ArticleTranslational vision science & technology2024
Hyaluronate Protects From Benzalkonium Chloride-Induced Ocular Surface Toxicity.
Article in Translational vision science & technology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Real-World Transition to a Preservative-Free Fixed Combination of Dorzolamide/Timolol: Impact on the Ocular Surface Microenvironment, Safety, Tolerability, and Efficacy.Medicina (Kaunas, Lithuania) · 2026Trial
- Aging and Corneal Nerve Health: Mechanisms of Degeneration and Emerging Therapies for the Cornea.Cells · 2025Review
- Effects of Benzalkonium Chloride, a Preservative in Topical Drugs, on the Barrier Function of Human Corneal Epithelial Cells.Translational vision science & technology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Purpose: The purpose of this study was to investigate the effect of sodium hyaluronate (SH) on benzalkonium chloride (BAK)-induced toxicity in the ocular surface epithelium and corneal nerves. Methods: Ocular surface epithelial cells from Balb/c mice were cultured with 0.1% to 0.4% SH and 0.001% to 0.01% BAK and their metabolic activity, viability, and wound repair capacity were assessed in vitro. Following a controlled corneal wound, re-epithelialization and recovery of epithelial barrier function and mechanosensitivity were measured in Balb/c mice treated with 0.4% SH 3 times/day and 0.01% BAK twice daily for 3 weeks. Nerve morphology was assessed by confocal microscopy of corneal whole mounts. Results: Whereas BAK exposure reduced metabolic activity, viability, and wound repair ability of ocular epithelial cells in vitro, pretreatment with SH ameliorated BAK toxicity in a concentration-dependent manner. The highest SH concentration partially reversed the effects of 0.01% BAK in vitro and increased the corneal healing rate of BAK-exposed mice. Although all corneal wounds closed after 4 days, continuous SH treatment improved corneal barrier dysfunction 18 days after wounding and accelerated the recovery of corneal mechanical sensitivity to baseline levels in BAK-exposed mice. SH treatment also increased corneal nerve density in the wounded area after 3 weeks. Conclusions: SH mitigates BAK-associated ocular epithelial and neurotoxicity in a concentration-dependent manner. Translational Relevance: Commercially available, high-concentration SH formulations may have added benefits in treating BAK-associated ocular surface toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.