| 2008-day-old Avian broliers were divided into 5 groups randomly, and fed on the diets as follows:control group(As O.lmg/kg+Se 0.2mg/kg), just arsenic group(As 3mg/kg), both selenium and arsenic group(As 3mg/kg+Se 5mg/kg; As 3mg/kg+Se 10mg/kg; As 3mg/kg+Se 15mg/kg) for 4 weeks respectively. Observing the growth of the chicken liver and determining the indicators of hepatic antioxidanU nitric oxide metabolism,apoptosis rate and enzymes to study the effect of arsenic and selenium on chicken liver. The results indicated that:the liver was growth retarded, the cells got fatty degeneration, the hepatic protein contents SOD and GSH-PX activity were decreased, the MDA content were increased, the hepatic NO content were decreased, the iNOS and tNOS activity were weakened, the ALT and AST activity were increased, the apoptosis rate were inceased by 3mg/kg arsenic diet, were significantly different from the control group(p<0.01); the growth retarded of the liver and fatty degeneration of the hepatic cells caused by arsenic were repaired, the hepatic protein contents SOD and GSH-PX activity were increased, the hepatic NO content iNOS and tNOS activity were increased, the ALT and AST activity were weakened, the apoptosis rate were decreased by both selenium and arsenic diet(As 3mg/kg+Se 5mg/kg; As 3mg/kg+Se 1Omg/kg), were significantly or not different from the control group(p<0.05或, p>0.05), and the 1Omg/kg Se group was better than the 5mg/kg group; the liver damage were more serious by the 15 mg/kg Se and As 3mg/ group, caused the liver growth retarded, the fatty degeneration of the cells, the hepatic protein content,SOD and GSH-PX activity were decreased, the MDA content were increased, the hepatic NO content were decreased, the iNOS and tNOS activity were weakened, the ALT and AST activity were increased, the apoptosis rate were inceased, were significantly different from the control group(p<0.01) and significantly or not different from the only arsenic group(p<0.05或p<0.01). |
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