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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)
To evaluate mechanisms of benzalkonium chloride toxicity in a human trabecular meshwork cell line and the possible role of gap junctions.
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.
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.
BAK induces time and dose dependent HTM cell cytotoxicity. Connexin43 is affected by the cytotoxic effects of BAK in this cell type.
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