Abstract

Aflatoxin B1 (AFB1) is a natural product of the Aspergillus genus of molds, which grow on several foodstuffs stored in hot moist conditions, and is among the most potent hepatocarcinogens and immunosuppression presently known. The latter was related to the up-regulated apoptosis of immune organs. However, the effect of expression of death receptor and endoplasmic reticulum molecules in AFB1-induced apoptosis of chicken splenocytes was largely unknown. The objective of this study was to investigate this unknown field. One hundred and forty four one-day-old chickens were randomly divided into control group (0 mg/kg AFB1) and AFB1 group (0.6 mg/kg AFB1), respectively and fed with AFB1 for 21 days. Histological observation demonstrated that AFB1 caused slight congestion and lymphocytic depletion in the spleen. TUNEL and flow cytometry assays showed the excessive apoptosis of splenocytes provoked by AFB1. Moreover, quantitative real-time PCR analysis revealed that AFB1 induced the elevated mRNA expression of Fas, FasL, TNF-α, TNF-R1, Caspase-3, Caspase-8, Caspase-10, Grp78 and Grp94 in the spleen. These findings suggested that AFB1 could lead the excessive apoptosis and alter the expression of death receptor and endoplasmic reticulum molecules in chicken spleen.

Highlights

  • Aflatoxins were difuranocoumarin compounds, and included B1, B2, G1, G2, M1, and M2, among which aflatoxin B1 (AFB1) showed highly hepatotoxic, genotoxic, immunotoxic and other adverse effects on humans and animals [1,2,3,4,5,6,7].Secondary to the effect on liver, the immuno­ suppressive nature of Aflatoxin B1 (AFB1) is the best documented area of its toxicity [4]

  • These findings suggested that AFB1 could lead the excessive apoptosis and alter the expression of death receptor and endoplasmic reticulum molecules in chicken spleen

  • This study demonstrated that AFB1 could reduce the splenic absolute weight and relative weight along with lymphocytic depletion, similar to the report by Chen et al [11], suggesting that this toxin had the detrimental effects on the development and immune function of spleen

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Summary

Introduction

Aflatoxins were difuranocoumarin compounds, and included B1, B2, G1, G2, M1, and M2, among which aflatoxin B1 (AFB1) showed highly hepatotoxic, genotoxic, immunotoxic and other adverse effects on humans and animals [1,2,3,4,5,6,7].Secondary to the effect on liver, the immuno­ suppressive nature of AFB1 is the best documented area of its toxicity [4]. AFB1 caused oxidative stress in lymphoid tissue [16, 17], cell cycle arrest [18], and mitochondria injury in the lymphoid organs [19]. Available information revealed that AFB1 caused excessive apoptosis of several poultry and mammal cells such as hepatocytes [21], thymocytes [19, 22], splenocytes [17], bursa of Fabricius cells [8], bronchial epithelial cells [23], jejunal mucosal cells [24], bone marrow cells [25], and renal www.impactjournals.com/oncotarget cells [26]. Our early researches have shown the possible link between mitochondrial molecules and apoptosis of hepatocytes [21], thymocytes [19], and bursa of Fabricius cells provoked by AFB1 [27]. Some death receptor molecules may not be related to AFB1-induced excessive cell death in the bursal cells [28], and the endoplasmic reticulum molecules may not be connected with the thymocyte apoptosis caused by AFB1 [19]

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