Purchase this article with an account.
Angela Qiao Zhang, Hong Liu, Christopher Byrne, Cindy Hutnik; Mechanisms of Benzalkonium Chloride Toxicity in a Human Trabecular Meshwork Cell Line. Invest. Ophthalmol. Vis. Sci. 2012;53(14):3252.
Download citation file:
© 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 increasing concentrations of benzalkonium chloride (BAK) ranging from 0.002 to 0.01% for 1, 3, 10 and 30 minutes and cell death was measured using the MTT assay. Cells were treated with BAK ranging from 0.0001 to 0.001% for 24 and 48 hours and cell death was measured using the MTT assay. Cells were treated with 0.0004% and 0.0008% BAK for 24 hours to assess apoptosis by Cell Death ELISA assay. HTM cells were up-regulated by retroviral transfection with Cx43-GFP and down-regulated with a dominant negative G138R mutant. Endogenous connexin43 expression was measured with Western Blot after 3 minutes BAK treatment and 24 hours incubation.
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 (n=3; p<0.001). HTM cells exhibited dose dependent decrease in cell viability when treated with 0.0001 to 0.001% BAK for 24 hours and 0.0001 to 0.0004% BAK for 48 hours (n=3; p<0.001). HTM cells exhibited dose dependent apoptosis when exposed to 0.0004 and 0.0008% BAK for 24 hours (n=3; p<0.05). Furthermore, endogenous connexin43 is upregulated upon BAK exposure.
BAK induces time and dose dependent HTM cell cytotoxicity through necrosis and apoptosis. Connexin43 is affected by the cytotoxic effects of BAK in this cell type.
This PDF is available to Subscribers Only