Abstract

Selenium (Se) deficiency induces pancreatic atrophy in chickens, but the molecular mechanism remains unclear. In this study, we investigated the effect of dietary Se deficiency on the expressions of 25 selenoproteins and the content of nitric oxide (NO) and examined the relationship between selenoproteins and NO. Chickens (180; 1day old) were randomly divided into two groups, low (L) group (fed with Se deficient (Se 0.033mg/kg) diet) and control (C) group (fed with normal (Se 0.2mg/kg) diet). Then, pancreas was collected at 15, 25, 35, 45, and 55days, and the content of NO, the activity of inducible NO synthase (iNOS), and the messenger RNA (mRNA) levels of 25 selenoproteins and iNOS were measured. The results showed that 25 selenoproteins were decreased (P < 0.05) by Se deficiency. Among them, thioredoxin reductase 1 (TXNRD1), selenoprotein S (SELS), selenoprotein U (SELU), selenoprotein X1 (SEPX1), and selenoprotein synthetase 2 (SPS2) were highly and extensively expressed than other types of selenoproteins in pancreas of chickens (P < 0.05). Thioredoxin reductase 2 (TXNRD2), glutathione peroxidase 1 (GPX1), glutathione peroxidase 3 (GPX3), selenoprotein I (SELI), iodothyronine deiodinase 1 (DIO1), selenoprotein P1 (SEPP1), selenoprotein W1 (SEPW1), selenoprotein O (SELO), selenoprotein T (SELT), selenoprotein M (SELM), selenoprotein X1 (SEPX1), and SPS2 were excessively decreased (P < 0.05). Meanwhile, NO content, iNOS activity, and mRNA level were increased strikingly compared with C group (P < 0.05). The correlation analysis suggested that NO had a strong negative correlation with GPX1, glutathione peroxidase 2 (GPX2), GPX3, DIO1, selenoprotein K (SELK), SELI, SEPX1, and SPS2. These results suggested that Se deficiency induced pancreatic injury by influencing NO and selenoproteins in pancreas of chickens. Thus, it offers some information on the mechanism of pancreatic injury induced by Se deficiency.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call