Deoxynivalenol induces apoptosis in PC12 cells via the mitochondrial pathway

Xichun Wang1, Wei Xu1, Mengxue Fan1

  • 1College of Animal Science and Technology, Anhui Agricultural University, 130 West Changjiang Road, Hefei 230036, China.

Insights

Deoxynivalenol (DON) triggers cell death in PC12 cells by activating the mitochondrial apoptosis pathway. This mycotoxin disrupts cell integrity and key protein expressions, leading to programmed cell death.

Area of Science:

  • Toxicology
  • Cell Biology
  • Molecular Biology

Background:

  • Deoxynivalenol (DON) is a prevalent mycotoxin with known toxicity to animals and humans.
  • Understanding DON's cellular mechanisms is crucial for assessing its health risks.

Purpose of the Study:

  • To investigate the impact of Deoxynivalenol (DON) on apoptotic pathways in PC12 cells.
  • To analyze DON's effects on cellular morphology, viability, and apoptosis markers.
  • To examine the expression of key apoptosis-related genes and proteins.

Main Methods:

  • PC12 cells were treated with varying concentrations of DON.
  • Evaluated typical apoptosis indicators: morphology, cell activity, lactate dehydrogenase (LDH) release, and apoptosis ratio.
  • Assessed the expression of apoptosis-related genes/proteins: Bcl-2, Bax, Bid, cytochrome C (Cyt C), apoptosis-inducing factor (AIF), cleaved-Caspase9, and cleaved-Caspase3.

Main Results:

  • DON inhibited PC12 cell proliferation and induced significant morphological changes and apoptosis.
  • DON promoted the release of cytochrome C (Cyt C) and apoptosis-inducing factor (AIF) from mitochondria.
  • DON increased cleaved-Caspase9 and cleaved-Caspase3 activities, decreased Bcl-2, and increased Bax and Bid expression.

Conclusions:

  • Deoxynivalenol (DON) induces apoptosis in PC12 cells.
  • The mechanism involves the activation of the mitochondrial apoptosis pathway.
  • DON alters the expression of critical proteins regulating apoptosis.

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