- Astaxanthin significantly reduced La2O3 nanoparticle-induced hepatic histopathological and ultrastructural damage and ameliorated altered hepatic oxidative stress parameters.
- ASX increased transsulfuration metabolites SAM, SAH, cysteine and homocysteine and prevented La2O3 NP-induced downregulation of pathway genes and proteins.
- Protection likely mediated by transsulfuration pathway activation with concurrent inhibition of oxidative stress, inflammatory responses and hepatocyte apoptosis.
J Agric Food Chem. 2026 Jul 23. doi: 10.1021/acs.jafc.6c04388. Online ahead of print.
ABSTRACT
The mechanism underlying hepatic toxicity induced by lanthanum oxide nanoparticles (La2O3 NPs), which are increasingly utilized in optical glasses, batteries, alloys and water treatment, remains unknown. Astaxanthin (ASX), a red carotenoid pigment with antioxidant, anticancer, and anti-inflammatory properties, exerts hepatoprotective properties via its antioxidant capacity. Treatment with ASX treatment significantly reduced La2O3 NP-induced histopathological liver injury and ultrastructural changes in liver cells and altered the oxidative stress parameters in the liver. ASX increased several metabolites of the transsulfuration pathway such as S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), cysteine, and homocysteine, and it prevented the decreased expression of transsulfuration pathway-related genes triggered by La2O3 NPs both at mRNA and protein levels. In conclusion, ASX had protective effects against La2O3 NP-induced damage, potentially by activating the transsulfuration pathway and inhibiting oxidative stress, inflammatory response, and hepatic apoptosis.
PMID:42489637 | DOI:10.1021/acs.jafc.6c04388
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