Hyaluronate Protects From Benzalkonium Chloride-Induced Ocular Surface Toxicity

Area of Science:

• Ophthalmology
• Cell Biology
• Neuroscience

Background:

• Benzalkonium chloride (BAK) is a common preservative in ophthalmic solutions, known to cause ocular surface toxicity.
• Ocular surface damage from BAK can affect epithelial cells and corneal nerves, leading to discomfort and impaired vision.

Purpose of the Study:

• To investigate the protective effects of sodium hyaluronate (SH) against benzalkonium chloride (BAK)-induced toxicity.
• To evaluate SH's impact on ocular surface epithelium and corneal nerve integrity.

Main Methods:

• In vitro assessment of ocular epithelial cell viability, metabolic activity, and wound repair with varying concentrations of SH and BAK.
• In vivo study in mice measuring corneal re-epithelialization, barrier function, and mechanosensitivity recovery after wounding and treatment.
• Confocal microscopy to analyze corneal nerve morphology and density.

Main Results:

• SH ameliorated BAK-induced toxicity in ocular epithelial cells in a concentration-dependent manner.
• SH treatment accelerated corneal healing, improved epithelial barrier function, and restored corneal mechanical sensitivity in BAK-exposed mice.
• SH administration increased corneal nerve density in the wounded area.

Conclusions:

• Sodium hyaluronate (SH) effectively mitigates benzalkonium chloride (BAK)-associated ocular epithelial and neurotoxicity.
• High-concentration SH formulations may provide therapeutic advantages for managing BAK-induced ocular surface damage.