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Benzalkonium Chloride and Glaucoma

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MARY ANN LIEBERT, INC
DOI: 10.1089/jop.2013.0174

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资金

  1. National Institutes of Health/National Eye Institute (University of Wisconsin-Madison Core Grant for Vision Research) [P30 EY016665, P51 RR000167]
  2. Merck, Inc.
  3. Research to Prevent Blindness, Inc., New York, NY
  4. Ocular Physiology Research and Education Foundation
  5. Walter Helmerich Chair from the Retina Research Foundation

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Glaucoma patients routinely take multiple medications, with multiple daily doses, for years or even decades. Benzalkonium chloride (BAK) is the most common preservative in glaucoma medications. BAK has been detected in the trabecular meshwork (TM), corneal endothelium, lens, and retina after topical drop installation and may accumulate in those tissues. There is evidence that BAK causes corneal and conjunctival toxicity, including cell loss, disruption of tight junctions, apoptosis and preapoptosis, cytoskeleton changes, and immunoinflammatory reactions. These same effects have been reported in cultured human TM cells exposed to concentrations of BAK found in common glaucoma drugs and in the TM of primary open-angle glaucoma donor eyes. It is possible that a relationship exists between chronic exposure to BAK and glaucoma. The hypothesis that BAK causes/worsens glaucoma is being tested experimentally in an animal model that closely reflects human physiology.

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