ArticleJournal of advanced research2026
Cuproptosis in atrazine-induced hepatotoxicity: ATOX1 as a therapeutic target for lycopene-mediated protection.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Mitochondrial-targeted actions of lycopene: evidence, mechanisms and future directions.Frontiers in pharmacology · 2026Review
- HMGB1/NF-κB Axis, IL-8, and Cuproptosis Contribute to Cisplatin-Induced Testicular Injury: Protective Potential Effect of Thymol.Biomolecules · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAtrazine (ATR) is a widely used herbicide in agriculture, and its residues pose a threat to biological organs, with particularly severe damage to the liver. Lycopene (LYC) is a natural pigment that exhibits beneficial effects on health, particularly liver health. However, the mechanism by which LYC mitigates liver injury induced by ATR remains unclear, and the hepatotoxicity induced by ATR requires further investigation.
objectivesThis study aimed to investigate cuproptosis involvement in ATR-induced hepatotoxicity and elucidate the protective mechanisms of LYC.
methodsWe established both chicken animal models and cell models to investigate the effects of LYC on ATR-induced liver injury. A variety of experimental approaches were utilized to evaluate the impacts of LYC and ATR on hepatic tissue damage, mitochondrial dysfunction, oxidative stress, and markers associated with cuproptosis.
resultsATR exposure was associated with increased copper ion accumulation and oxidative stress markers, along with decreased antioxidant enzyme activities. Severe liver damage and mitochondrial dysfunction were observed in ATR-treated groups through histopathological analysis, and these effects were alleviated by LYC. Mechanistic studies revealed that ATR induced the expression of cuproptosis-related proteins and metabolic markers, indicating activation of cuproptosis pathways. These effects were mitigated by LYC treatment. Strong binding affinity between LYC and ATOX1 was revealed by molecular docking. ATR-induced cuproptosis was significantly inhibited by ATOX1 knockdown, confirming its critical role.
conclusionOverall, it was determined that ATOX1-mediated cuproptosis is involved in ATR-induced hepatotoxicity and the therapeutic effects of LYC. The findings enrich the understanding of the pathogenesis of ATR-induced liver toxicity and provide data to support further cuproptosis studies.
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