April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Mechanisms of Benzalkonium Chloride Toxicity in a Human Trabecular Meshwork Cell
Author Affiliations & Notes
  • Cindy M. Hutnik
    Ophthalmology, Ivey Eye Institute, London, Ontario, Canada
  • Angela Q. Zhang
    Ophthalmology, Ivey Eye Institute, London, Ontario, Canada
  • Christopher Byrne
    Ophthalmology, Ivey Eye Institute, London, Ontario, Canada
  • Hong Liu
    Ophthalmology, Ivey Eye Institute, London, Ontario, Canada
  • Grayson Roumeliotis
    Ophthalmology, Ivey Eye Institute, London, Ontario, Canada
  • Cindy Q. Shao
    Ophthalmology, Ivey Eye Institute, London, Ontario, Canada
  • Footnotes
    Commercial Relationships  Cindy M. Hutnik, None; Angela Q. Zhang, None; Christopher Byrne, None; Hong Liu, None; Grayson Roumeliotis, None; Cindy Q. Shao, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4661. doi:
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      Cindy M. Hutnik, Angela Q. Zhang, Christopher Byrne, Hong Liu, Grayson Roumeliotis, Cindy Q. Shao; Mechanisms of Benzalkonium Chloride Toxicity in a Human Trabecular Meshwork Cell. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4661.

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

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Abstract

Purpose: : To evaluate mechanisms of benzalkonium chloride toxicity in a human trabecular meshwork cell line and the possible role of gap junctions.

Methods: : A human trabecular meshwork (HTM) cell line was established in culture. Cells were treated with different concentrations of benzalkonium chloride (BAK) (ranging from 0.002% to 0.01%) for different time courses (1, 3, 10 and 30 minutes) and cell death was measured using the MTT assay. An apoptosis assay by caspase-3 activity and ELISA were also tested on the cells treated with BAK. Establishing overexpression Cx43 HTM cells by retroviral transfection with Cx43-GFP and non-functional Cx43 expression cell lines with a dominant negative G138R mutant. Connexin43 expression was measured with Western Blot and RT-PCR. Gap junction intercellular communication was determined with scrape loading/dye transfer assay with 5% Lucifer yellow.

Results: : HTM cells exhibited time and dose dependent decrease in cell viability when treated with 0.002 to 0.01% BAK for 1 to 30 minutes. Up-regulation of connexin43 enhanced cell viability while dominant negative of Cx43 mutant (G138R) contributed to further cellular demise.

Conclusions: : BAK induces time and dose dependent HTM cell cytotoxicity. Connexin43 is affected by the cytotoxic effects of BAK in this cell type.

Keywords: trabecular meshwork • stress response • apoptosis/cell death 
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