Liao S.,Guangdong Academy of Agricultural Sciences |
Shi D.,South China Agricultural University |
Shi D.,Nature Technology |
Shi D.,Guangdong Provincial Key Laboratory of Prevention and Control for Severe Clinical Animal Diseases of Guangdong Province |
And 13 more authors.
Biological Trace Element Research | Year: 2014
Aflatoxin B1 (AFB1) is a mycotoxin which causes toxicity through oxidative damage. Selenium (Se), an antioxidative agent, can antagonize some toxicity induced by oxidative stress. The aim of this work was to investigate the toxicity of AFB1 and the protective effects of Se on duckling liver in vivo. The study consisted of three groups: AFB1, AFB1Tx, and a control group. AFB1 group was administered aflatoxin intragastrically (0.1 mg/kg body weight). AFB1Tx group was administered AFB1 intragastrically (0.1 mg/kg body weight) plus sodium selenite (1 mg/kg body weight). The control group was given the same volume of dimethyl sulfoxide (DMSO) via intragastric intubation. All three groups received daily administrations for 28 days. Blood samples were obtained on the 14th, 21st, and 28th days of post-administration, and the serum alanine aminotransferase (ALT) and aspartate transaminase (AST) were evaluated. A high level of serum ALT and AST was observed in AFB1 group. The activity of ALT and AST was significantly lower in Se treatment group than those in AFB1 group. Liver samples were collected on the 14th, 21st, and 28th days of post-administration, and concentrations of Bcl-2, Bax, caspase-3, and p53 were measured. Increased expression level of Bax, caspase-3, and p53 and decreased Bcl-2 expression level and Bcl-2/Bax ratio were observed in AFB1 group. Se diminished hepatic dysfunction, or damage and modulated the expression of apoptotic related proteins, in a time-dependent manner. In conclusion, concurrent treatment with Se reduced the AFB1-induced hepatic dysfunction and apoptosis. © 2014, Springer Science+Business Media New York.