文摘
To investigate the protection of selenium on hepatic mitochondrial functions, 90 7-day-old ducklings were randomly divided into three groups (groups I–III). Group I was used as a blank control. Group II was administered with aflatoxin B1 (0.1?mg/kg body weight). Group III was administered with aflatoxin B1 (0.1?mg/kg body weight) plus selenium (sodium selenite, 1?mg/kg body weight). All treatments were given once daily for 21?days. The results showed that the activities of hepatic mitochondrial complexes I–IV in group II ducklings significantly decreased when compared with group I (P-lt;-.01). Furthermore, the activities of hepatic mitochondrial complexes I–IV in group III significantly increased when compared with group II (P-lt;-.05). The hepatic mitochondrial respiratory control ratio (RCR) in group II ducklings significantly decreased when compared with group I (P-lt;-.01). In addition, the hepatic mitochondrial RCR in group III significantly increased when compared with group II (P-lt;-.05). These results revealed that the aflatoxin B1 significantly induced hepatic mitochondrial dysfunction in the activities of hepatic mitochondrial respiratory chain complexes I–IV and the RCR in ducklings. However, sodium selenite could significantly ameliorate the negative effect induced by aflatoxin B1.