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Related Experiment Video

Updated: Jul 10, 2026

Generating Retinal Injury Models in Xenopus Tadpoles
09:29

Generating Retinal Injury Models in Xenopus Tadpoles

Published on: October 13, 2023

Zeaxanthin Mitigates Hydroxychloroquine-Induced Retinal Toxicity and Metabolic Reprogramming in ARPE-19 Cells.

Münire Berna Asal Altıparmak1, Emine Merve Yıldırım1, Ozan Kaplan2

  • 1Department of Biochemistry, Faculty of Pharmacy, University of Hacettepe, Ankara, Turkiye.

Journal of Biochemical and Molecular Toxicology
|July 9, 2026
PubMed
Summary

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Zeaxanthin (ZEA) protects against hydroxychloroquine (HCQ)-induced retinotoxicity by reducing oxidative stress and improving mitochondrial function. This study suggests ZEA as a potential therapeutic agent for preventing vision damage from HCQ.

Area of Science:

  • Ophthalmology
  • Pharmacology
  • Cell Biology

Background:

  • Long-term hydroxychloroquine (HCQ) use for autoimmune diseases can cause retinal toxicity.
  • This toxicity is linked to lysosomal pH changes, mitochondrial damage, and oxidative stress.

Purpose of the Study:

  • To investigate the protective effects of zeaxanthin (ZEA) against HCQ-induced cytotoxicity, oxidative stress, mitochondrial dysfunction, and metabolic changes.
  • To evaluate ZEA's potential as a therapeutic agent against HCQ-induced retinotoxicity.

Main Methods:

  • ARPE-19 cells were treated with HCQ and/or ZEA.
  • Assessed cell viability, apoptosis/necrosis, reactive oxygen species (ROS), mitochondrial membrane potential, and lysosomal acidification.
  • Performed untargeted metabolomics and pathway enrichment analysis.
Keywords:
ARPE‐19hydroxychloroquinemetabolomicsmitochondrial dysfunctionzeaxanthin

Related Experiment Videos

Last Updated: Jul 10, 2026

Generating Retinal Injury Models in Xenopus Tadpoles
09:29

Generating Retinal Injury Models in Xenopus Tadpoles

Published on: October 13, 2023

Main Results:

  • HCQ significantly reduced cell viability, increased necrosis and ROS, and altered mitochondrial and lysosomal function.
  • ZEA (10 μM) co-treatment increased cell viability, reduced ROS and necrosis, and modulated metabolic pathways, including glutathione synthesis.
  • ZEA demonstrated significant protection against HCQ-induced cellular stress.

Conclusions:

  • Zeaxanthin exhibits significant protective effects against hydroxychloroquine-induced retinotoxicity.
  • ZEA may be a promising therapeutic agent for mitigating HCQ-related vision damage.