June 2013
Volume 54, Issue 15
ARVO Annual Meeting Abstract  |   June 2013
Benzalkonium Chloride is Cytotoxic While Preservative-free Tafluprost is Cytoprotective in Human Trabecular Meshwork Cells
Author Affiliations & Notes
  • Caitlin Chang
    Faculty of Medicine and Dentistry, University of Western Ontario, London, ON, Canada
  • Cindy Hutnik
    Ophthalmology, Ivey Eye Institute, London, ON, Canada
  • Footnotes
    Commercial Relationships Caitlin Chang, None; Cindy Hutnik, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 3535. doi:
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      Caitlin Chang, Cindy Hutnik; Benzalkonium Chloride is Cytotoxic While Preservative-free Tafluprost is Cytoprotective in Human Trabecular Meshwork Cells. Invest. Ophthalmol. Vis. Sci. 2013;54(15):3535.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: The use of the preservative benzalkonium chloride (BAK) in topical ophthalmic medications is controversial. It is effective as an antimicrobial and antifungal compound, and is the most frequently used preservative in topical ophthalmic medications. However, as BAK adversely affects the surface of the eye and reduces patient comfort and compliance, there is interest in alternative or preservative-free formulations. Tafluprost is the first preservative-free PGA, has good tolerability and safety, and its IOP-lowering effect is comparable to that of other PGAs. Like other PGAs, it acts on the prostaglandin F2α receptor, which is known to have anti-apoptotic effects. The purpose of this study was to investigate the effect of BAK toxicity and tafluprost in primary human trabecular meshwork (HTM) cells, and to study the cytoprotective effect of tafluprost in HTM cells stressed with BAK. Our objective was to determine whether BAK or tafluprost have an in vitro cytotoxic effect on primary HTM cells, and if BAK-tafluprost co-incubation attenuates BAK cytotoxicity.

Methods: Primary HTM cells were treated with various BAK and tafluprost free acid concentrations over multiple exposure times, and cell viability was measured with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenol tetrazolium bromide (MTT) assay. HTM cells were co-treated with BAK and tafluprost free acid for 30 min and cell viability was assessed.

Results: BAK treatment induced a time- and dose-dependent reduction in HTM cell viability. Tafluprost treatment did not significantly affect cell viability. Co-treatment of BAK with tafluprost showed an increase in cell viability as compared to BAK treatment alone.

Conclusions: These results demonstrate that BAK is harmful to the health of the HTM cells, and its use in topical ophthalmic medications should perhaps be re-evaluated. Tafluprost is both safe and cytoprotective for the HTM. The finding that tafluprost has a positive effect on HTM cell viability, with minimal or no negative effects, further supports the merits of the use of preservative-free ophthalmic medications in the treatment of glaucoma. Further clinical investigations are needed to clarify whether BAK reduces the efficacy of anti-glaucoma medications and whether tafluprost may provide additional benefits for glaucoma patients besides lowering IOP.

Keywords: 735 trabecular meshwork • 426 apoptosis/cell death • 503 drug toxicity/drug effects  

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