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Direct and microsomal activated aflatoxin B1 exposure and its effects on turkey peritoneal macrophage functions in

D L Neldon-Ortiz1, M A Qureshi

  • 1Department of Poultry Science, North Carolina State University, Raleigh 27695-7608.

Insights

Turkey macrophages resist direct aflatoxin B1 (AFB1) exposure. However, metabolic activation of AFB1 by mixed function oxidases (MFOs) significantly impairs macrophage functions, indicating AFB1

Area of Science:

  • Immunology
  • Toxicology
  • Cell Biology

Background:

  • Aflatoxin B1 (AFB1) is a mycotoxin with potential adverse effects on animal health.
  • Macrophages are critical immune cells involved in pathogen clearance and host defense.
  • Understanding AFB1's impact on macrophage function is crucial for assessing its toxicological risks.

Purpose of the Study:

  • To investigate the direct effects of AFB1 on turkey macrophage functions.
  • To determine if metabolic activation of AFB1 by mixed function oxidases (MFOs) alters its toxicity to macrophages.

Main Methods:

  • Established adherent turkey macrophage monolayers from peritoneal exudate cells.
  • Exposed macrophages directly to varying doses of AFB1.
  • Exposed macrophages to AFB1 in the presence of a chicken microsomal MFO system.
  • Assessed macrophage adherence, cell damage, phagocytic activity, and AFB1-induced alterations.
  • Utilized piperonyl butoxide (a P450 inhibitor) to investigate the role of MFOs.

Main Results:

  • Direct exposure to AFB1 did not negatively impact macrophage adherence, damage, or phagocytosis.
  • Co-incubation with MFOs and low doses of AFB1 caused significant morphological changes, reduced adherence, and impaired phagocytic potential.
  • Piperonyl butoxide blocked the AFB1-MFO induced alterations, confirming the role of metabolic activation.

Conclusions:

  • Turkey macrophages exhibit resistance to the direct cytotoxic effects of AFB1.
  • Metabolic activation of AFB1 by MFOs is responsible for its detrimental effects on macrophage effector functions.
  • These findings highlight the importance of metabolic activation in AFB1 toxicity to avian immune cells.

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