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Published on: October 13, 2018
Astaxanthin Alleviated La2O3 Nanoparticle-Induced Liver Injury by Activating the Transsulfuration Pathway in Mice
Lu Yuan1, Zhixue Song2, Peng Liang3
1School of Psychology and Mental Health, Hebei Key Laboratory of Mental Health and Brain Science, North China University of Science and Technology, 21 Bohai Road, Tang'shan, Tangshan, Hebei Province063210, P. R. China.
Journal of Agricultural and Food Chemistry
|July 23, 2026
Summary
Astaxanthin (ASX) protects the liver from lanthanum oxide nanoparticle (La2O3 NP) toxicity. It reduces liver injury by activating the transsulfuration pathway and combating oxidative stress.
Area of Science:
- Nanotechnology
- Toxicology
- Biochemistry
Background:
- Lanthanum oxide nanoparticles (La2O3 NPs) are widely used but their liver toxicity mechanism is unclear.
- Astaxanthin (ASX), a potent antioxidant, is known for its potential hepatoprotective effects.
Purpose of the Study:
- To investigate the protective mechanism of Astaxanthin (ASX) against La2O3 NP-induced liver toxicity.
- To explore the role of the transsulfuration pathway in ASX's hepatoprotective effects.
Main Methods:
- Assessing histopathological and ultrastructural liver changes in response to La2O3 NPs and ASX treatment.
- Measuring oxidative stress parameters and transsulfuration pathway metabolites (SAM, SAH, cysteine, homocysteine).
- Analyzing the expression of transsulfuration pathway-related genes at mRNA and protein levels.
Main Results:
- ASX treatment significantly reduced La2O3 NP-induced liver injury and cellular damage.
- ASX altered oxidative stress markers and increased key transsulfuration pathway metabolites.
- ASX prevented the downregulation of transsulfuration pathway genes caused by La2O3 NPs.
Conclusions:
- Astaxanthin (ASX) demonstrates significant hepatoprotective effects against La2O3 NP-induced toxicity.
- ASX's protective action is linked to the activation of the transsulfuration pathway.
- ASX mitigates liver damage by inhibiting oxidative stress, inflammation, and apoptosis.
