作者
Jia‐Hong Chu,Yu-Xue Yan,Pei‐Chao Gao,Xuewei Chen,Ruifeng Fan
摘要
Kidney is a primary target organ for mercuric chloride (HgCl 2 ) toxicity. Selenium (Se) can exert antagonistic effect on heavy metals–induced organ toxicity by regulating the expression of selenoproteins. The objective of this study was to investigate the effect of HgCl 2 on the gene expression of selenoproteins in chicken kidney. Sixty male Hyline brown chickens were randomly and evenly divided into two groups. After acclimatization for one week, chickens were provided with the standard diet as well as non-treated water (CON group), and standard diet as well as HgCl 2 -treated water (250 ppm, HgCl 2 group). After seven weeks, kidney tissues were collected to examine the mRNA expression levels of 25 selenoproteins genes and protein expression levels of 4 selenoproteins. Moreover, correlation analysis and principal component analysis (PCA) were used to analyze the expression patterns of 25 selenoproteins. The results showed that HgCl 2 exposure significantly decreased the mRNA expression of Glutathione peroxidase 1 (GPX1), GPX4, Thioredoxin reductase 2 (TXNRD2), Iodothyronine deiodinase 1 (DIO1), Methionine-Rsulfoxide reductase 1 (SELR), 15-kDa selenoprotein (SEP15), selenoprotein I (SELI), SELK, SELM, SELN, SELP, SELS, SELT, SELW, and SEPHS2. Meanwhile, HgCl 2 exposure significantly increased the mRNA expression of GPX3, TXNRD1, and SELU. Western blot analysis showed that the expression levels of GPX3, TXNRD1, SELK, and SELN were concordant with these mRNA expression levels. Analysis results of selenoproteins expression patterns showed that HgCl 2 -induced the main disorder expression of selenoproteins with antioxidant activity and endoplasmic reticulum resident selenoproteins. In conclusion, selenoproteins respond to HgCl 2 exposure in a characteristic manner in chicken kidney. • Selenoproteins respond to HgCl 2 exposure in a characteristic manner. • HgCl 2 -induced the disorder expression of selenoproteins with antioxidant activity. • HgCl 2 -induced the disorder expression of ER resident selenoproteins.