Abstract
T-2 toxin is a representative trichothecene that is widely detected in corn, wheat and other grain feeds. T-2 toxin has stable physical and chemical properties, making it difficult to remove from food and feed. Hence, T-2 toxin has become an unavoidable pollutant in food for humans and animals. T-2 toxin can enter brain tissue by crossing the blood–brain barrier and leads to congestion, swelling and even apoptosis of neurons. T-2 toxin poisoning can directly lead to clinical symptoms (anti-feeding reaction and decline of learning and memory function in humans and animals). Maternal T-2 toxin exposure also exerted toxic effects on the central nervous system of offspring. Oxidative stress is the core neurotoxicity mechanism underlying T-2 toxin poison. Oxidative stress-mediated apoptosis, mitochondrial oxidative damage and inflammation are all involved in the neurotoxicity induced by T-2 toxin. Thus, alleviating oxidative stress has become a potential target for relieving the neurotoxicity induced by T-2 toxin. Future efforts should be devoted to revealing the neurotoxic molecular mechanism of T-2 toxin and exploring effective therapeutic drugs to alleviate T-2 toxin-induced neurotoxicity.
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This work was supported by the National Natural Science Foundation of China (32202877; 32102739), the Science and Technology Innovation Fund of Henan Agricultural University (KJCX2021A06), and the Key scientific research projects of colleges and universities in Henan Province (22A230010; 23A230008).
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Wang, Y., Wang, B., Wang, P. et al. Review of neurotoxicity of T-2 toxin. Mycotoxin Res 40, 85–95 (2024). https://doi.org/10.1007/s12550-024-00518-5
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DOI: https://doi.org/10.1007/s12550-024-00518-5