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 Despite this conclusive analysis, the United States has not withdrawn its allegations and declares that the issue has not been fully resolved.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 chrondocytes (cartilage cells). When exposed to T-2 mycotoxin. Furthermore, the level of Fas, an apoptosis-related cell-surface