Delineating hierarchy of selenotranscriptome expression and their response to selenium status in chicken central nervous system

Selenium deficiency may induce exudative diathesis (ED) in broiler chick, and this damage is closely related to oxidative damage. Long noncoding RNA (LncRNA) can regulate the redox state in vivo. The aim of the present study was to clarify the LncRNA expression profile in broiler veins and filter and verify the LncRNAs related to oxidative damage of ED. This study established an ED model induced by selenium deficiency and presented the expression and characterization of LncRNAs in normal and ED samples. A total of 15412 LncRNAs (including 8052 novel LncRNAs) were generated in six cDNA libraries using the Illumina Hi-Seq 4000 platform. 635 distinct changes in LncRNAs (up-regulated fold change > 1.5, down-regulated fold change < 0.67 and differentially expressed LncRNAs) were filtered. Gene ontology enrichment on LncRNAs target genes showed that the oxidative reduction process was important. This study also defined and verified 19 target mRNAs of 23 LncRNAs related to the oxidative reduction process. The in vivo and vitro experiments also demonstrated these 23 LncRNAs can participate in the oxidative reduction process. This study presents LncRNAs expression profile in broiler chick veins for the first time and confirmed 23 LncRNAs involving in the vein oxidative damage in ED.

Atrazine (ATR) is one of the most widely detected contaminant in the ecosystem. Nuclear xenobiotic receptors are activated by herbicides and induce the transcription of CYP450 isoforms involved in xenobiotic metabolism and transport. However, little is known about hepatic nuclear xenobiotic receptors in birds are responsible for ATR-induced hepatotoxicity via regulating the cytochrome P450 enzyme systems (CYP450s). The objective of this study was to investigate the mechanism of ATR hepatotoxicity in quails. For this purpose, male quails were dosed by oral gavage from sexual immaturity to maturity with 0, 50, 250, and 500 mg/kg/day ATR for 45 days. The results showed that ATR exposure caused the hepatotoxicity damage and endoplasmic reticulum (ER) degeneration. It suggested that ER is a target organelle of ATR toxicity in hepatocytes. ATR exposure disrupted the hepatic CYP450s homeostasis. This study also demonstrated that ATR triggered the CYP450 isoforms transcription via activating the hepatic CAR/PXR pathway. The present study provides new insights regarding the mechanism of the ATR-induced hepatotoxicity through activating nuclear xenobiotic receptors and triggering ER stress and hepatic CYP450s in quails.

Selenophosphate synthetase (SPS) is essential for selenoprotein biosynthesis. In two SPS paralogues, SPS1 was only cloned from a cDNA library prepared from avian organ. However, the biological function of SPS1 in chicken central nervous system (CNS) remains largely unclear. To investigate the role of avian SPS1 in the development and selenium (Se) homeostasis of CNS, fertile eggs, chicken embryos, embryo neurons and chicks were employed in this study. The response of SPS1 transcription to the development and Se levels of CNS tissues was analyzed using qRT-PCR. SPS1 gene exists extensively in the development of chicken CNS. The wide expression of avian SPS1 can be controlled by the Se content levels, which suggests that SPS1 is important in the regulation of Se homeostasis. The fundamental mechanism of these effects is that Se alters the half-life and stability of SPS1 mRNA. Therefore, SPS1 exerts an irreplaceable biological function in chicken CNS and Se homeostasis is closely related to the expression of SPS1. These results suggested that SPS1 was required for the development and Se homeostasis of CNS in chicken.