Trichothecene

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Chemical structure of Trichothecenes

Trichothecenes are a very large family of chemically related mycotoxins produced by various species of Fusarium, Myrothecium, Trichoderma, Trichothecium, Cephalosporium, Verticimonosporium, and Stachybotrys. Trichothecenes belong to sesquiterpene compounds. These compounds were used in chemical warfare by the Soviet Union on several occasions.^{[1] [2]}

The most important structural features causing the biological activities of trichothecenes are: the 12,13-epoxy ring, the presence of hydroxyl or acetyl groups at appropriate positions on the trichothecene nucleus and the structure and position of the side-chain. They are produced on many different grains like wheat, oats or maize by various Fusarium species such as F. graminearum, F. sporotrichioides, F. poae and F. equiseti.

Some molds that produce trichothecene mycotoxins, such as Stachybotrys chartarum, can grow in damp indoor environments. It has been found that macrocyclic trichothecenes produced by Stachybotrys chartarum can become airborne and thus contribute to health problems among building occupants.^[3][4]

This group of structurally related mycotoxins has a strong impact on the health of animals and humans. Trichothecenes are powerful inhibitors of protein synthesis. They do this by reacting with components of the ribosomes: the structure within the cell where proteins are made. The specific site of action of T-2 toxin, which is a reaction with a critical site on the ribosomal RNA (rRNA) is known. Protein synthesis is an essential function in all tissues, but tissues where cells are actively and rapidly growing and dividing are very susceptible to the toxins. ^[5]

Trichothecenes are different from most other potential weapons toxins because they can act through the skin. Compared with some of the other mycotoxins such as aflatoxin, the trichothecenes do not appear to require metabolic activation to exert their biological activity. After direct dermal application or oral ingestion, the trichothecene mycotoxins can cause rapid irritation to the skin or intestinal mucosa. In cell-free systems or single cells in culture, these mycotoxins cause a rapid inhibition of protein synthesis and polyribosomal disaggregation. Thus, we can postulate that the trichothecene mycotoxins have molecular capability of direct reaction with cellular components. Despite this direct effect, it is possible to measure the toxicokinetics and the metabolism of the trichothecene mycotoxins. ^[1]

When it comes to animal and human food, type A trichothecenes (e.g. T-2 toxin, HT-2 toxin, diacetoxyscirpenol) are of special interest because they are even more toxic than the related type B trichothecenes (e.g. deoxynivalenol, nivalenol, 3- and 15-acetyldeoxynivalenol). Their major effects – related to their concentration in the commodity – are reduced feed uptake, vomiting and immuno-suppression.

Only few countries have recommended levels for these mycotoxins in food and animal feed but it is often tested for to prevent them from entering the food chain and to prevent losses in animal production.

The poisonous mushroom in Japan and China, Podostroma cornu-damae contains six trichothecenes; satratoxin H, roridin E, verrucarin and others.

CIA, UN, and other reports implicate Soviet trichothecenes in chemical attacks in Laos, Afghanistan, and other countries during the 1980s.^[2]

Epoxitrichothecenes are a variation of the above, and were once explored for military use in east Germany, and possibly the whole Soviet bloc.^[6] There is no feasible treatment once symptoms of epoxithichothecene poisoning set in, though the effects can subside without leaving any permanent damage.

The plans for use as a large-scale bioweapon were dropped, as the relevant epoxitrichothecenes degrade very quickly under UV light and heat, as well as chlorine exposure, making them useless for open attacks and the poisoning of water supplies.

The first symptoms exhibited are general discomfort, dry eyes, and drowsiness. A red rash appears shortly, starting in blotches and swiftly covering the entire body. Symptoms of a classic hemorrhagic fever set in, which include blood-red eyes, vomiting/urinating of blood, nosebleed, and patches of skin ranging from quarter- to A4-sheet size begin to bleed sponateously. Brain function is also impaired, with the victim progressing from slurred speech to classic 'fever dreams' to various psychological conditions from multiple personality disorder to paranoia^{[citation needed]}. The victim succumbs to loss of blood, fever, or systemic hyperinfection brought on by the weakened immune system, whichever comes first.

If the patient survives, he will recover from most of the symptoms, although patches of skin will still bleed spontaneously for short periods of time. His immune system remains weakened, and his mental faculties will be severely damaged.

References

1. ^ ^{a b} Trichothecene mycotoxins
2. ^ ^{a b} Use of toxins and other lethal chemicals in southeast Asia and Afganistan
3. ^ Detection of Airborne Stachybotrys chartarum Macrocyclic Trichothecene Mycotoxins in the Indoor Environment
4. ^ Etzel RA (2002). "Mycotoxins". Journal of the American Medical Association 287: 425-427. 
5. ^ [1] T-2 Toxin, Essential Data
6. ^ Die Chemie der Kampfstoffe, GDR Government publishing, 1988

External links

• Detailed information about mycotoxins
• Vendor's Product Website
• Structures of some of the Commoner Trichothecene Mycotoxins.
• Robert W. Wannemacher and Stanley L. Weiner: Trichothecene mycotoxins, chapter 34, Medical Aspects of Chemical and Biological Warfare