PUBLICATION
Lanthanum oxide nanoparticles induce AHR-mediated hepatotoxicity in zebrafish via oxidative stress and metabolic dysregulation
- Authors
- Wang, J.X., Liu, Y., Ding, Y., Zhang, B.F., Liao, Y.L., Zuo, S.J., Zhou, Q.H., Li, Y., Pei, D.S.
- ID
- ZDB-PUB-250608-2
- Date
- 2025
- Source
- Ecotoxicology and environmental safety 300: 118463118463 (Journal)
- Registered Authors
- Pei, Desheng
- Keywords
- Hepatotoxicity, La(2)O(3) NPs, Metabolism disorder, Zebrafish
- MeSH Terms
-
- Reactive Oxygen Species/metabolism
- Metal Nanoparticles*/toxicity
- Apoptosis/drug effects
- Liver/drug effects
- Liver/metabolism
- Oxidative Stress/drug effects
- Oxides*/toxicity
- Zebrafish*/metabolism
- Animals
- Lanthanum*/toxicity
- Water Pollutants, Chemical*/toxicity
- Receptors, Aryl Hydrocarbon*/metabolism
- Nanoparticles*/toxicity
- PubMed
- 40480128 Full text @ Ecotoxicol. Environ. Saf.
Citation
Wang, J.X., Liu, Y., Ding, Y., Zhang, B.F., Liao, Y.L., Zuo, S.J., Zhou, Q.H., Li, Y., Pei, D.S. (2025) Lanthanum oxide nanoparticles induce AHR-mediated hepatotoxicity in zebrafish via oxidative stress and metabolic dysregulation. Ecotoxicology and environmental safety. 300:118463118463.
Abstract
Lanthanum oxide nanoparticles (La2O3 NPs) are extensively utilized in industrial, medical, and technological fields and are increasingly infiltrating aquatic ecosystems; however, their ecotoxicological impacts remain poorly understood. This study used zebrafish to elucidate the hepatotoxicity induced by La2O3 NPs through oxidative stress, apoptosis, and metabolic dysregulation. Exposure to La2O3 NPs triggered reactive oxygen species (ROS) overload in the liver of larvae, provoking oxidative damage and hepatocyte apoptosis. Transcriptomic analysis revealed altered expression of genes critical for liver function, including cytochrome P450 enzymes, implicating activation of the aryl hydrocarbon receptor (ahr) signaling pathway as a key mechanistic driver. Following 90 days of chronic exposure, the La content in the liver of zebrafish exposed to 10 mg/L La2O3 NPs reached as high as 5.637 ± 0.188 μg/g, and histopathological evaluation confirmed that La2O3 NPs accumulation induces hepatic vacuolation and elevated ALT/AST levels, underscoring structural and functional hepatic impairments. Furthermore, the liver area in the 10 mg/L exposure group was reduced by 39 % compared to the control group, manifesting a small liver phenotype. La2O3 NPs promote lipid and glycogen accumulation in the liver, inhibit enzyme activity, and disrupt lipid metabolism genes (ppar-α and cpt1aa) and glucose metabolism genes (hk1, gys2, and pdhx), indicating profound metabolic dysfunction. This study provides the first evidence linking La2O3 NPs to ahr-mediated hepatotoxicity in aquatic organisms, highlighting their capacity to impair liver development, induce metabolic disorders, and bioaccumulate in zebrafish. These findings emphasize the urgent need for environmental monitoring and regulatory frameworks to mitigate ecological risks posed by rare earth nanomaterials, safeguarding aquatic health and trophic integrity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping