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

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.