4.7 Article

Dietary aflatoxin B1 (AFB1) reduces growth performance, impacting growth axis, metabolism, and tissue integrity in juvenile gilthead sea bream (Sparus aurata)

Journal

AQUACULTURE
Volume 533, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.aquaculture.2020.736189

Keywords

Aflatoxin B1; Stress axis; Growth regulation; Metabolism; Sparus aurata

Funding

  1. Spanish Ministry of Economy and Business-MINECO [AGL2016-76069-C2-1-R]
  2. Agencia Estatal de InvestigaciOn (MINECO, Spanish Government) [AGL2016-81808-REDT]
  3. University of Cadiz Ph.D. scholarship [PIF UCA/RECO2VIT/2014]
  4. Foundation for Science and Technology (FCT) [UIDB/04326/2020]

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The use of aflatoxin B1 in the feed of gilthead sea bream resulted in inhibited growth, altered energy metabolism, disrupted tissue integrity, and affected gene transcription responses without residue detection in the liver or muscle.
Mycotoxins are an increasing threat to all the related commodities from agriculture. Its occurrence is expected to increase due to climate change. Here, we examined the impacts of dietary toxicity of aflatoxin B1 (AFB1) in gilthead sea bream (Sparus aurata) at levels of 1 or 2 mg AFB1 kg(-1)- fish feed. Inclusion of AFB1 in the diet resulted in 80% inhibition of the total weight gain during the 85-day trial. Carbohydrate and lipid energetic metabolites, both in plasma and liver, were depleted. Moreover, the histopathological analysis revealed several tissue anomalies in the liver, kidney, and spleen. Furthermore, the relative expression of gene transcripts for growth regulation was affected by AFB1. Adenohypophyseal gh and hepatic igf1 were inversely correlated due to AFB1 effects. Relative expression levels of gene transcripts as stress indicators were increased at AFB1 highest doses, such as hypothalamic trh, crh, and crhbp, as well as star in head kidney. Interestingly circulating levels of cortisol were unaffected. Overall, our results showed that aquafeeds with AFB1 impaired growth, alter metabolism, tissue integrity, and transcriptomic responses. However, we did find AFB1 residue neither in the liver nor muscle.

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