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The Protective Role of Selenium in AFB1-Induced Tissue Damage and Cell Cycle Arrest in Chicken's Bursa of Fabricius

Ping Hu1, Zhicai Zuo1, Fengyuan Wang1

  • 1Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, 611130, Sichuan, People's Republic of China.

Insights

Selenium (Se) supplementation protects chickens from Aflatoxin B1 (AFB1) immune toxicity. Se alleviates AFB1-induced tissue damage and cell cycle arrest in the bursa of Fabricius, mitigating oxidative stress.

Area of Science:

  • Poultry immunology
  • Toxicology
  • Nutritional biochemistry

Background:

  • Aflatoxin B1 (AFB1) is a toxic fungal metabolite causing significant damage.
  • Selenium (Se) is an essential trace element with antioxidant and detoxification properties.

Purpose of the Study:

  • To investigate the protective effects of dietary Selenium (Se) against Aflatoxin B1 (AFB1)-induced toxicity in the chicken bursa of Fabricius (BF).

Main Methods:

  • Histological examination to assess tissue damage and oxidative stress.
  • Flow cytometry to analyze cell cycle arrest.
  • mRNA expression analysis of key cell cycle regulatory genes (ATM, Chk2, p53, p21, cdc25, PCNA, cyclins, CDKs).

Main Results:

  • Dietary Se (0.4 mg·kg⁻¹) reduced AFB1-induced histological lesions, vacuoles, nuclear debris, and oxidative stress in the BF.
  • Se supplementation prevented AFB1-induced G2M phase arrest (7 days) and G0G1 phase arrest (14-21 days).
  • Se restored the expression of ATM, Chk2, p53, p21, cdc25, PCNA, cyclin D1, cyclin E1, cyclin B3, CDK6, CDK2, and cdc2 towards control levels.

Conclusions:

  • Dietary Se (0.4 mg·kg⁻¹) mitigates AFB1-induced immune toxicity in chicken BF.
  • Se alleviates oxidative damage and cell cycle arrest via the ATM-Chk2-cdc25 and ATM-Chk2-p21 pathways.
  • Se supplementation is a viable strategy to counteract AFB1 toxicity in poultry.

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