College of Veterinary Medicine, Sichuan Province Key Laboratory of Animal Disease & Human Health; Key Laboratory of Environmental Hazard and Human Health of Sichuan Province, Sichuan Agricultural University, Ya'an, 625014, China.
Leshan City, Shizhong District of Animal Husbandry Bureau, Leshan, 614000, China.
Biol Trace Elem Res. 2021 Mar;199(3):1080-1089. doi: 10.1007/s12011-020-02222-8. Epub 2020 May 31.
The aim of the present study was to investigate the abilities of selenium to counteract the toxic damage of arsenic (As). Two hundred 1-day-old healthy male broilers were randomly divided into five groups and fed the following diets: control group (0.1 mg/kg As + 0.2 mg/kg Se), As group (3 mg/kg As + 0.2 mg/kg Se), As + Se group I (3 mg/kg As + 5 mg/kg Se), As + Se group II (3 mg/kg As + 10 mg/kg Se), and As + Se group III (3 mg/kg As + 15 mg/kg Se), respectively. The relative weight of the liver, hepatic protein content, GSH-Px levels, SOD activities, NO contents, iNOS and tNOS activities, and increased malondialdehyde contents, ALT and AST activities, and the apoptotic hepatocytes were analyzed. Adding 3 mg/kg arsenic to the diet caused the growth and development of chicken liver to be blocked, resulting in decrease of protein contents in liver tissue, decrease of SOD and GSH-Px activities, increase of MDA contents, decrease of NO contents, decrease of iNOS and TNOs activities, increase of ALT and AST activities, increase of apoptosis rates of liver cells. Compared to the 3-mg/kg arsenic group, adding 5 mg/kg and 10 mg/kg selenium, respectively, could repair the liver growth retardation and steatosis caused by arsenic, increase the protein contents in liver tissue, increase the activities of SOD and GSH-Px, reduce the contents of MDA, increase the contents of NO, enhance the activities of iNOS and TNOs, reduce the activities of ALT and AST, and reduce the rates of apoptosis of liver cells, in which the best effects are to add 10 mg/kg selenium. While 15 mg/kg of sodium selenite may induce progression of As-induced hepatic lesions, the results indicated that 5 and 10 mg/kg of sodium selenite supplied in the diet, through mechanisms of oxidative stress and apoptosis regulation, may ameliorate As-induced hepatic lesions in a dose-dependent manner.
本研究旨在探讨硒对抗砷毒性损害的能力。将 200 只 1 日龄健康雄性肉鸡随机分为 5 组，分别饲喂以下日粮：对照组（0.1mg/kg 砷+0.2mg/kg 硒）、砷组（3mg/kg 砷+0.2mg/kg 硒）、砷+硒组 I（3mg/kg 砷+5mg/kg 硒）、砷+硒组 II（3mg/kg 砷+10mg/kg 硒）和砷+硒组 III（3mg/kg 砷+15mg/kg 硒）。分析肝相对重量、肝组织蛋白含量、GSH-Px 水平、SOD 活性、NO 含量、iNOS 和 tNOS 活性、MDA 含量、ALT 和 AST 活性、凋亡的肝细胞。添加 3mg/kg 砷到饲料中会导致鸡肝脏的生长发育受阻，导致肝组织蛋白含量降低，SOD 和 GSH-Px 活性降低，MDA 含量增加，NO 含量降低，iNOS 和 TNOs 活性降低，ALT 和 AST 活性增加，肝细胞凋亡率增加。与 3mg/kg 砷组相比，分别添加 5mg/kg 和 10mg/kg 硒可以修复砷引起的肝脏生长迟缓和脂肪变性，增加肝组织蛋白含量，提高 SOD 和 GSH-Px 的活性，降低 MDA 含量，增加 NO 含量，增强 iNOS 和 TNOs 的活性，降低 ALT 和 AST 的活性，降低肝细胞的凋亡率，其中添加 10mg/kg 硒的效果最好。而 15mg/kg 亚硒酸钠可能会诱导砷引起的肝损伤进展，结果表明，日粮中添加 5 和 10mg/kg 的亚硒酸钠，通过氧化应激和凋亡调节机制，可能会以剂量依赖的方式改善砷引起的肝损伤。
