T-2 toxin is a trichothecene mycotoxin that has been found in Fusarium. It binds to and inhibits peptidyltransferase in the 60S ribosomal subunit, inducing a ribotoxic stress response that triggers JNK and p38 MAPK signaling. T-2 toxin (3 nM) decreases toll-like receptor expression and LPS-induced production of IL-1β, TNF-α, and nitric oxide (NO) in, and is cytotoxic to (IC50 = 19.47), primary pig alveolar macrophages (PAMs). In vivo, T-2 toxin induces production of reactive oxygen species (ROS), lipid peroxidation, and glutathione (GSH) depletion in mouse brain and is lethal to mice (LD50s = 1.54-5.94 mg/kg). It also induces hepatocyte apoptosis and dyslipidemias in mice. T-2 toxin has been found in Fusarium-infected wheat, barley, and rice crops both in fields and in storage.
T-2 Toxin is a tricothecene mycotoxin produced by fungi of the genus Fusarium. T-2 Toxin induces DNA damage and cell death on prolonged administration.
ChEBI: T-2 toxin is a trichothecene mycotoxin produced by fungi of the genus Fusarium. It is a common contaminant in food and feedstuffs of cereal origin and is known to cause a range of toxic effects in humans and animals. It has a role as a mycotoxin, a cardiotoxic agent, a neurotoxin, an environmental contaminant, an apoptosis inducer, a DNA synthesis inhibitor and a fungal metabolite. It is a trichothecene, an acetate ester and an organic heterotetracyclic compound. It is functionally related to a HT-2 toxin.
T-2 Toxin is found to be a potent trichothecene mycotoxin produced by the genus fusarium fungi in feedstuffs and cereal grains.
Poison by ingestion,
intramuscular, subcutaneous, intraperitoneal,
intracerebral, and intravenous routes.
Moderately toxic by inhalation.
Experimental teratogenic and reproductive
effects. A skin irritant. Questionable
carcinogen with experimental neoplastigenic
data. Mutation data reported. When heated
to decomposition it emits acrid smoke and
irritating fumes.
