In Vitro and in Vivo Experimental Studies on Trabecular Meshwork Degeneration Induced by Benzalkonium Chloride (An American Ophthalmological Society Thesis)
Christophe Baudouin (1,2,3,4), Alexandre Denoyer (1,2), Nicolas Desbenoit (2), Gregory Hamm (5), and Alice Grise (1,2)
1 From the Department of Ophthalmology III, Quinze-Vingts National Ophthalmology Hospital, Paris, France.
2 Institut National de la Santé¸ et de la Recherche Médicale (INSERM), University Paris 06, Institut de la Vision, and Centre National de la Recherche Scientifique (CNRS), Paris, France.
3 Ambroise Paré¸ Hospital, Assistance Publique-Hôpitaux de Paris, Boulogne, France
4 University of Versailles, St-Quentin-en-Yvelines, France
5 ImaBiotech, Parc Eurasanté, Loos, France
Long-term antiglaucomatous drug administration may cause irritation, dry eye, allergy, subconjunctival fibrosis, or increased risk of glaucoma surgery failure, potentially due to the preservative benzalkonium chloride (BAK), whose toxic, proinflammatory, and detergent effects have extensively been shown experimentally. We hypothesize that BAK also influences trabecular meshwork (TM) degeneration.
BAK enhances all characteristics of TM degeneration typical of glaucoma trabecular apoptosis, oxidative stress, induction of inflammatory chemokines and causes degeneration in acute experimental conditions, potentially mimicking long-term accumulation. BAK was also shown to access the TM after repeated instillations. These findings support the hypothesis that antiglaucoma medications, through toxicity of their preservative, may cause further long-term trabecular degeneration and therefore enhance outflow resistance, reducing the impact of IOP-lowering agents.