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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]

Excessive fat deposition in the hepatocytes, associated with excess dietary fat intake, was related to the occurrence of fatty livers in fish. miR-101b plays the important roles in controlling lipid metabolism, but the underlying mechanism at the post-transcriptional level remains unclear. The purpose of this study is to explore the roles and mechanism of miR-101b-mediating lipid deposition and metabolism in yellow catfish Pelteobagrus fulvidraco. We found that miR-101b directly targeted fatty acid translocase (cd36), caspase9 (casp9) and autophagy-related gene 4A (atg4a). Furthermore, using palmitic acid (PA) or oleic acid (OA) to incubate the primary hepatocytes of yellow catfish, we demonstrated that miR-101b inversely regulated cd36, casp9, and atg4a expression at the transcriptional level; the inhibition of miR-101b aggravated fatty acids (FAs, PA or OA)-induced lipid accumulation, indicating that miR-101b mediated FAs-induced variations of lipid metabolism in yellow catfish. Taken together, our study gave novel insight into the regulatory mechanism of lipid deposition and metabolism and might provide potential targets for the prevention and treatment of fatty livers in fish. [ABSTRACT FROM AUTHOR]

Enrofloxacin (ENR) is a kind of widespread hazardous pollutant on aquatic ecosystems and causes toxic effects, such as disorders of metabolism, on aquatic animals. However, its potential mechanisms at an environmental concentration on metabolic disorders of aquatic organisms remain unclear. Herin, we found that hepatic lipotoxicity was induced by ENR exposure, which led to ENR accumulation, oxidative stress, mitochondrial fragmentation, and fatty acid transfer blockage from lipid droplets into fragmented mitochondria. ENR-induced lipotoxicity and mitochondrial β-oxidation down-regulation were mediated by reactive oxygen species (ROS). Moreover, dynamin-like protein 1 (DRP1) mediated ENR-induced mitochondrial fragmentation and changes of lipid metabolism. Mechanistically, ENR induced increment of DRP1 mitochondrial localization via dephosphorylating DRP1 at S627 and promoted its interaction with mitochondrial fission factor (MFF), leading to mitochondria fragmentation. For the first time, our study provides an innovative mechanistic link between hepatic lipotoxicity and mitochondrial fragmentation under ENR exposure, and thus identifies previously unknown mechanisms for the direct relationship between environmental ENR concentration and lipotoxicity in aquatic animals. Our study provides innovative insights for toxicological mechanisms and environmental risk assessments of antibiotics in aquatic environment. [Display omitted] • Enrofloxacin (ENR) induced lipotoxicity and promoted mitochondrial fragmentation. • ENR blocked fatty acids transfer from lipid droplets into mitochondria. • Reactive oxygen species mediated ENR-induced lipotoxicity. • Dynamin-like protein 1 (DRP1) mediated ENR-induced mitochondrial fragmentation. • ENR induced mitochondria fragmentation via dephosphorylating DRP1 at S627. [ABSTRACT FROM AUTHOR]