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Pathway underlying small intestine apoptosis by dietary nickel chloride in broiler chickens
Bangyuan Wu1, Hongrui Guo1, Hengmin Cui2
1Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Sichuan, China.
Abstract:
The aims of this study were to investigate the pathways which dietary nickel chloride (NiCl2) affects small intestine apoptosis in broiler chickens by observing the ultrastructure, and bcl-2, bax, and caspase-3 protein expression and mRNA expression, and cytochrome C, bak and caspase-9 mRNA expression of the small intestine. A total of 240 one-day-old avian broilers were divided into four groups and fed a corn-soybean basal diet as the control diet or three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. Ultrastructurally, the microvilli were apparently exfoliated, and the mitochondria were swollen and the number of lysosomes increased in the intestinal cells of three experimental groups. As measured by TUNEL and flow cytometry (FCM), the percentage of apoptotic cells in the small intestine and the lymphocytes in the ileum were significantly increased in three experimental groups when compared with those of the control group. Meanwhile, immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immuno-sorbent assay (ELISA) tests showed that the protein expression, mRNA expression levels were decreased in the bcl-2, whereas those of bax and caspase-3, and the cytochrome C, bak and caspase-9 mRNA expression levels were increased in three experimental groups. The abovementioned results show that pathway of dietary NiCl2-induced small intestine apoptosis is related to the mitochondrial damage and promotion of the cytochrome C release from mitochondria, which activates the mitochondrion-mediated apoptosis pathway.
Insights
Dietary nickel chloride (NiCl2) induces small intestine apoptosis in broiler chickens by damaging mitochondria and releasing cytochrome C. This activates the mitochondrion-mediated apoptosis pathway, impacting cell integrity and function.
Area of Science:
- Poultry nutrition and toxicology
- Cellular and molecular biology
- Apoptosis research
Background:
- Dietary nickel chloride (NiCl2) is a potential toxicant in animal feed.
- Understanding the mechanisms of NiCl2-induced apoptosis in broiler chickens is crucial for poultry health and food safety.
Purpose of the Study:
- To investigate the pathways by which dietary NiCl2 affects small intestine apoptosis in broiler chickens.
- To analyze the ultrastructural changes and the expression of key apoptosis-related proteins and genes.
Main Methods:
- Broiler chickens were fed diets with varying NiCl2 concentrations (0, 300, 600, 900 mg/kg) for 42 days.
- Ultrastructural analysis, TUNEL assay, flow cytometry (FCM), immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR), and enzyme-linked immuno-sorbent assay (ELISA) were employed.
Main Results:
- NiCl2 exposure caused microvilli exfoliation, mitochondrial swelling, and increased lysosomes in intestinal cells.
- Apoptotic cell percentages in the small intestine and ileum lymphocytes significantly increased.
- Bcl-2 expression decreased, while Bax, Caspase-3, Cytochrome C, Bak, and Caspase-9 expression increased.
Conclusions:
- Dietary NiCl2 induces small intestine apoptosis in broiler chickens.
- The primary pathway involves mitochondrial damage and subsequent release of cytochrome C, activating the mitochondrion-mediated apoptosis pathway.
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