DNA methylation and RASSF4 expression are involved in T-2 toxin-induced hepatotoxicity

Toxicology
Aimei LiuZonghui Yuan

Abstract

T-2 toxin is a secondary metabolite produced by Fusarium species and commonly contaminates food and animal feed. T-2 toxin can induce hepatotoxicity through apoptosis and oxidative stress; however, the underlying mechanism is not clear. Recent studies indicated that RASSF4, a member of the RASSF family, participates in cell apoptosis and some cancers due to its inactivation via DNA hypermethylation. However, its role in T-2 toxin-induced liver toxicity is poorly understood. Therefore, in this study, female Wistar rats were given a single dose of T-2 toxin at 2 mg/kg b.w. and were sacrificed at 1, 3 and 7 days post-exposure. A normal rat liver cell line (BRL) was exposed to different concentrations of T-2 toxin (10, 20, 40 nM) for 4, 8, 12 h, respectively. Histopathological analysis revealed with apoptosis in some liver cells and clear proliferation under T-2 toxin exposure. Expression analysis by immunohistochemical assays, quantitative real-time PCR (qPCR) and western blot demonstrated that T-2 toxin activated PI3K-Akt/Caspase/NF-κB signaling pathways. Additionally, DNA methylation assays revealed that the expression of RASSF4 was silenced by promoter hypermethylation after exposure to T-2 toxin for 1 and 3 days as compared to...Continue Reading

Citations

Apr 3, 2020·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Pu GuoXu Wang
Apr 1, 2021·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Jun JiangYiqun Deng
Apr 10, 2021·Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association·Qirong LuXu Wang
Sep 24, 2021·Journal of Cellular Physiology·Aimei LiuIrma Ares

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