Deoxynivalenol protein synthesis inhibition

Azcona-Olivera, J. I. et al. Induction of cytokine mRNAs in mice after oral exposure to the trichothecene vomitoxin (deoxynivalenol) Relationship to toxin distribution and protein synthesis inhibition. Toxicol. Appl. Pharmacol. 133, 109, 1995. 

The toxic efiects of the 12,13-epoxytrichothecenes are associated with the more highly oxidized members such as T-2 toxin (9.8) and vomitoxin (deoxynivalenol) (9.6) together with their macrocychc esters. The symptoms of alimentary toxic aleukia in test animals (cats) were detected on administration of T-2 toxin at a level of 0.08 mg kg per day. Structure activity studies on T-2 toxin revealed a requirement for the presence of the 12,13-epoxide and the 9-ene. The compounds exert their activity by the inhibition of protein synthesis. The trichothecenes interfere with the peptidyl transferase in the ribosomes. 

Casale, W. L. Inhibition of protein synthesis in maize and wheat by trichothecene mycotoxins and hybridoma-based enzyme immunoassay for deoxynivalenol. 168 pp. Avail. Univ. Microfilms Int., Order No. DA8722822. From Diss. Abstr. Int B 1988,48(8), 2167. 1987. 

TRICHOTHECENE MYCOTOXINS. A family of structurally related poisonous substances produced by various species of fungi, especially Acremorium (Cephalosporium), Fusarium, Myrothe-cium, Stachybotrys, Trichderme, and Verticumonosporium. Tri-chothecene mycotoxins are toxic to humans because they inhibit cellular protein synthesis. Prominent examples are deoxynivalenol (sometimes referred to as vomitoxin because it induces vomiting), diacetoxyscirpenol, HT-2, nivalenol, and T-2. These five toxins gained some notoriety in the so-caUed yellow rain events in Southeast Asia because of allegations that they were associated with Soviet-inspired use of chemical weapons (CW). 

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