Selenium Ameliorates AFB1-Induced Excess Apoptosis in Chicken Splenocytes Through Death Receptor and Endoplasmic Reticulum Pathways

Aflatoxin B-1 (AFB(1)) can cause hepatotoxicity, genotoxicity, and immunosuppressive effects for a variety of organisms. Selenium (Se), as an essential nutrient element, plays important protective effects against cell apoptosis induced by AFB(1). This research aimed to reveal the ameliorative effects of selenium on AFB(1)-induced excess apoptosis in chicken splenocytes through death receptor and endoplasmic reticulum pathways in vivo. Two hundred sixteen neonatal chickens, randomized into four treatments, were fed with basal diet (control treatment), 0.4mg/kg Se supplement (+Se treatment), 0.6mg/kg AFB(1) (AFB(1) treatment), and 0.6mg/kg AFB(1)+0.4mg/kg Se (AFB(1)+Se treatment) during 21days of experiment, respectively. Compared with the AFB(1) treatment, the levels of splenocyte apoptosis in the AFB(1)+Se treatment were obviously dropped by flow cytometry and TUNEL assays although they were still significantly higher than those in the control or+Se treatments. Furthermore, the mRNA expressions of CASP-3, CASP-8 and CASP-10, GRP78, GRP94, TNF-, TNF-R1, FAS, and FASL of splenocytes in the AFB(1)+Se treatment by qRT-PCR assay were significantly decreased compared with the AFB(1) treatment. These results indicate that Se could partially ameliorate the AFB(1)-caused excessive apoptosis of chicken splenocytes through downregulation of endoplasmic reticulum and death receptor pathway molecules. This research may rich the knowledge of the detoxification mechanism of Se on AFB(1)-induced apoptosis.