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The molecular mechanism of G2M cell cycle arrest induced by AFB1 in the jejunum

Heng Yin1, Min Jiang1, Xi Peng1,2

  • 1Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Chengdu, Sichuan, PR China.

Oncotarget
|May 28, 2016
PubMed

Insights

Aflatoxin B1 (AFB1) exposure in broilers causes intestinal damage and G2/M cell cycle arrest. This occurs via the ATM pathway, impacting key cell cycle regulatory proteins.

Area of Science:

  • Veterinary Toxicology
  • Molecular Biology
  • Animal Science

Background:

  • Aflatoxin B1 (AFB1) is a mycotoxin with significant toxicological effects.
  • AFB1 poses risks to both human and animal health, including hepatotoxicity and carcinogenicity.
  • Understanding AFB1's impact on animal intestinal health is crucial for food safety.

Purpose of the Study:

  • To elucidate the molecular mechanisms behind AFB1-induced G2/M cell cycle arrest in broiler jejunum.
  • To investigate the specific signaling pathways involved in AFB1 toxicity in poultry.

Main Methods:

  • Broilers were fed a diet containing 0.6 mg/kg AFB1 for three weeks.
  • Jejunal tissues were analyzed for morphological changes and protein/mRNA expression.
  • Key cell cycle regulatory proteins and signaling molecules were quantified.

Main Results:

  • AFB1 exposure led to reduced jejunal villus height and villus height/crypt ratio.
  • AFB1 induced G2/M cell cycle arrest in broiler jejunum.
  • This arrest was associated with increased ATM, p53, Chk2, and p21 expression, and decreased Mdm2, cdc25C, cdc2, cyclin B, and PCNA.

Conclusions:

  • AFB1 disrupts intestinal integrity and induces cell cycle arrest in broilers.
  • The G2/M cell cycle arrest is mediated through the ATM signaling pathway.
  • These findings highlight AFB1's detrimental effects on broiler jejunum at a molecular level.
Keywords:
AFB1G2/M phasePathology Sectioncell cycle arrestjejunummechanism

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