Abstract
Aflatoxin B1 (AFB1) is a potent immunosuppressive agent in endotherms, which can be related to the up-regulated apoptosis of immune organs. In this study, we investigated the roles of the mitochondrial, death receptor, and endoplasmic reticulum pathways in Aflatoxin B1 induced thymocytes apoptosis. Chickens were fed an aflatoxin B1 containing diet (0.6 mg/kg AFB1) for 3 weeks. Our results showed that (1) AFB1 diet induced the decrease of T-cell subsets, morphological changes, and excessive apoptosis of thymus. (2) The excessive apoptosis involved the mitochondrial pathway (up-regulation of Bax, Bak, cytC and down-regulation of Bcl-2 and Bcl-xL) and death receptor pathway (up-regulation of FasL, Fas and FADD). (3) Oxidative stress, an apoptosis inducer, was confirmed in the thymus. In conclusion, this is the first study to demonstrate that mitochondrial and death receptor pathways involved in AFB1 induced thymocytes apoptosis in broilers.
Highlights
Aflatoxins, a group of mutagenic compounds and a contaminant of many food sources, especially in some parts of Africa, Asia and Latin America
The morphology of the epithelial reticular cells was clear in the contex and medulla, and there were no obvious histopathological changes in the thymus (Figure 1A, 1C)
Broilers are sensitive to Aflatoxin B1 (AFB1), and a low dosage of AFB1 can induce immunosuppression, which showed as the decrease of T cell subsets, some cytokines contents, antibody titers, and complement activity [27,28,29,30]
Summary
Aflatoxins, a group of mutagenic compounds and a contaminant of many food sources, especially in some parts of Africa, Asia and Latin America. Williams et al [4] have estimated that 4.5 billion of the world’s population is exposed to aflatoxins In animals, these toxins impair growth and are immunosuppressive. Several studies suggested that AFB1 treatment could induce oxidative stress, cell cycle arrest, excessive apoptosis, and mitochondria injury in lymphoid tissues [15,16,17,18]. These findings indicated that the injuries of immune organs might play critical roles in immunosuppression induced by AFB1 administration, but its mechanisms need to be further clarified
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