The role of Nrf2 pathway in alleviating fluorine-induced apoptosis by different selenium sources in the chicken duodenum and jejunum

Abstract

In order to evaluate the alleviative effects and molecular mechanisms of sodium selenite (SS) and selenomethionine (SM) on excessive apoptosis induced by high fluorine (HF) in the duodenum and jejunum of broilers, 720 1 day old Lingnan Yellow broilers were randomly divided into 4 groups (each group assigned 180 chickens with 6 replicates) and offered either a control diet or test diets (800 mg/kg F, HF group; 800 mg/kg F + 0.15 mg selenium (Se)/kg as SS (SS group) or SM (SM group)) for 50 days. High F intake significantly increased (P < 0.05) apoptosis rates of duodenum and jejunum by inducing oxidative stress and leading to mitochondrial damage. Selenomethionine supplementation effectively alleviated mitochondrial damage and severe apoptosis of duodenum and jejunum caused by HF through decreasing oxidative stress parameters. Selenomethionine added group significantly increased (P < 0.05) nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA and nuclear Nrf2 protein levels as well as Nrf2 downstream antioxidant enzymes expressions in the duodenum and jejunum when compared with the HF group. Selenomethionine was superior to SS in activating the Nrf2 pathway and reducing the apoptosis rate of duodenum. It was concluded that dietary SM supplementation could ameliorate F-induced excessive apoptosis by inducing the Nrf2 pathway. Our findings will bring a promising tactics for the utilization of SM as an efficient antioxidant additive for reducing the intestinal damage caused by fluorosis in poultry.

Keywords

• Selenomethionine
• Sodium selenite
• Fluorine
• Duodenum
• Jejunum
• Apoptosis