The Full Wiki

Trichothecene: Wikis


Note: Many of our articles have direct quotes from sources you can cite, within the Wikipedia article! This article doesn't yet, but we're working on it! See more info or our list of citable articles.


From Wikipedia, the free encyclopedia

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. 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.[1][2]. The poisonous mushroom in Japan and China, Podostroma cornu-damae contains six trichothecenes; satratoxin H, roridin E, verrucarin and others.


Toxicity Mechanisms

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. [3] 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. [4]

Regulatory Issues

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 more toxic than the other foodborne trichothecenes i.e. type B group (e.g. deoxynivalenol, nivalenol, 3- and 15-acetyldeoxynivalenol). However, deoxynivalenol is of concern as it is the most prevalent trichothecene in Europe [5]. The major effects of trichothecenes – related to their concentration in the commodity – are reduced feed uptake, vomiting and immuno-suppression. Only few countries (mostly EU) 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.

Occurence and Outbreaks

Trihothecenes have been reported throughout the world [6]. In the modern history, incidences of emesis in animals and humans after consumption of cereals infected with Fusarium species have been described in early 1900’s [7] [8]. Around 100,000 people in Soviet Union died due to alimentary toxic aleukia, a disease apparently caused by consuming grains infested with Fusarium sp. which are high producers of T-2 toxin [9]. A disease of similar etiology, Akakabibyo (in case of equine, “bean-hulls poisoning”), has also been associated with trichothecene contaminated grains in Japan [10]. Cereals or their products contaminated with trichothecenes including DON, T-2 toxin, and NIV, have also been associated with outbreaks of gastrointestinal disorders in China [11].

Trichothecenes including DON, T-2 toxin, and diacetoxyscirpenol are also important from the view of biological warfare [12] and though controversial, have also been associated with ‘yellow rain’ in southeast Asia [13] [14]


Epoxitrichothecenes are a variation of the above, and were once explored for military use in east Germany, and possibly the whole Soviet bloc.[15] 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. 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.


  1. ^ Detection of Airborne Stachybotrys chartarum Macrocyclic Trichothecene Mycotoxins in the Indoor Environment
  2. ^ Etzel RA (2002). "Mycotoxins". Journal of the American Medical Association 287: 425–427.  
  3. ^ [1] T-2 Toxin, Essential Data
  4. ^ Trichothecene mycotoxins
  5. ^ Miller, J. D. 2003. Aspects of the eology of fusarium toxins in cereals. In: Mycotoxins and Food Safety. Vries, J. W. de, M. W. Trucksess, L. S. Jakson (eds.). Kluwer Aademic/Plenum Publishers, New York. pp. 19-27.
  6. ^ Dohnal, V., A. Jezkova, D. Jun and K. Kuca. 2008. Metabolic pathways of T-2 toxin. Current Drug Metabolism. 9: 77-82.
  7. ^ Naumov, N. A. 1916. Intoxicating bread. Min. Yeml. (Russia), Trudy Ruiri Miwel. i. Fitopatol. Uchen, Kom. 216.
  8. ^ Dounin, M. 1930. The fusariosis of cereal crops in European-Russia in 1923. Phytopathol. 16: 305-308.
  9. ^ Joffe, A. Z. 1950. Toxicity of fungi on cereals overwintered in the field: on the etiology of alimentary toxic aleukia. Dissertation, Inst. Bot. Acad. Sci. Leningrad. P. 205.
  10. ^ Ueno, Y., K. Ishii, K. Sakai, S. Kanaeda and H. Tsunoda. 1972. Toxicological approaches to the metabolites of Fusaria. IV. Microbial survey on “bean-hulls poisoning of horses” with the isolation of toxic trichothecenes, neosolaniol and T-2 toxin of Fusarium solani M-1-1. Japanese J. Exp. Med. 42: 187-203.
  11. ^ Lou, X. Y. 1988. Fusarium toxins contamination of cereals in China. Proc. Japanese Assoc. Mycotoxicology. Suppl. 1: 97-98.
  12. ^ Henghold II, W. B. 2004. Other biologic toxin bioweapons: Ricin, staphylococcal enterotoxin B, and trichothecene mycotoxins. Dermatologic Clinics. 22: 257-262.
  13. ^ Rosen, R. T. and J. D. Rosen. 1982. Presence of four Fusarium mycotoxins and synthetic material in 'yellow rain'. Evidence for the use of chemical weapons in Laos. Biomed. Mass Spectrom. 9: 443-450.
  14. ^ Watson, S. A., C. J. Mirocha and A. W. Hayes. 1984. Analysis for trichothecenes in samples from southeast Asia associated with 'yellow rain'. Fundamental Appl. Toxicol. 4: 700-717.
  15. ^ Die Chemie der Kampfstoffe, GDR Government publishing, 1988

External links



Got something to say? Make a comment.
Your name
Your email address