database. GSE25151 consists of liver samples from SeY-treated and the control broilers. Six hundred four differentially expressed genes (DEGs) were identified in livers between SeY-treated and control. Gene ontology (GO) enrichment analysis indicated that those DEGs are mainly involved in metabolism-related biological processes, such as biological regulation, molecular processes, responses to stimuli, cell communication and proliferation, and growth. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed the DEGs mainly enriched in metabolism-related signaling pathways, including PI3K, Akt, Wnt, calcium, IGF1 receptor, and MAPK signaling pathways. Moreover, many genes, such as NMUR1, NMU, and GPRC6A, might contribute to the regulation of SeY to broiler liver metabolism and health. In conclusion, the current study enhances our understanding of the regulation of SeY in liver metabolism and health of the birds and will assist studies of the molecular mechanisms of SeY regulation in chicken liver.
... Endogenous H 2 S is mainly produced from L-cysteine by cystathionine-γ-lyase (CSE) and cystathionine-β-synthase, and from β-mercaptopyruvic acid catalyzed by 3-mercaptopyruvate sulfurtransferase in the mitochondria. In vasculature, endogenous H 2 S is mainly produced by CSE and 3-MST [10][11][12][13] . H 2 S has many important functions, including modifying neuronal conduction, regulating vascular tone, protecting tissues from oxidative stress, anti-oxidation, anti-apoptosis, and anti-inflammatory 14 . ...
Inhibition of RhoA-ROCK pathway is involved in the H 2 S-induced cerebral vasodilatation and H 2 S-mediated protection on endothelial cells against oxygen-glucose deprivation/reoxygenation injury. However, the inhibitory mechanism of H 2 S on RhoA-ROCK pathway is still unclear. The aim of this study was to investigate the target and mechanism of H 2 S in inhibition of RhoA/ROCK. GST-RhoA wild and GST-RhoA S188A proteins were constructed and expressed, and were used for phosphorylation assay in vitro. Recombinant RhoA wild -pEGFP-N1 and RhoA S188A -pEGFP-N1 plasmids were constructed and transfected into primary hippocampal nerve cells (HNCs) to evaluate the neuroprotective mechanism of endothelial H 2 S by using transwell co-culture system with endothelial cells from cystathionine-γ-lyase knockout (CSE −/− ) mice and 3-mercaptopyruvate sulfurtransferase knockout (3-MST −/− ) rats, respectively. We found that NaHS, exogenous H 2 S donor, promoted RhoA phosphorylation at Ser188 in the presence of cGMP-dependent protein kinase 1 (PKG1) in vitro. Besides, both exogenous and endothelial H 2 S facilitated the RhoA phosphorylation at Ser188 in HNCs, which induced the reduction of RhoA activity and membrane transposition, as well as ROCK 2 activity and expression. To further investigate the role of endothelial H 2 S on RhoA phosphorylation, we detected H 2 S release from ECs of CSE +/+ and CSE −/− mice, and 3-MST +/+ and 3-MST −/− rats, respectively, and found that H 2 S produced by ECs in the culture medium is mainly catalyzed by CSE synthase. Moreover, we revealed that both endothelial H 2 S, mainly catalyzed by CSE, and exogenous H 2 S protected the HNCs against hypoxia-reoxygenation injury via phosphorylating RhoA at Ser188.
... LC3 and ATG5 have been shown to participate in the formation of the autophagosome (Bansal et al. 2018). Dyneins are large multi-component microtubule-based molecular motors involved in many fundamental cellular processes, and may act as transporters critically functioning in the combination of autophagosomes with lysosomes induced by Se deficiency (Wenzhong et al. 2017). Beclin1 is involved in the early stages of autophagosome formation, promoting autophagosome nucleation (Aguilera et al. 2012). ...
To investigate the effects of Selenium (Se) deficiency on testis development and autophagy in chicks. 20 1-day old cocks were randomly divided into two groups, named the control check (CK) group [a basic diet (containing 0.333 mg Se/kg) was fed] and the Se-deficiency (Low Se) group [a selenium deficiency diet (containing 0.033 mg Se/kg) was supplied]. After 30 days, the body and testicle weights of the chicks were measured, and the organ coefficient was calculated. While haematoxylin–eosin staining, enzyme-linked immunosorbent assay, colorimetric method was used to assess the histopathological changes of testis, the changes of sex hormone levels, and antioxidant enzyme activities in two groups of chicks, respectively, the mRNA and protein expression of autophagy-related factors in the testes was determined by using quantitative PCR and western blotting. We found that Se deficiency resulted in a significant decrease in body and testicle weights of the chicks, a reduction in organ coefficients, and damaged testis tissue. The levels of sex hormone testosterone, oestradiol, the activities of serum antioxidant enzymes T-AOC, GSH-ST and GSH-PX in the Low-Se group were significantly lower than those in the CK group. Furthermore, the level of autophagy was significantly increased in the Low-Se group compared with the CK counterpart. The mRNA levels of Beclin1, Dynein, ATG-4B, ATG5, LC3-A and LC3-B genes in the Low-Se group were significantly higher than those in the CK group, while the protein expression of ATG5 and LC3-B was significantly increased in the Low-Se group compared with the CK counterpart. These data indicates dietary selenium-deprived chicks exhibit poor testicular development, impaired sex hormone synthesis, reduced antioxidant enzyme activity, and increased mRNA and protein expression of autophagy-related factors.
• HIGHLIGHTS
• Se-deprived chicks display poor testicular development, impaired sex hormone synthesis, reduced activity of antioxidant enzymes, and increased mRNA and protein levels of autophagy-related factors.
... H 2 S, which has a characteristic "rotten egg" smell, is one of the predominant noxious gases and is second only to NH 3 in animal production because of its low odour threshold and high toxicity [11,12]. The exposure of animals to certain concentrations of H 2 S has been linked to liver, spleen and respiratory diseases and immune system damage [13][14][15]. Exposure to more than 20 ppm of H 2 S may lead to activated inflammatory responses and higher relative weight losses of the bursa, spleen and thymus in chickens [16]. ...
Odour is one of the main environmental concerns in the laying hen industry and may also influence animal health and production performance. Previous studies showed that odours from the laying hen body are primarily produced from the microbial fermentation (breakdown) of organic materials in the caecum, and different laying hen species may have different odour production potentials. This study was conducted to evaluate the emissions of two primary odorous gases, ammonia (NH3) and hydrogen sulphide (H2S), from six different laying hen species (Hyline, Lohmann, Nongda, Jingfen, Xinghua and Zhusi). An in vitro fermentation technique was adopted in this study, which has been reported to be an appropriate method for simulating gas production from the microbial fermentation of organic materials in the caecum. The results of this study show that Jingfen produced the greatest volume of gas after 12 h of fermentation (p < 0.05). Hyline had the highest, while Lohmann had the lowest, total NH3 emissions (p < 0.05). The total H2S emissions of Zhusi and Hyline were higher than those of Lohmann, Jingfen and Xinghua (p < 0.05), while Xinghua exhibited the lowest total H2S emissions (p < 0.05). Of the six laying hen species, Xinghua was identified as the best species because it produced the lowest total amount of NH3 + H2S (39.94 µg). The results for the biochemical indicators showed that the concentration of volatile fatty acids (VFAs) from Zhusi was higher than that for the other five species, while the pH in Zhusi was lower (p < 0.01), and the concentrations of ammonium nitrogen (NH4+), uric acid and urea in Xinghua were lower than those in the other species (p < 0.01). Hyline had the highest change in SO42− concentration during the fermentation processes (p < 0.05). In addition, the results of the correlation analysis suggested that NH3 emission is positively related to urease activities but is not significantly related to the ureC gene number. Furthermore, H2S emission was observed to be significantly related to the reduction of SO42− but showed no connection with the aprA gene number. Overall, our findings provide a reference for future feeding programmes attempting to reduce odour pollution in the laying hen industry.
... For example, it has been reported that copper and/or arsenic induced autophagy while inhibiting AKT/MTOR pathway in chicken skeletal muscle [119] and cadmium modulated MIR-33-AMPK axis and led to BNIP3-dependent autophagy in chicken spleen [120]. In this domain, autophagy was mostly studied at the tissue level, more precisely in muscle [119,121], intestine [122], gizzard [123], heart [124], brain [125], liver [126][127][128], kidney [129], testis [130], and immune organs [120,[131][132][133]. The methods combined the quantification of key proteins involved in macroautophagy (LC3, SQSTM1, BECN1, ATG4B, ATG5, ATG12), sometimes mitophagy (MFN1, MFN2, BNIP3) and associated signaling pathways by western blot and/or their transcript by RT-qPCR and ultrastructure imaging by TEM. ...
Autophagy (a process of cellular self-eating) is a conserved cellular degradative process that plays important roles in maintaining homeostasis and preventing nutritional, metabolic, and infection-mediated stresses. Surprisingly, little attention has been paid to the role of this cellular function in species of agronomical interest, and the details of how autophagy functions in the development of phenotypes of agricultural interest remain largely unexplored. Here, we first provide a brief description of the main mechanisms involved in autophagy, then review our current knowledge regarding autophagy in species of agronomical interest, with particular attention to physiological functions supporting livestock animal production, and finally assess the potential of translating the acquired knowledge to improve animal development, growth and health in the context of growing social, economic and environmental challenges for agriculture. © 2020
... Therefore, H 2 may act as a novel bridge between gut and liver, and play a central role among the colonic gas mixture in modulating liver homeostasis. stress, hepatic mitochondrial bioenergetics (modulating mitochondrial structure and function, respiratory chain, and cellular bioenergetics), hepatic fibrosis and autophagy et al. (Mani et al., 2014;Sun et al., 2015;Ci et al., 2017;Wang et al., 2017;Wenzhong et al., 2017;Untereiner and Wu, 2018;Wu et al., 2019). However, genetically manipulating the H 2 S-producing enzymes in mammalian cells could not exclude the biological effects of endogenous H 2 S produced by sulphate-reducing bacteria in animals. ...
Basic and clinical studies have shown that hydrogen (H2), the lightest gas in the air, has significant biological effects of anti-oxidation, anti-inflammation, and anti-apoptosis. The mammalian cells have no abilities to produce H2 due to lack of the expression of hydrogenase. The endogenous H2 in human body is mainly produced by anaerobic bacteria, such as Firmicutes and Bacteroides, in gut and other organs through the reversible oxidation reaction of 2 H⁺ + 2 e⁻ ⇌ H2. Supplement of exogenous H2 can improve many kinds of liver injuries, modulate glucose and lipids metabolism in animal models or in human beings. Moreover, hepatic glycogen has strong ability to accumulate H2, thus, among the organs examined, liver has the highest concentration of H2 after supplement of exogenous H2 by various strategies in vivo. The inadequate production of endogenous H2 play essential roles in brain, heart, and liver disorders, while enhanced endogenous H2 production may improve hepatitis, hepatic ischemia and reperfusion injury, liver regeneration, and hepatic steatosis. Therefore, the endogenous H2 may play essential roles in maintaining liver homeostasis.
