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Effect of Artificial Tear Formulations on the Metabolic Activity of Human Corneal Epithelial Cells after Exposure to Desiccation
Published on: May 2, 2020
Altered Carnitine Homeostasis Modulates Hyperosmolarity-Induced Mitochondrial Dysfunction and Lipotoxicity in Human
Richard Kontoh-Twumasi1,2, Antonella Aliste1,2, Alexander Scheid1,2
1Center for Biotechnology and Genomic Medicine, Augusta University, Augusta, Georgia, United States.
Investigative Ophthalmology & Visual Science
|February 19, 2026
Summary
Dry eye disease causes hyperosmolarity, damaging corneal cells. L-carnitine supplementation protects against this damage by restoring mitochondrial function and reducing oxidative stress.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Tear hyperosmolarity is a key factor in dry eye disease (DED), leading to corneal epithelial injury and mitochondrial dysfunction.
- Carnitine metabolism plays a crucial role in cellular energy production and lipid handling within mitochondria.
Purpose of the Study:
- To investigate the impact of hyperosmolar stress on mitochondrial carnitine metabolism in corneal epithelial cells.
- To evaluate the potential of L-carnitine as an osmoprotective agent against hyperosmolarity-induced cellular damage.
Main Methods:
- Human telomerase-immortalized corneal epithelial (hTCEpi) cells were subjected to hyperosmolar conditions (490 mOsM) with or without L-carnitine supplementation.
- Assays were performed to quantify free fatty acid uptake, triglyceride accumulation, lipid peroxidation, mitochondrial reactive oxygen species (mtROS), and intracellular ATP levels.
- Expression and activity of key enzymes in carnitine metabolism (CPT1, CPT2, CrAT) and PPARα were assessed.
Main Results:
- Hyperosmolar stress increased lipid uptake, triglyceride accumulation, lipid peroxidation, and mtROS generation, while decreasing ATP levels and carnitine metabolism enzyme activity.
- L-carnitine supplementation mitigated lipid accumulation and peroxidation, reduced mtROS, and partially restored ATP production and carnitine shuttle function.
- Inducible nitric oxide synthase (iNOS) expression was upregulated under hyperosmolar conditions, and L-carnitine partially normalized this.
Conclusions:
- Hyperosmolarity disrupts corneal epithelial cell carnitine homeostasis, causing lipotoxicity, oxidative stress, and impaired mitochondrial function.
- L-carnitine supplementation effectively restores carnitine-dependent mitochondrial pathways, offering a potential therapeutic strategy for DED.
- These findings highlight L-carnitine's role in protecting the ocular surface from hyperosmolar injury.
