
Metabolites, Год журнала: 2025, Номер 15(3), С. 165 - 165
Опубликована: Март 1, 2025
Background/Objectives: Deoxynivalenol (DON), known as vomitoxin, is one of the most common mycotoxins produced by Fusarium graminearum, with high detection rates in feed worldwide. Ferroptosis a novel mode cell death characterized lipid peroxidation and accumulation reactive oxygen species. Although it has been demonstrated that DON can induce ferroptosis liver, specific mechanisms pathways are still unknown. The aim this experiment was to investigate iron metabolism disorders livers mice, thereby triggering causing toxic damage liver. Methods: Male C57 mice were treated at 5 mg/kg BW concentration an vivo model. After sampling, organ coefficient monitoring, liver function test, histopathological analysis, Fe2+ content oxidative stress-related indexes performed. mRNA protein expression Nrf2 its downstream genes also detected using series methods including quantitative real-time PCR, immunofluorescence double-labeling, Western blotting analysis. Results: cause mouse. Specifically, we found mouse group exhibited pathological necrosis, inflammatory infiltration, cytoplasmic vacuolization, elevated relative weight, significant changes indexes. Meanwhile, substantial reduction levels glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), total antioxidant capacity (T-AOC) indicated caused stress Notably, exposure increased Malondialdehyde (MDA) which provides strong evidence for occurrence disorders. Most importantly, Nrf2, important pathway ferroptosis, along genes, heme oxygenase (HO-1), quinone oxidoreductase (NQO1), peroxidase (GPX4), solute carrier gene (SLC7a11), significantly inhibited group. Conclusions: Based on our results, closely associated DON-induced livers, suggesting maintaining hepatic homeostasis activating may be potential target mitigating hepatotoxicity future.
Язык: Английский