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.

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.