Effects of Selenium on Arsenic-Induced Liver Lesions in Broilers.

Abstract

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 (0.1mg/kg As + 0.2mg/kg Se), As group (3mg/kg As + 0.2mg/kg Se), As + Se group I (3mg/kg As + 5mg/kg Se), As + Se group II (3mg/kg As + 10mg/kg Se), and As + Se group III (3mg/kg As + 15mg/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 3mg/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 5mg/kg and 10mg/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 10mg/kg selenium. While 15mg/kg of sodium selenite may induce progression of As-induced hepatic lesions, the results indicated that 5 and 10mg/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.