A new study in Food and Chemical Toxicology, led by H. Zhao, reports that combined exposure to T-2 and HT-2 mycotoxins induces ferroptosis — a form of iron-dependent programmed cell death — in Caco-2 human intestinal epithelial cells. The researchers identify down-regulation of the SLC7A11/GPX4 antioxidant axis and the NAD(P)H/FSP1/CoQ10 pathway as the key mechanisms driving cell death.

T-2 and HT-2 are trichothecene mycotoxins produced by Fusarium species, common contaminants of cereal grains and animal feed worldwide. Because Caco-2 is a standard human intestinal model, the findings are directly relevant to how these mycotoxins may damage the gut barrier in humans following dietary or environmental exposure.

Earlier work has linked trichothecene exposure to nausea, immune dysregulation, and gut inflammation. This paper adds a specific mechanistic explanation — dual antioxidant pathway suppression — for that pattern. Full text via PubMed (PMID 42128264).