Degradation of trichothecene mycotoxins by chicken intestinal microbes.

The degradation of 12 trichothecene mycotoxins by chicken intestinal microbes was monitored by liquid chromatography-ultraviolet-mass spectrometry under positive ion atmospheric pressure chemical ionization. Two pathways were observed: deacylation and deepoxidation. Essentially complete conversions to the deepoxy metabolites were observed for the non-acylated trichothecenes 4-deoxynivalenol, nivalenol, and verrucarol. However, deacetylation was the predominant pathway for the monoacetyl trichothecenes 3-acetyldeoxynivalenol, 15-acetyldeoxynivalenol (15ADON), and fusarenon X. Small amounts of the deepoxy metabolites were observed from 15ADON and large amounts from 15-monoacetoxyscirpenol where steric hindrance protected the C-15 acetyl groups from enzymatic attack. Diacetylated trichothecenes diacetoxyscirpenol and neosolaniol exhibited only deacetylation. The larger isovaleryl functionality was resistant to removal and deepoxidation was the prevalent reaction in HT-2 toxin and T-2 triol, whereas T2 toxin showed only deacetylation.