Growth, serum biochemistry, complement activity, and liver gene expression responses of Pekin ducklings to graded levels of cultured aflatoxin B1

Chen, X.; Horn, Nathan; Cotter, P. F.; Applegate, T. J.

doi:10.3382/ps.2014-03904

Cited by 44 publications

(35 citation statements)

References 40 publications

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“…Similarly, feed consumption was decreased in AFB1-exposed quail, but body weight and feed conversion were unaffected [126]. In ducks fed AFB1, both feed intake and weight gain were reduced but without affecting feed efficiency [127].…”

Section: Production Lossesmentioning

confidence: 92%

“…This is exemplified by AFB1-reduced total serum protein levels, as the liver is responsible for production of most circulating proteins [88,115,[117][118][119]123,127,129,140,141]. Aflatoxicosis negatively affects albumin, globulin, cholesterol, and triglyceride levels in serum [88,115,117,119,127,129,136,[140][141][142].…”

Section: Hepatotoxicitymentioning

confidence: 99%

“…Total serum complement is decreased by feeding AFB1 to chickens, ducks and turkeys [115,127,[173][174][175]. Antibody titers are often reduced, whether measured as total serum levels of IgA, IgG and IgM [139,141,167], as production of specific antibodies in response to sheep red blood cells [122,152,159] or as exposure response to infectious bronchitis virus, infectious bursal disease virus, Newcastle disease virus or Pasteurella multocida [128,176,177].…”

Section: Immunotoxicitymentioning

confidence: 99%

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Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

2015

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This review is a comprehensive introduction to the effects of poultry exposure to the toxic and carcinogenic mycotoxin aflatoxin B1 (AFB1). The relationship between AFB1 sensitivity and metabolism, major direct and indirect effects of AFB1, recent studies of gene expression and transcriptome responses to exposure, and mitigation strategies to reduce toxicity are discussed. Exposure to AFB1 primarily occurs by consumption of contaminated corn, grain or other feed components. Low levels of residual AFB1 in poultry feeds can cause reduction in growth, feed conversion, egg production, and compromised immune functions, resulting in significant economic costs to producers. Thus, AFB1 acts as a "force multiplier" synergizing the adverse effects of microbial pathogens and other agents, and factors detrimental to poultry health. Domestic turkeys (Meleagris gallopavo) are one of the most sensitive animals known to AFB1 due, in large part, to a combination of efficient hepatic bioactivation by cytochromes P450 1A5 and 3A37, and deficient hepatic glutathione-S-transferase (GST)-mediated detoxification. Because of their sensitivity, turkeys are a good model to investigate chemopreventive treatments and feed additives for their ability to reduce AFB1 toxicity. Transcriptome analysis (RNA-seq) of turkey poults (liver and spleen) has identified AFB1-induced gene expression changes in pathways of apoptosis, carcinogenesis, lipid regulation, antimicrobial activity, cytotoxicity and antigen presentation. Current research focuses on further identifying the molecular mechanisms OPEN ACCESSAgriculture 2015, 5 743 underlying AFB1 toxicity with the goal of reducing aflatoxicosis and improving poultry health.

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Section: Production Lossesmentioning

confidence: 92%

Section: Hepatotoxicitymentioning

confidence: 99%

Section: Immunotoxicitymentioning

confidence: 99%

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Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

2015

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“…For FB 1 , our estimated IC 50 based on 48 and 72 h incubation was 14.27 μg ml –1 (19.8 μ m ) and 4.19 μg ml –1 (5.8 μ m ), respectively, while Creppy et al ( reported that IC 50 values of FB 1 were 45, 31 and 64 μ m in C6 glioma cells, Caco‐2 cells and Vero cells after 48 h incubation. With an IC 50 of 3.69 μg ml –1 (11.8 μ m ) in primary DEF, toxicity potential of AFB 1 was intermediate of the three mycotoxins tested herein, yet in livestock, AFB 1 tend to be the most potent mycotoxin in impairing performance and health (Andretta et al , ; Chen et al , ; Yunus et al , ). This inconsistency might be due to limited activity of hepatic enzymes in the fibroblasts, as AFB 1 needs to undergo an extensive transformation by the hepatic cytochrome P450 family into the metabolically active metabolite, exo‐AFB 1 ‐8, 9‐epoxide, to exert its toxicity (Yunus et al , ).…”

Section: Discussionmentioning

confidence: 87%

“…As secondary metabolites of Aspergillus and Fusarium species, AFB 1 , FB 1 and DON are known to be highly prevalent contaminants in a variety of food and feedstuffs. When consumed by humans or animals, these mycotoxins can cause diverse toxic effects, including growth depression, immunosuppression, liver damage and carcinogenic effects (Chen et al , ; Henry et al , ; Mirocha and Christensen, ; Rotter, ). Similar to our results with testing chemicals, a difference in cell sensitivity has been observed for the three mycotoxins tested.…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity of various chemicals and mycotoxins in fresh primary duck embryonic fibroblasts: a comparison to HepG2 cells

Chen

Murdoch²,

Shafer³

et al. 2016

J. Appl. Toxicol.

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To screen cost-effectively the overall toxicity of a sample, particularly in the case of food and feed ingredient quality control, a sensitive bioassay is necessary. With the wide variety of cytotoxicity assays, performance comparison between assays using different cells has become of interest. Fresh primary duck embryonic fibroblasts (DEF) were hypothesized to be a sensitive tool for in vitro cytotoxicity screening; cell viability of DEF in response to various cytotoxins was determined and compared with response of HepG2 cells. The IC50 values by the alamar blue assay in the DEF cells had a high correlation (R(2) = 0.96) with those obtained in HepG2 cells. Within the same toxin, primary DEF yielded significantly lower IC50 values than that obtained from HepG2 cells using the MTT and alamar blue assay. Additionally, primary DEF responded to all mycotoxins tested using the alamar blue assay, while HepG2 was less sensitive, particularly at short exposure times. The estimated IC50 for aflatoxin B1 , fumonisins B1 and deoxynivalenol in DEF after 72 h incubation were 3.69, 4.19 and 1.26 μg ml(-1) , respectively. Results from the current study suggest that primary DEF are more sensitive to cytotoxins and mycotoxins compared to HepG2, and thus may have great potential as an effective tool for cytotoxicity assessment. The question remains whether in vitro IC50 values can accurately predict in vivo toxicity; however, the current study accentuates the need for further attention to identify sensitive cell models for in vitro cytotoxicity screening and subsequent exploration of species-specific prediction models for in vivo toxicity. Copyright © 2016 John Wiley & Sons, Ltd.

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