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C Blondin, P Hamard, G Sultan, C Baudouin; In Vitro Effects of Topical Beta-blockers on Human Complement System . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3392.
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Purpose: To investigate the action of topical beta-blockers, used with or without preservative in the treatment of glaucoma, on human complement system. Methods: Normal human serum was used as a source of complement. The effect of antiglaucomatous eyedrops on complement was assessed in a standard CH50 hemolytic assay. In addition, the ability of beta-blockers to prevent activation of the complement classical pathway induced by immune complexes was examined. Results: timolol maleate (0.5%), betaxolol chlorhydrate (0.25%), carteolol (1% or 2%), both preserved or preservative-free, as well as unpreserved latanoprost (0.005%), did not induce significant activation of complement system. However, benzalkonium chloride (BAC, 0.01%) induced a slight activation (12%) of complement. The capability of preserved or unpreserved beta-blockers to prevent activation of complement induced by immune complexes was then investigated. Corteolol and latanoprost failed to inhibit complement activation, whereas benzalkonium chloride increased IgG-induced complement activation (p = 0.033). On the contrary, a significant inhibition of complement activation was detected with preserved (p = 0.037) or preservative-free (p < 0.001) timolol maleate, as well as with preserved (p = 0.0015) or preservative-free (p < 0.001) betaxolol chlorhydrate. No statistical differences were observed between the inhibitory effect of preserved or unpreserved timolol (21 ± 8% versus 24 ± 5%, respectively) as well as between preserved or unpreserved betaxolol (34 ± 6% versus 37 ± 6%, respectively). Conclusion: Functional complement is present in most anterior segment tissues including tears, cornea, posterior sclera, vitreous and aqueous humor. Activation of complement system generates activated fragments that mediate inflammation and chemotaxis of inflammatory cells. The anti-glaucomatous drugs tested in this study were all devoid of intrinsic complement-activating potency. Benzalkonium chloride was slightly complement-activating and increased the IgG-induced complement activation. On the opposite, timolol maleate and betaxolol chlorhydrate significantly prevented complement activation induced by immune complexes, indicating that the tendency of benzalkonium to activate complement was somehow inhibited within the preserved eyedrops, possibly through complexation of BAC with the beta-blocker.
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