T-2 mycotoxin is a trichothecene mycotoxin. It is a naturally occurring mold byproduct of Fusarium spp. fungus which is toxic to humans and other animals. The clinical condition it causes is alimentary toxic aleukia and a host of symptoms related to organs as diverse as the skin, airway, and stomach. Ingestion may come from consumption of moldy whole grains. T-2 can be absorbed through human skin. Although no significant systemic effects are expected after dermal contact in normal agricultural or residential environments, local skin effects can not be excluded. Hence, skin contact with T-2 should be avoided.
History Alimentary toxic aleukia (ATA), a disease which is caused by trichothecenes like T-2 mycotoxin, killed many thousands of USSR citizens in the Orenburg District in the 1940s. It was reported that the mortality rate was 10% of the entire population in that area. During the 1970s it was proposed that the consumption of contaminated food was the cause of this mass poisoning. Because of World War II, harvesting of grains was delayed and food was scarce in Russia. This resulted in the consumption of grain that was contaminated with Fusarium molds, which produce T-2 mycotoxin. In 1981, the United States Secretary of State Alexander Haig and his successor George P. Shultz accused the Soviet Union of using T-2 mycotoxin as a chemical weapon known as "yellow rain" in Laos (1975–81), Kampuchea (1979–81), and Afghanistan (1979–81), where it allegedly caused thousands of casualties. Although several US chemical weapons experts claim to have identified "yellow rain" samples from Laos as trichothecenes, other experts believe that this exposure was due to naturally occurring T-2 mycotoxin in contaminated foods. Another alternative theory was developed by Harvard biologist Matthew Meselson, who proposed that the "yellow rain" found in Southeast Asia originated from the excrement of jungle bees. The first indication for this theory came from finding high levels of pollen in the collected samples, giving the substance its yellow color. It was also found that jungle bees in this area fly collectively in great numbers, at altitudes too high to be easily seen, producing showers of feces that could have been mistaken for sprays from aircraft. Further testing later determined that the oily liquid was, in fact, the pollen-filled feces of jungle bees. A similar case in China was brought to light, and in this instance the cause of the phenomenon had also been bee excrement. Despite this conclusive analysis, the United States has not withdrawn its allegations and declares that the issue has not been fully resolved. T-2 mycotoxin is also thought to be a cause of Gulf War syndrome. US troops suffered from mycotoxicosis-like symptoms after an Iraqi missile detonated in a US military camp in Saudi Arabia during Operation Desert Storm in the Persian Gulf War, in 1991. It has been shown that Iraq researched trichothecene mycotoxins, among other substances, and thus was capable of its possession and employment in chemical warfare. Nevertheless, much of the key information from these incidents remains classified, leaving these matters still unresolved.
Chemical properties This compound has a tetracyclic sesquiterpenoid 12,13-epoxytrichothene ring system, which relates it to the trichothecenes. These compounds are generally very stable and are not degraded during storage/milling and cooking/processing of food. They do not degrade at high temperatures either. This compound has an epoxide ring, and several acetyl and hydroxyl groups on its side chains. These features are mainly responsible for the biological activity of the compound and make it highly toxic. T-2 mycotoxin is able to inhibit DNA and RNA synthesis in vivo and in vitro and can induce apoptosis. However, in vivo the compound rapidly metabolizes to HT-2 mycotoxin (a major metabolite).
Mechanism of action The toxicity of T-2 toxin is due to its 12,13-epoxy ring. Epoxides are in general toxic compounds; these react with nucleophiles and then undergo further enzymatic reactions. The reactivity of epoxides can lead to reactions with endogenous compounds and cellular constituents like DNA bases and proteins. These reactions could be the reason for the noticed actions and effects of T-2 mycotoxin. The toxic compound influences the metabolism of membrane phospholipids, leads to an increase of liver lipid peroxidases and has an inhibiting effect on DNA and RNA synthesis. In addition it can bind to an integral part of the 60s ribosomal subunit, peptidyltransferase, thereby inhibiting protein synthesis. These effects are thought to be the explanation for T-2 toxin inducing apoptosis (cell death) in different tissues as the immune system, the gastrointestinal tissue and also fetal tissue. With regard to apoptosis there has been noticed that the level of the pro-apoptotic factor Bas (Bcl-2-associated X protein) was increased and the level of Bcl-xl, an anti-apoptotic factor, was decreased in human chondrocytes (cartilage cells). When exposed to T-2 mycotoxin. Furthermore, the level of Fas, an apoptosis-related cell-surface antigen and p53, a protein regulating the cell cycle, were increased.
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