T-2 Toxin [BSA]

Trichothecenes (TCT) are a group of chemically related mycotoxin compounds produced by different species of filamentous fungi such as Fusarium, Myrothecium, Stachybotrys, Trichoderma, Trichothecium, and Spicellum, which pose a threat to human and animal health. TCT is a non-volatile, low molecular weight sesquiterpenoid synthesized via the terpenoid biosynthesis pathway, slightly soluble in water and very soluble in polar organic solvents. TCT can be found in foods and feeds such as wheat, barley, oats, hay, and straw. Poisoning in humans through consumption of meat, milk and eggs from livestock and poultry fed TCT-contaminated feeds. Due to its low molecular weight and amphiphilic nature, TCT is easily absorbed through the gastrointestinal membrane and distributed to different tissues and organs.

T-2 toxin is a type A TCT, produced by different species of Fusarium, and is the most toxic of all TCTs. T-2 is resistant to degradation under different environmental conditions (e.g., high temperature and UV). However, it is effectively inactivated in strong acidic or alkaline environments and can be detoxified by co-existing fungi or bacteria, resulting in changes in the chemical structure of T-2. TCTs share a common structure, a tricyclic molecule known as 12,13-epoxytrichothec-9-ene (EPT). Cyclohexene (A ring) is fused to tetrahydropyran (B ring), which is bridged by a two-carbon chain at C-2 and C-5 to form a cyclopentyl molecule (C ring). T-2 toxin, a type A TCT, contains a double bond between C-9 and C-10 and an epoxy group between C-12 and C-13. Its chemical structure is characterized by a hydroxyl group (OH) at the C-3 position, acetoxy groups (-OCOCH₃) at the C-4 and C-15 positions, a hydrogen atom at the C-7 position, and an isoamyl [OCOCH₂CH(CH₃)₂] group linked to the ester at the C-8 position.

Figure 1. Chemical structure of T-2 toxin
(Source: Janik E, et al. 2021)

The toxicity of T-2 varies according to dose, age, and mode of exposure, with acute toxicity manifesting as food refusal, vomiting, hemorrhage, gastric necrosis, and dermatitis. At the cellular level, the primary role of T-2 is to inhibit protein synthesis, which leads to secondary DNA destruction and RNA synthesis. The most important molecular target of TCT is the 60S ribosomal unit, which prevents the initiation of polypeptide chains. This inhibition is most pronounced in proliferating cells in the gastrointestinal tract, skin, thyroid, bone marrow, and erythrocytes. T-2 toxicity also affects oxidative stress-related responses such as increased lipid peroxidation, nuclear and mitochondrial DNA damage, disturbances in cell signaling and inflammatory pathways. In addition, the toxin affects the cell cycle and induces apoptosis.