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Background: Selenium (Se) appears in the selenoproteins in the form of selenocysteine (Sec) and is important for the growth and development of vertebrates. The present study characterized seven selenoproteins, consisting of the GPX1, GPX3, GPX4, SELENOW, SELENOP, TXNRD2 and TXNRD3 cDNAs in various tissues of yellow catfish, explored their regulation to dietary Se addition., Methods: 3' and 5' RACE PCR were used to clone full-length cDNA sequences of seven selenoprotein genes (GPX1, GPX3, GPX4, SELENOW, SELENOP, TXNRD2 and TXNRD3). Their molecular characterizations were analyzed, including conservative motifs and the SECIS elements. The phylogenetic trees were generated through neighbor-joining (NJ) method with MEGA 6.0 with 1000 bootstrap replications. Quantitative real-time PCR was used to explore their mRNA tissue distribution in the heart, anterior intestine, dorsal muscle, head kidney, gill, liver, brain, spleen and mesenteric fat. Yellow catfish (mixed sex) were fed diets with dietary Se contents at 0.03 (low Se), 0.25 (adequate Se) and 6.39 (high Se) mg Se/kg, respectively, for 12 weeks, and their spleen, kidney, testis and brain were used for the determination of the mRNA levels of the seven selenoproteins., Results: The seven selenoproteins had similar domains to their corresponding members of other vertebrates. They were widely expressed in nine tissues, including heart, liver, brain, spleen, head kidney, dorsal muscle, mesenteric fat, anterior intestine and gill, but showed tissue-dependent expression patterns. Dietary Se addition affected the expression of the seven genes in spleen, kidney, testis and brain tissues of yellow catfish., Conclusion: Taken together, our study demonstrated the characterization, expression and regulation of seven selenoproteins, which increased our understanding of the biological functions of Se and selenoproteins in fish., (Copyright © 2020 Elsevier GmbH. All rights reserved.)

Aims: Studies demonstrated that oxidized fish oil (OFO) promoted oxidative stress and induced mitochondrial dysfunction and lipotoxicity, which attenuated beneficial effects of fish oil supplements in the treatment of nonalcoholic fatty liver disease (NAFLD). The current study was performed on yellow catfish, a good model to study NAFLD, and its hepatocytes to explore whether selenium (Se) could alleviate OFO-induced lipotoxicity via the inhibition of oxidative stress and determine its potential mechanism. Results: The analysis of triglycerides content, oxidative stress parameters, and histological and transmission electronic microscopy observation showed that high dietary Se supplementation alleviated OFO-induced lipotoxicity, oxidative stress, and mitochondrial injury and dysfunction. RNA-sequencing and immunoblotting analysis indicated that high dietary Se reduced OFO-induced decline of peroxisome-proliferator-activated receptor alpha (Pparα) and ubiquitin-specific protease 4 (Usp4) protein expression. High Se supplementation also alleviated OFO-induced reduction of thioredoxin reductase 2 (txnrd2) messenger RNA (mRNA) expression level and activity. The txnrd2 knockdown experiments revealed that txnrd2 mediated Se- and oxidized eicosapentaenoic acid (oxEPA)-induced changes of mitochondrial reactive oxygen species (mtROS) and further altered Usp4 mediated-deubiquitination and stabilization of Pparα, which, in turn, modulated mitochondrial fatty acid β-oxidation and metabolism. Mechanistically, Usp4 deubiquitinated Pparα and ubiquitin-proteasome-mediated Pparα degradation contributed to oxidative stress-induced mitochondrial dysfunction. Innovation: These findings uncovered a previously unknown mechanism by which Se and OFO interacted to affect lipid metabolism via the Txnrd2-mtROS-Usp4-Pparα pathway, which provides the new target for NAFLD prevention and treatment. Conclusion: Se ameliorated OFO-induced lipotoxicity via the inhibition of mitochondrial oxidative stress, remodeling of Usp4-mediated deubiquitination, and stabilization of Pparα. Antioxid. Redox Signal. 40, 433–452. [ABSTRACT FROM AUTHOR]

The current study is conducted to determine the influences of dietary selenium (Se) and oxidized fish oil (OFO) on growth, nutritional composition, muscle development, antioxidant responses and selenoprotein expression in the muscle of yellow catfish. We used the 2 × 2 factorial experimental design, which included two dietary Se levels at 0.25 (adequate) and 0.5 (high) mg Se/kg diets, and each Se level had fresh fish oil (FFO) and OFO, respectively. The experiment continued for 10 weeks. Compared to FFO group, dietary OFO reduced final body weight (FBW), specific growth rate (SGR) and weight gain (WG), and the contents of n-6 polyunsaturated fatty acid (PUFA), 18: 2n-6, 20: 4n-6, n-3 PUFA, 20: 5n-3, 22: 6n-3 and total PUFA, the diameters of muscle fibers >80 μm, mRNA expression of mef2d , myf5 , myod , s6kb and mTOR, and the ratio of p-mTOR to mTOR protein expression, but increased feed conversion rate (FCR), muscle lipid content, malic enzyme (ME) and isocitrate dehydrogenase (ICDH) activities, the number of the muscle fiber with the diameter lower than 50 μm; high dietary Se addition alleviated OFO- induced variations of these indices mentioned above. Dietary OFO also reduced muscle catalase (CAT) and glutathione peroxidase (GPX) activities and total antioxidant capacity (AOC), and mRNA expression of gpx1 , gpx2 , gpx3 , selenoe , selenok and selenos , but increased total superoxide dismutase (SOD) activity, malondialdehyde (MDA) content and NRF2 protein expression, and high dietary Se addition alleviated OFO-induced changes of these parameters involved in antioxidant responses and selenoprotein expression in the muscle of yellow catfish. Based on these observations above, dietary Se addition alleviated OFO-induced lipogenesis, and reversed the OFO-induced inhibition of muscle growth and development, and oxidative damage of muscle. Our study provides new mechanistic insights into the Se and OFO interaction in fish. The biological basis through which dietary OFO and Se diets interacted to affect muscle metabolism and physiology is scarce. Our study indicated that dietary Se could alleviate OFO-induced negative effects on muscle metabolism and physiology, which will be helpful to the feed formulation and fish farm. • Se alleviated dietary OFO-induced reduction of growth performance. • Se alleviated dietary OFO-induced reduction of muscle PUFA content. • Se alleviated dietary OFO-induced reduction of muscle growth and development. • Se alleviated dietary OFO-induced increase of lipogenesis and lipid deposition. • Se reversed dietary OFO-induced oxidative stress and selenoprotein expression. [ABSTRACT FROM AUTHOR]

Selenium (Se) functions through selenoproteins and is essential to growth and metabolism of vertebrates. The present study was conducted to identify twelve selenoproteins genes (selenoe , selenof , selenoh , selneoi , selenom , selenok , selneon , selenoo , selenot , selenos , selenou and msrb1) from yellow catfish. Their mRNA expression patterns, as well as their response to dietary oxidized fish oils and Se addition were explored. We use 3′and 5′ RACE PCR to clone full-length cDNA sequence of twelve selenoprotein genes from yellow catfish. Their mRNA expression patterns were assessed via quantitative real-time PCR. Yellow catfish were fed diet adequate Se+ fresh fish oil, adequate Se+ oxidized fish oil, high Se+ fresh fish oil and high Se+ oxidized fish oil, respectively, for 10 weeks. Their kidney, heart, brain and testis were used to assess the mRNA expression of twelve selenoprotein. Twelve selenoprotein genes had similar domains with mammals and the other fish. Their mRNAs were expressed widely in eleven tissues but varied with the tissues. Dietary oxidized fish oils and Se addition influenced their mRNA abundances of twelve selenoproteins in a tissue-dependent manner. Our study demonstrated the characterization and expression of twelve selenoproteins, and elucidated their responses in yellow catfish fed diets varying in oxidized fish oils and Se addition, which increased our knowledge into the biological function and regulatory mechanism of Se and selenoproteins in fish. [ABSTRACT FROM AUTHOR]

• We obtained the 1993-bp, 2000-bp and 1959-bp promoters of three selenoproteins. • Se increase the activities of the selenok , selenot and selenop promoters. • Functional FoxO4, Nrf2, KLF4 and ATF4 sites were identified on their promoters. • Se promoted FoxO4, Nrf2, KLF4 and ATF4 binding ability to their promoters. The selenok , selenot and selenop are three key selenoproteins involved in stress response. Our study, using the yellow catfish Pelteobagrus fulvidraco as the experimental animal, obtained the 1993-bp, 2000-bp and 1959-bp sequences of selenok , selenot and selenop promoters, respectively, and predicted the binding sites of several transcriptional factors on their promoters, such as Forkhead box O 4 (FoxO4), activating transcription factor 4 (ATF4), Kruppel-like factor 4 (KLF4) and nuclear factor erythroid 2-related factor 2 (NRF2). Selenium (Se) increased the activities of the selenok , selenot and selenop promoters. FoxO4 and Nrf2 can directly bind with selenok promoter and controlled selenok promoter activities positively; KLF4 and Nrf2 can directly bind with selenot promoter and controlled selenot promoter activities positively; FoxO4 and ATF4 can directly bind to selenop promoter and regulated selenop promoter activities positively. Se promoted FoxO4 and Nrf2 binding to selenok promoter, KLF4 and Nrf2 binding to selenot promoter, and FoxO4 and ATF4 binding to selenop promoter. Thus, we provide the first evidence for FoxO4 and Nrf2 bindnig elements in selenok promoter, KLF4 and Nrf2 binding elements in selenot promoter, and FoxO4 and ATF4 binding elements in selenop promoter, and offer novel insight into regulatory mechanism of these selenoproteins induced by Se. [ABSTRACT FROM AUTHOR]

Selenium (Se) is an essential micro-mineral and plays important roles in antioxidant responses, and also influences lipid metabolism and selenoprotein expression in vertebrates, but the effects and mechanism remain unknown. The study was undertaken to decipher the insights into dietary Se influencing lipid metabolism and selenoprotein expression in the anterior and middle intestine (AI and MI) of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (weight: 8.27 ± 0.03 g) were fed a 0.03- (M-Se), 0.25- (A-Se), or 6.39- (E-Se) mg Se/kg diet for 12 wk. AI and MI were analyzed for triglycerides (TGs) and Se concentrations, histochemistry and immunofluorescence, enzyme activities, and gene and protein levelsassociated with antioxidant responses, lipid metabolism, endoplasmic reticulum (ER) stress, and selenoproteome. Compared to the A-Se group, M-Se and E-Se diets significantly decreased weight gain (WG) and increased TGs concentration in the AI and MI. In the AI, compared with A-Se group, M-Se and E-Se diets significantly increased activities of fatty acid synthase, expression of lipogenic genes, and suppressed lipolysis. In the MI, compared to the A-Se group, M-Se and E-Se diets significantly increased activities of lipogenesis and expression of lipogenic genes. Compared with A-Se group, E-Se diet significantly increased glutathione peroxidase (GPX) activities in the AI and MI, and M-Se diet did not significantly reduce GPX activities in the AI and MI. Compared with the A- Se group, E-Se diet significantly increased glutathione peroxidase (GPX) activities in the plasma and liver, and M-Se diet significantly reduced GPX activities in the plasma and liver. Compared with the A-Se group, M-Se and E-Se groups also increased glucose-regulated protein 78 (GRP78, ER stress marker) protein expression of the intestine. Dietary Se supplementation also differentially influenced the expression of the 28 selenoproteins in the AI and MI, many of which possessed antioxidant characteristics. Compared with the A-Se group, the M-Se group significantly decreased mRNA levels of txnrd2 and txnrd3, but made no difference on mRNA levels of these seven GPX proteins in the MI. Moreover, we characterized sterol regulatory element binding protein 1c (SREBP1c) binding sites of three ER-resident proteins (selenom, selenon, and selenos) promoters, and found that Se positively controlled selenom, selenon, and selenos expression via SREBP1c binding to the selenom, selenon, and selenos promoter. Thus, dietary marginal and excess Se increased TGs deposition of yellow catfish P. fulvidraco, which might be mediated by ER-resident selenoproteins expression and ER stress. [ABSTRACT FROM AUTHOR]