Cell Viability Score as an Integrated Indicator for Cytotoxicity of Benzalkonium Chloride-Containing Antiglaucoma Eyedrops

Introduction: Most intraocular pressure (IOP)-lowering eye drops are preserved with benzalkonium chloride (BAK). This can increase side effects and decrease adherence. Particularly, damage to the mucin-producing conjunctival goblet cells may be an issue due to instability of the tear film. We aimed to investigate the effect of IOP-lowering eye drops preserved with BAK on cultured human conjunctival goblet cells. Methods: Eye drops Brimonidine Tartrate Teva (BT) with 0.005% BAK, Dorzolamide Stada (DS) with 0.0075% BAK, Optimol® (OP) with 0.01% BAK, and Latanoprost Teva (LT) with 0.02% BAK were included. Human primary cultured goblet cell survival was evaluated using a lactate dehydrogenase assay on human goblet cells after treatment for 30 min and 6 h with the different anti-glaucoma drug formulations. Results: All eye drops examined, except BT, reduced goblet cell survival. The impact of eye drops on goblet cell viability was correlated with the time of exposure as well as to the concentration of BAK. After 30 min of exposure, cell viability was 93% for BT (0.005% BAK; p = 0.93), 71% for DS (0.0075% BAK; p = 0.067), 70% for OP (0.01% BAK; p = 0.054), and 69% for LT (0.02% BAK; p = 0.022), and exposure for 6 h reduced cell survival to 74% for BT (p = 0.217), 52% for DS (p = 0.011), 34% for OP (p = 0.017), and 31% for LT (p = 0.0007). Conclusion: LT, OP, and DS reduced human goblet cell survival in a time-dependent manner. BT did not affect goblet cell survival. Cell survival was correlated with the BAK concentration in the eye drops making 0.02% BAK-preserved LT most toxic and 0.005% BAK-preserved BT least toxic. Based on the present study, decreasing BAK in eye drops for chronic use seems important to reduce damage to the goblet cells. However, future studies are needed to further explore this finding.

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Effects of benzalkonium chloride on cell viability, inflammatory response, and oxidative stress of human alveolar epithelial cells cultured in a dynamic culture condition

Toxicology in Vitro ◽

10.1016/j.tiv.2019.04.027 ◽

2019 ◽

Vol 59 ◽

pp. 221-227 ◽

Cited By ~ 5

Author(s):

Haejun Jeon ◽

Dongjoo Kim ◽

Jean Yoo ◽

Soonjo Kwon

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Cell Viability ◽

Culture Condition ◽

Benzalkonium Chloride ◽

Alveolar Epithelial Cells ◽

Alveolar Epithelial ◽

And Oxidative Stress ◽

Cells Cultured ◽

Human Alveolar Epithelial Cells

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Allergic contact sensitivity to benzalkonium chloride. Cutaneous, ophthalmic, and general medical implications

Archives of Dermatology ◽

10.1001/archderm.106.2.169 ◽

1972 ◽

Vol 106 (2) ◽

pp. 169-171 ◽

Cited By ~ 10

Author(s):

A. A. Fisher

Keyword(s):

Benzalkonium Chloride ◽

Contact Sensitivity ◽

Allergic Contact

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Cytoprotective Effect of Tocotrienol-Rich Fraction and α-Tocopherol Vitamin E Isoforms Against Glutamate-Induced Cell Death in Neuronal Cells

International Journal for Vitamin and Nutrition Research ◽

10.1024/0300-9831/a000201 ◽

2014 ◽

Vol 84 (3-4) ◽

pp. 0140-0151 ◽

Cited By ~ 11

Author(s):

Thilaga Rati Selvaraju ◽

Huzwah Khaza’ai ◽

Sharmili Vidyadaran ◽

Mohd Sokhini Abd Mutalib ◽

Vasudevan Ramachandran ◽

...

Keyword(s):

Vitamin E ◽

Cell Viability ◽

Neuronal Cells ◽

Positive Control ◽

Post Treatment ◽

Mitochondrial Activity ◽

Before And After ◽

Pre Treatment ◽

Tocotrienol Rich Fraction ◽

Major Mediator

Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100 - 300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76 % and 79 % in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2 %, 95.0 %, and 95.6 %, respectively (p < 0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.

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