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.
The aim of the study was to investigate the effect of selenium on hepatic mitochondrial antioxidant capacity in ducklings administrated with aflatoxin B(1) (AFB(1)). Ninety 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 AFB(1) (0.1 mg/kg body weight). Group III was administered with AFB(1) (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 mitochondrial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione reductase (GR) in group II ducklings significantly decreased when compared with group I (P < 0.01). Furthermore, the content of hepatic mitochondrial malondialdehyde (MDA) significantly increased (P < 0.01). However, the activities of hepatic mitochondrial SOD, CAT, GSH-Px, and GR in group III ducklings significantly increased when compared with group II (P < 0.05). In addition, the content of hepatic mitochondrial MDA significantly decreased (P < 0.01). These results revealed that AFB(1) significantly induced hepatic mitochondrial antioxidant dysfunction. However, sodium selenite could significantly ameliorate the negative effect induced by AFB(1).
Copper is an important trace mineral in the diet of poultry due to its biological activity. However, limited information is available concerning the effects of high copper on mitochondrial dysfunction. In this study, 72 broilers were used to investigate the effects of high dietary copper on liver mitochondrial dysfunction and electron transport chain defect. Birds were fed with different concentrations [11, 110, 220, and 330 mg of copper/kg dry matter (DM)] of copper from tribasic copper chloride (TBCC). The experiment lasted for 60 d. Liver tissues on d 60 were subjected to histopathological observation. Additionally, liver mitochondrial function was recorded on d 12, 36, and 60. Moreover, a site-specific defect in the electron transport chain in liver mitochondria was also identified by using various chemical inhibitors of mitochondrial respiration. The results showed different degrees of degeneration, mitochondrial swelling, and high-density electrons in hepatocytes. In addition, the respiratory control ratio (RCR) and oxidative phosphorylation rate (OPR) in liver mitochondria increased at first and then decreased in high-dose groups. Moreover, hydrogen peroxide (H2O2) generation velocity in treated groups was higher than that in control group, which were magnified by inhibiting electron transport at Complex IV. The results indicated that high dietary copper could decline liver mitochondrial function in broilers. The presence of a site-specific defect at Complex IV in liver mitochondria may be responsible for liver mitochondrial dysfunction caused by high dietary copper.
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 B(1) (0.1 mg/kg body weight). Group III was administered with aflatoxin B(1) (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 < 0.01). Furthermore, the activities of hepatic mitochondrial complexes I-IV in group III significantly increased when compared with group II (P < 0.05). The hepatic mitochondrial respiratory control ratio (RCR) in group II ducklings significantly decreased when compared with group I (P < 0.01). In addition, the hepatic mitochondrial RCR in group III significantly increased when compared with group II (P < 0.05). These results revealed that the aflatoxin B(1) 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 B(1).
To investigate the influence of selenium on body weights and the immune organ indexes in ducklings administrated with aflatoxin B(1) (AFB(1)), 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 AFB(1) (0.1 mg/kg body weight). Group III was administered with AFB(1) (0.1 mg/kg body weight) plus sodium selenite (1 mg/kg body weight). All treatments were given once daily for 21 days. It showed that the ducklings' bursa of fabricius, thymus indexes, and body weights in group II significantly decreased when compared with group I (P < 0.01). Furthermore, the spleen indexes significantly decreased (P < 0.01). However, the ducklings' bursa of fabricius and thymus indexes, body weights in group III ducklings significantly increased when compared with group II (P < 0.01). In addition, the spleen indexes significantly decreased (P < 0.01). These results revealed that AFB(1) significantly affect ducklings' growth and immune organs development. However, selenium significantly ameliorated the negative effects induced by AFB(1).
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