The Role of Ferroptosis in Hepatocyte Injury Induced by α-Amanitin.
Year: 2025
Type: article
Abstract: OBJECTIVES: To explore whether ferroptosis is involved in α-amanitin-induced hepatocyte injury by detecting iron deposition in mice liver tissues, oxidative stress indicators in hepatocytes and L-02 cells, and expressions of ferroptosis-related proteins after α-amanitin exposure. METHODS: The poisoning models of α-amanitin C57BL/6J mice and L-02 cell were established. The Lillie ferrous iron staining and Prussian blue staining were used to detect iron deposition; the kits were applied to detect the levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and glutathione (GSH). Western blotting was performed to analyze expressions of p53, solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4). RESULTS: in mice liver tissues increased significantly. In the liver tissues of medium (0.35 mg/kg) and high (0.45 mg/kg) dose groups and L-02 cells treated with 1 μmol/L α-amanitin, the level of GSH decreased, the level of MDA increased, and the activities of SOD and CAT decreased significantly. In addition, α-amanitin upregulated the expression of p53 in a concentration- and time-dependent manner and inhibited the expressions of SLC7A11 and GPX4. CONCLUSIONS: Ferroptosis plays an important role in α-amanitin-induced hepatocyte injury. Abnormalities of ferroptosis-related indicators can provide references for the forensic identification of α-amanitin poisoning.
Source: PubMed
Authors: Hao-Wei Wang, Xiao-Xing Zhang, Gen-Meng Yang, Shang-Wen Wang, Xiao-Feng Zeng
Institution: Kunming Medical University
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W4413139574