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.

本研究的目的是研究硒抵抗砷（As）毒性损害的能力。将200只1天大的健康雄性肉鸡随机分为五组，并按以下饮食喂养：对照组（0.1 mg / kg As + 0.2 mg / kg Se），As组（3 mg / kg As + 0.2 mg / kg Se），As + Se组I（3 mg / kg As + 5 mg / kg Se），As + Se组II（3 mg / kg As + 10 mg / kg Se）和As + Se组III（3毫克/千克砷+ 15毫克/千克硒）。分析肝脏的相对重量，肝蛋白含量，GSH-Px水平，SOD活性，NO含量，iNOS和tNOS活性，以及​​丙二醛含量增加，ALT和AST活性以及凋亡的肝细胞。在饮食中添加3 mg / kg的砷会导致鸡肝的生长和发育受阻，导致肝脏组织蛋白质含量降低，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活性升高，肝细胞凋亡率增加。与3 mg / kg砷组相比，分别添加5 mg / kg和10 mg / kg硒可以修复砷引起的肝发育迟缓和脂肪变性，增加肝脏组织中的蛋白质含量，增加SOD活性和GSH-Px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，并降低肝细胞的凋亡率，其中最好的作用是添加10 mg / kg硒。虽然15 mg / kg的亚硒酸钠可能会诱发As诱发的肝损伤，