ArticleBiological trace element research2024
Copper Exposure Induced Chicken Hepatotoxicity: Involvement of Ferroptosis Mediated by Lipid Peroxidation, Ferritinophagy, and Inhibition of FSP1-CoQ10 and Nrf2/SLC7A11/GPX4 Axis.
Article in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Chicken hepatic injury and food safety: From etiological drivers to pathogenic mechanisms.Poultry science · 2026Review
- Crosstalk between autophagy and ferroptosis in liver diseases (Review).International journal of molecular medicine · 2026Review
- The use of new approach methodologies (high-throughput transcriptomics) to study nanoagrochemicals: mechanisms of toxicity of a commercial copper oxychloride to soil model invertebrates (Enchytraeus crypticus).Archives of toxicology · 2026Article
- Copper deprivation reprograms antioxidant defense to suppress ferroptosis via SLC7A11.Redox biology · 2026Article
- Metallic Contaminants and Osteoporosis: a Review of the Gut-Bone Axis.Biological trace element research · 2026Review
- Boron Triggers Hepatic Ferroptosis: Unveiling the Dual-Pathogenic Nexus of Oxidative Stress and SLC7A11/GPX4 Dysregulation.Animals : an open access journal from MDPI · 2026Article
- The Role of COQ10B in Tumor Progression and Its Association with Immune Escape in Esophageal Squamous Cell Carcinoma: A Multi-Omics and Functional Analysis.International journal of general medicine · 2026Article
- Nanozyme-Driven Ferroptosis-Cuproptosis Interplay in Lung Cancer.International journal of nanomedicine · 2026Review
- Phloretin inhibits ferroptosis by restoring the antioxidant capacity of bovine adipose and muscle cells via the AMPK-PPAR signaling pathway.Stress biology · 2025Article
- Ferroptosis as a key player in the pathogenesis and intervention therapy in liver injury: focusing on drug-induced hepatotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The Regulation of Trace Metal Elements in Cancer Ferroptosis.Advanced biology · 2025Review
- Copper Toxicity in Animals: A Review.Biological trace element research · 2025Review
- Functional nanozyme system for synergistic tumor immunotherapy via cuproptosis and ferroptosis activation.Journal of nanobiotechnology · 2025Article
- Ferritinophagy: multifaceted roles and potential therapeutic strategies in liver diseases.Frontiers in cell and developmental biology · 2025Review
- Deciphering the Role of Copper Homeostasis in Atherosclerosis: From Molecular Mechanisms to Therapeutic Targets.International journal of molecular sciences · 2024Review
- Hepatic oxylipin profiles in mouse models of Wilson disease: New insights into early hepatic manifestations.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2024Article
- Copper metabolism in osteoarthritis and its relation to oxidative stress and ferroptosis in chondrocytes.Frontiers in molecular biosciences · 2024Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper (Cu) is one of the most significant trace elements in the body, but it is also a widespread environmental toxicant health. Ferroptosis is a newly identified programmed cell death, which involves various heavy metal-induced organ toxicity. Nevertheless, the role of ferroptosis in Cu-induced hepatotoxicity remains poorly understood. In this study, we found that 330 mg/kg Cu could disrupt the liver structure and cause characteristic morphological changes in mitochondria associated with ferroptosis. Additionally, Cu treatment increased MDA (malondialdehyde) and LPO (lipid peroxide) production while reducing GSH (reduced glutathione) content and GCL (glutamate cysteine ligase) activity. However, it is noticeable that there were no appreciable differences in liver iron content and key indicators of iron metabolism. Meanwhile, our further investigation found that 330 mg/kg Cu-exposure changed multiple ferroptosis-related indicators in chicken livers, including inhibition of the expression of SLC7A11, GPX4, FSP1, and COQ10B, whereas enhances the levels of ACLS4, LPCAT3, and LOXHD1. Furthermore, the changes in the expression of NCOA4, TXNIP, and Nrf2/Keap1 signaling pathway-related genes and proteins also further confirmed 330 mg/kg Cu exposure-induced ferroptosis. In conclusion, our results indicated that ferroptosis may play essential roles in Cu overload-induced liver damage, which offered new insights into the pathogenesis of Cu-induced hepatotoxicity.
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