Zhao Xia, Yao Haidong, Fan Ruifeng, Zhang Ziwei, Xu Shiwen
College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, People's Republic of China.
Biol Trace Elem Res. 2014 Dec;161(3):341-9. doi: 10.1007/s12011-014-0139-9. Epub 2014 Oct 16.
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; 1 day old) were randomly divided into two groups, low (L) group (fed with Se deficient (Se 0.033 mg/kg) diet) and control (C) group (fed with normal (Se 0.2 mg/kg) diet). Then, pancreas was collected at 15, 25, 35, 45, and 55 days, 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.
硒（Se）缺乏会导致雏鸡胰腺萎缩，但其分子机制尚不清楚。在本研究中，我们调查了日粮缺硒对25种硒蛋白表达及一氧化氮（NO）含量的影响，并检测了硒蛋白与NO之间的关系。将180只1日龄雏鸡随机分为两组，低硒（L）组（饲喂缺硒（硒含量0.033 mg/kg）日粮）和对照组（C组，饲喂正常（硒含量0.2 mg/kg）日粮）。然后，在第15、25、35、45和55天采集胰腺，检测NO含量、诱导型一氧化氮合酶（iNOS）活性以及25种硒蛋白和iNOS的信使核糖核酸（mRNA）水平。结果显示，缺硒使25种硒蛋白表达下降（P<0.05）。其中，硫氧还蛋白还原酶1（TXNRD1）、硒蛋白S（SELS）、硒蛋白U（SELU）、硒蛋白X1（SEPX1）和硒蛋白合成酶2（SPS2）在雏鸡胰腺中的表达高于其他类型的硒蛋白，且差异显著（P<0.05）。硫氧还蛋白还原酶2（TXNRD2）、谷胱甘肽过氧化物酶1（GPX1）、谷胱甘肽过氧化物酶3（GPX3）、硒蛋白I（SELI）、碘甲腺原氨酸脱碘酶1（DIO1）、硒蛋白P1（SEPP1）、硒蛋白W1（SEPW1）、硒蛋白O（SELO）、硒蛋白T（SELT）、硒蛋白M（SELM）、硒蛋白X1（SEPX1）和SPS2表达显著降低（P<0.05）。同时，与C组相比，L组NO含量、iNOS活性及mRNA水平显著升高（P<0.05）。相关性分析表明，NO与GPX1、谷胱甘肽过氧化物酶2（GPX2）、GPX3、DIO1、硒蛋白K（SELK）、SELI、SEPX1和SPS2呈显著负相关。这些结果表明，缺硒通过影响雏鸡胰腺中的NO和硒蛋白诱导胰腺损伤。因此，本研究为缺硒诱导胰腺损伤的机制提供了一些信息。
