Enniatin B1

The Fusarium avenaceum

Antifungal effects of the bioactive compounds enniatins A, A(1), B, B(1).[Pubmed:20417654]

Toxicon. 2010 Sep 1;56(3):480-5.

To produce enniatin (ENs), Fusarium tricinctum CECT 20150 was grown in a liquid medium of potato (PDB), being mycotoxin purified by high performance liquid chromatography (HPLC) with a reverse phase semipreparative column using a mobile phase of acetonitrile/water using gradient condition. The purity of the ENs fractions was verified by analytical HPLC and LC/MS-MS. The pure fractions of ENs were utilized to study the biological activity on several mycotoxigenic moulds as Fusarium verticilloides, Fusarium sporotrichioides, Fusarium tricinctum, Fusarium poae, Fusarium oxysporum, Fusarium proliferatum, Beauveria bassiana, Trichoderma harzianum, Aspergillus flavus, Aspergillus parasiticus, Aspergillus fumigatus, Aspergillus ochraceus and Penicillium expansum. The results obtained demonstrated that in several antibiograms, ENs induced the inhibition of the grown microorganisms tested.

Pilot toxicokinetic study and absolute oral bioavailability of the Fusarium mycotoxin enniatin B1 in pigs.[Pubmed:24239892]

Food Chem Toxicol. 2014 Jan;63:161-5.

The aim of present study was to reveal the toxicokinetic properties and absolute oral bioavailability of Enniatin B1 in pigs. Five pigs were administered this Fusarium mycotoxin per os and intravenously in a two-way cross-over design. The toxicokinetic profile fitted a two-compartmental model. Enniatin B1 is rapidly absorbed after oral administration (T(1/2a)=0.15 h, Tmax=0.24h) and rapidly distributed and eliminated as well (T(1/2elalpha)=0.15 h; T(1/2elbeta)=1.57 h). The absolute oral bioavailability is high (90.9%), indicating a clear systemic exposure. After intravenous administration, the mycotoxin is distributed and eliminated rapidly (T(1/2elalpha)=0.15 h; T(1/2elbeta)=1.13 h), in accordance with oral administration.

The emerging mycotoxin, enniatin B1, down-modulates the gastrointestinal toxicity of T-2 toxin in vitro on intestinal epithelial cells and ex vivo on intestinal explants.[Pubmed:23649843]

Arch Toxicol. 2013 Dec;87(12):2233-41.

Enniatins, the most prevalent emerging mycotoxins, represent an emerging food safety issue, because of their common co-occurrence with other fusariotoxins such as trichothecenes co-produced by Fusarium spp on field grains and because of their extensive prevalence in grains. In this study, the intestinal toxicity of Enniatin B1 (ENN) alone and mixed with the most toxic trichothecene T-2 toxin (T2) was characterized by using two biological models from pig, the most sensitive species: the intestinal cell line IPEC1 (in vitro exposure) and jejunal explants (ex vivo exposure). Dose-dependent decreases in cell proliferation in IPEC1 and in the histopathological scores of explants were observed for ENN at muM-levels and for T2 at nM-levels, with IC50 values for ENN of 15.8 and 29.7 muM, and for T2 of 9.3 and 15.1 nM in vitro and ex vivo, respectively. Interaction analysis by probabilistic and by determinist approaches showed a less than additive effect both in vitro and ex vivo, at IC50 values, with increasing antagonism with decreasing concentrations of toxins. The results obtained by the determinist median-effect dose analysis and by the nonlinear regression analysis were concordant. All the median-effect doses estimated for IPEC cells were included in the IC50 confidence intervals of the nonlinear regression fitting. Given the occurrence of enniatins, potential synergy following the co-occurrence of enniatins and the major fusariotoxins, especially trichothecene B deoxynivalenol should be investigated.

Enniatins A1, B and B1 from an endophytic strain of Fusarium tricinctum induce apoptotic cell death in H4IIE hepatoma cells accompanied by inhibition of ERK phosphorylation.[Pubmed:19065580]

Mol Nutr Food Res. 2009 Apr;53(4):431-40.

Enniatins are mycotoxins which have important impact on human health, e.g. as contaminants of cereals, but also are discussed as possible anticancer agents. We investigated toxic effects of enniatins A1, B and B1 isolated from Fusarium tricinctum on different cancer cell lines. The enniatins showed moderate activity in HepG2 and C6 cells (EC(50)-values approximately 10-25 microM), but were highly toxic in H4IIE cells (EC(50)-values approximately 1-2.5 microM). In H4IIE cells, all enniatins increased caspase 3/7 activity and nuclear fragmentation as markers for apoptotic cell death. Enniatin A1, Enniatin B1, and, to a lesser extent, also enniatin B decreased the activation of extracellular regulated protein kinase (ERK) (p44/p42), a mitogen-activated protein kinase which is associated with cell proliferation. Furthermore, enniatins A1 and B1, but not enniatin B were able to inhibit moderately tumor necrosis factor alpha (TNF-alpha)-induced NF-kappaB activation. Screening of 24 additional protein kinases involved in signal transduction pathways (cell proliferation, survival, angiogenesis and metastasis) showed no inhibitory activity of enniatins. We conclude that enniatins A1 and B1 and, to a lesser extent, enniatin B may possess anticarcinogenic properties by induction of apoptosis and disruption of ERK signalling pathway. Further analysis of these substances is necessary to analyse their usefulness for cancer therapy.

Enniatin B1 is a Fusarium mycotoxin. Enniatin B1 inhibits acyl-CoA: cholesterol acyltransferase (ACAT) activity with an IC50 of 73 μM in an enzyme assay using rat liver microsomes. Enniatin B1 crosss the blood-brain barrier. Enniatin B1 decreases the activation of ERK (p44/p42). Enniatin B1 inhibits moderately TNF-α-induced NF-κB activation.

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