Dietary Selenium Deficiency and Excess Accelerate Ubiquitin-Mediated Protein Degradation in the Muscle of Rainbow Trout (Oncorhynchus mykiss) via Akt/FoxO3a and NF-κB Signaling Pathways.

Abstract

Selenium (Se) deficiency and excess can lead to protein degradation in fish. However, the underlying mechanisms remain unclear. Ubiquitin proteasome system (UPS) is the main pathway of muscle proteolysis. This study aimed to investigate the effect and molecular mechanism of dietary Se on ubiquitin-mediated muscle protein degradation in rainbow trout (Oncorhynchus mykiss). The fish were fed with the Se-deficient diet (0 mg/kg, DSe), Se-adequate diet (4 mg/kg, ASe), and Se-excessive diet (16 mg/kg, ESe), respectively. After a 10-week feeding trial, the growth performance, body composition, antioxidant enzyme activities, and UPS-related gene and protein expressions were detected. Results indicated that DSe and ESe diets significantly decreased the weight gain rate, specific growth rate, feed efficiency, and muscle crude protein content compared with ASe diet. The histological analysis showed that the mean diameter of muscle fibers was significantly decreased in DSe and ESe groups. And DSe and ESe diets significantly increased the contents of malondialdehyde and nitric oxide, but reduced the glutathione peroxidase activity. Additionally, the abundance of muscle ubiquitinated proteins and the expression levels of MuRF1 and Atrogin-1 were significantly increased in DSe and ESe groups. Compared to ASe diet, DSe and ESe diets significantly decreased the phosphorylation level of Akt Ser473 and the ratio of p-FoxO3a/FoxO3a, but significantly increased the phosphorylation level of IκBα and upregulated the expressions of TNF-α, IL-8, and NF-κB. Overall, this study indicated that dietary Se deficiency and excess accelerated the ubiquitin-mediated muscle protein degradation through regulating Akt/FoxO3a and NF-κB signaling pathways in rainbow trout.