Trichothecene mycotoxins acute effects

Cresia, D.A., Lambert, R.J. (1989). Acute respiratory tract toxicity of the trichothecene mycotoxin, T-2 toxin. In Trichothecene Mycotoxicosis Pathophysiological Effects, Vol. 1 (V.R. Beasley, ed.), pp. 161-70. CRC Press, Boca Raton, FL. 

There are many reports on toxicological effects of trichothecene mycotox-ins to animal and livestock. In general,acute toxicity of trichothecene mycotoxins is highest in Type D compounds such as Verrucarin A and Roridin A, followed by Type A, such as T-2 toxin and Type B trichothecene mycotoxins. Table 3 shows the LD50 of trichothecene mycotoxins. 

The pathological effects and clinical signs for many toxic materials can vary with the route and type (acute, single dose vs chronic, subacute doses) of exposure. For the trichothecene mycotoxins, however, a number of the toxic responses are similar, regardless of the route of exposure. As we discussed earlier in this chapter, once they enter the systemic circulation, trichothecene mycotoxins affect rapidly proliferating tissue regardless of the... 

Limited data are available on the respiratory effects of inhaled trichothecene mycotoxins, although acute pulmonary edema is one of the serious, often lethal consequences of a yellow rain attack.16,27 One of the major symptoms following the yellow rain attacks was an upper respiratory irritation (sore throat, hoarseness, nonproductive cough),716,27 which can be relieved by steam inhalation, codeine, or another substance to suppress the cough, and other simple measures.85 A casualty who develops severe respiratory symptoms should be under the care of a physician skilled in respiratory care. 

Prophylactic induction of enzymes involved in the conjugation of xenobiotics reduced or prevented the acute toxic effects of T-2 toxin in the rat, while inhibition of these enzymes resulted in a higher toxicity for this trichothecene.96 Pretreatment with flavonoids,97 ascorbic acid,98 vitamin E," selenium,100 or chemoprotective compounds such as emetine101 that block trichothecene-cell association all reduce acute toxicity of these mycotoxins. However, none of these chemoprotective treatments have undergone extensive efficacy studies to evaluate their ability to protect against an aerosol or dermal exposure to trichothecene mycotoxins. 

Contamination occurs primarily in wheat, barley, rye, and maize. Type A trichothecenes include mainly T-2 toxin, HT-2, and diacetoxyscirpenol (DAS) mycotoxins of the group B include mainly 4-deoxynivalenol (DON), commonly known as vomitoxin, and nivalenol (NIV). Toxic effects include nausea, vomiting, visual disorder, vertigo, throat irritation, and feed refusal in farm animals. The most toxic is T-2, followed by DAS and NIV, with DON being the least toxic in acute toxicity studies but the most widespread in grains worldwide and therefore the most studied. Issues related to chemical and physical data, occurrence, toxicity, absorption, distribution, and metabolism of trichothecenes are reviewed in WHO (89) and IARC (34). Physicochemical data for some selected Fusarium toxins is given by Sydenham et al. (90). The molecular structures of the main trichothecenes are shown in Fig. 9. 

---