T-2 mycotoxin (T-2 toxin)

T-2 mycotoxin is a type A trichothecene produced by Fusarium species that contaminates grains such as wheat, barley, and oats. Its toxicity is largely attributed to the 12,13-epoxy ring and high-affinity binding to the peptidyl transferase center of the 60S ribosomal subunit, blocking polypeptide chain initiation and thereby inhibiting protein synthesis; it also inhibits DNA and RNA synthesis, perturbs membrane phospholipid metabolism, induces oxidative stress, and triggers apoptosis in rapidly dividing tissues (GI mucosa, bone marrow, immune cells). Exposure causes acute and systemic toxicosis across dermal, inhalational, and gastrointestinal routes with symptoms ranging from local irritation/necrosis to systemic weakness, ataxia, GI distress, respiratory effects, and cardiovascular collapse; late effects include cytopenias due to bone marrow suppression. In the liver, T-2 reduces microsomal CYP activities and causes hepatotoxicity with elevated ALT/AST/ALP and reduced total protein; oxidative stress is a central mechanism, and selenium/selenomethionine can mitigate injury by supporting antioxidant enzymes such as glutathione peroxidase and thioredoxin reductase. T-2 is nonvolatile, environmentally stable, and undergoes biotransformation (notably to HT-2) in vivo.

Other names

Fusariotoxin T-2Mycotoxin T-2EpoxytrichotheceneNSC 138780HT-2 precursorInsariotoxin

Binds the peptidyl transferase center of the 60S ribosomal subunit to inhibit protein synthesis; Inhibits DNA and RNA synthesis; Induces oxidative stress and activates stress MAPKs (e.g., JNK/p38); Alters membrane phospholipid metabolism; Inhibits monoamine oxidase activity; Disrupts mitochondrial respiration