Abstract

This study was conducted with objective of evaluating the toxic effects of nickel chloride (NiCl2) on development of bursa of Fabricius in broilers fed on diets supplemented with 0, 300, 600 and 900 mg/kg of NiCl2 for 42 days by using the methods of experimental pathology, flow cytometry (FCM), and quantitative real-time polymerase chain reaction (qRT-PCR). The results showed that dietary NiCl2 in 300 mg/kg and over induced toxic suppression in the bursal development, which was characterized by decreasing lymphocytes histopathologically and relative weight, increasing G0/G1 phase (a prolonged nondividing state), reducing S phase (DNA replication) and proliferating index, and increasing percentages of apoptotic cells. Concurrently, the mRNA expression levels of bax, cytochrome c (cyt c), apoptotic peptidase activating factor 1 (Apaf-1), caspase-3, caspase-6, caspase-7 and caspase-9 were increased and the bcl-2 mRNA expression levels were decreased. The toxic suppression of bursal development finally impaired humoral immunity duo to the reduction of B lymphocyte population and B lymphocyte activity in the broiler chicken. This study provides new evidences for further studying the effect mechanism of Ni and Ni compoundson B-cell or bursa of Fabricius.

Highlights

  • Nickel (Ni), an essential element of more than one hundred compounds used widely in industry and commerce, is considered to be a nutritionally essential trace metal for several animal species, microorganisms and plants [1,2,3,4]

  • This study was conducted with objective of evaluating the toxic effects of nickel chloride (NiCl2) on development of bursa of Fabricius in broilers fed on diets supplemented with 0, 300, 600 and 900 mg/kg of NiCl2 for 42 days by using the methods of experimental pathology, flow cytometry (FCM), and quantitative realtime polymerase chain reaction

  • The relative weight of bursa in NiCl2-treated groups was lower than that in control group, implying that dietary NiCl2 in 300 mg/kg and over inhibited the bursal development, and impaired the bursal function, which was consistent with the cell cycle arrest

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Summary

Introduction

Nickel (Ni), an essential element of more than one hundred compounds used widely in industry and commerce, is considered to be a nutritionally essential trace metal for several animal species, microorganisms and plants [1,2,3,4]. There have been more reports on Ni or Ni compound toxicity than on Ni nutritional deficiency at present. Nickel chloride (NiCl2) at a level of 1200 mg/kg can cause weight loss and reduction of food intake [8]. Ling and Leach [9] have reported that diets supplemented with Ni 300 mg/kg or over are toxic to male chicks. It has been proved that longterm exposure to Ni is deleterious to the upper respiratory tract, skin, kidney, immune system [10,11,12,13], embryos, and the breeding system [14,15,16], and that Ni causes DNA damage and inhibits DNA repair in mammalian cells [17-

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