Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Feb;40(1):85-95.
doi: 10.1007/s12550-024-00518-5. Epub 2024 Jan 13.

Review of neurotoxicity of T-2 toxin

Youshuang Wang  1 , Bo Wang  1 , Peilin Wang  1 , Zeao Hua  1 , Shanshan Zhang  1 , Xuebing Wang  1 , Xu Yang  1   2 , Cong Zhang  3   4
Affiliations
Review

Review of neurotoxicity of T-2 toxin

Youshuang Wang et al. Mycotoxin Res. 2024 Feb.

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.

Keywords: Apoptosis; Mitochondrial damage; Neurotoxicity; Oxidative stress; T-2 toxin.

PubMed Disclaimer

Similar articles

See all similar articles

References

    1. Adegbeye MJ, Reddy PRK, Chilaka CA, Balogun OB, Elghandour M, Rivas-Caceres RR, Salem AZM (2020) Mycotoxin toxicity and residue in animal products: prevalence, consumer exposure and reduction strategies-A review. Toxicon 177:96–108. https://doi.org/10.1016/j.toxicon.2020.01.007 - DOI - PubMed
    1. Agrawal M, Bhaskar AS, Lakshmana Rao PV (2015) Involvement of mitogen-activated protein kinase pathway in T-2 toxin-induced cell cycle alteration and apoptosis in human neuroblastoma cells. Mol Neurobiol 51(3):1379–1394. https://doi.org/10.1007/s12035-014-8816-4 - DOI - PubMed
    1. Blasiak J, Pawlowska E, Chojnacki J, Szczepanska J, Chojnacki C, Kaarniranta K (2020) Zinc and Autophagy in age-related macular degeneration. Int J Mol Sci 21(14). https://doi.org/10.3390/ijms21144994
    1. Candelario-Jalil E, Dijkhuizen RM, Magnus T (2022) Neuroinflammation, stroke, blood-brain barrier dysfunction, and imaging modalities. Stroke 53(5):1473–1486. https://doi.org/10.1161/strokeaha.122.036946 - DOI - PubMed - PMC
    1. Cha H, Choi JH, Jeon H et al (2023) Aquaporin-4 deficiency is associated with cognitive impairment and alterations in astrocyte-neuron lactate shuttle. Mol Neurobiol 60(11):6212–6226. https://doi.org/10.1007/s12035-023-03475-9 - DOI - PubMed

LinkOut - more resources