The Molecular Mechanisms of Protective Role of Se on the G0/G1 Phase Arrest Caused by AFB1 in Broiler's Thymocytes

Biol Trace Elem Res. 2019 Jun;189(2):556-566. doi: 10.1007/s12011-018-1491-y. Epub 2018 Sep 10.

Abstract

This research was designed to explore the protective effects of sodium selenite on G0/G1 phase arrest induced by AFB1 in thymocytes of broilers. Two hundred eighty-eight Cobb broilers were divided into control group, + Se group (0.4 mg/kg Se), AFB1 group (0.6 mg/kg AFB1), and AFB1 + Se group (0.6 mg/kg AFB1 + 0.4 mg/kg Se). The results revealed that 0.4 mg/kg Se supplement in diets could improve the AFB1-induced histological lesions in the thymus consisting of the more vacuoles and nuclear debris in thymic cortical area. The results of flow cytometric detect showed that 0.4 mg/kg Se relieved the G0/G1 phase arrest caused by AFB1 in thymocytes. The results of transcription levels of ATM, p53, p21, p27, p15, p16, CyclinD1, CyclinE, Cdk6, Cdk2, and PCNA genes by qRT-PC, and protein expression level of PCNA by immunohistochemistry demonstrated that 0.4 mg/kg Se could reduce the adverse effects of AFB1 on these parameters. In conclusion, Se could relieve AFB1-induced G0/G1 phase arrest by p15 (or p16)-CyclinD1/Cdk6, ATM-p53-p21-CyclinE/Cdk2, p27-CyclinE/Cdk2 pathways.

Keywords: AFB1; Cell cycle; G0/G1 phase; Sodium selenite; Thymus.

MeSH terms

  • Aflatoxin B1 / metabolism
  • Animals
  • Apoptosis / drug effects
  • Cell Cycle / drug effects
  • Chickens
  • Dietary Supplements
  • G1 Phase / drug effects
  • Sodium Selenite / pharmacology*
  • Thymocytes / drug effects*
  • Thymocytes / metabolism*

Substances

  • Aflatoxin B1
  • Sodium Selenite