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The role of Nrf2 pathway in alleviating fluorine-induced apoptosis by different selenium sources in the chicken
Hao Ju1, Siyuan Chen1, Yajie Xue1
1Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, College of Animal Science and Technology • College of Veterinary Medicine, Zhejiang A & F University, Linan 311300, China.
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.
Insights
Selenomethionine effectively reduces high fluorine-induced apoptosis in broiler intestines by activating the Nrf2 pathway and decreasing oxidative stress. This antioxidant strategy shows promise for mitigating intestinal damage from fluorosis in poultry.
Area of Science:
- Animal Nutrition
- Toxicology
- Molecular Biology
Background:
- High fluorine (HF) intake induces excessive apoptosis and oxidative stress in the duodenum and jejunum of broilers.
- This damage can impair intestinal health and poultry productivity.
Purpose of the Study:
- To evaluate the effects of sodium selenite (SS) and selenomethionine (SM) on HF-induced apoptosis in broiler intestines.
- To elucidate the molecular mechanisms underlying the protective effects of SS and SM, particularly the Nrf2 pathway.
Main Methods:
- 720 broiler chickens were divided into four groups: control, HF, HF + SS, and HF + SM.
- Diets were administered for 50 days, and apoptosis rates, oxidative stress markers, mitochondrial damage, and Nrf2 pathway activation were assessed in the duodenum and jejunum.
Main Results:
- HF significantly increased apoptosis and oxidative stress, leading to mitochondrial damage.
- SM supplementation effectively alleviated apoptosis and mitochondrial damage by reducing oxidative stress.
- SM significantly upregulated Nrf2 mRNA and protein levels and downstream antioxidant enzymes compared to the HF group.
Conclusions:
- Dietary SM ameliorates fluorine-induced excessive apoptosis in broiler intestines by activating the Nrf2 pathway.
- SM is superior to SS in activating the Nrf2 pathway and reducing duodenal apoptosis.
- SM presents a promising antioxidant additive for reducing intestinal damage caused by fluorosis in poultry.
