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

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.