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Abstract #9896 Published in IGR 5-3
Metipranolol attenuates lipid peroxidation in rat brain: a comparative study with other antiglaucoma drugs
Melena J; Osborne NNGraefe's Archive for Clinical and Experimental Ophthalmology 2003; 241: 827-833
BACKGROUND: Free radical production seems to be involved in the pathogenesis of a number of ocular diseases. Certain β-adrenoceptor antagonists display antioxidant properties, but these have not been ascribed to any of the presently used ophthalmic β-adrenoceptor antagonists. Therefore, the authors examined the influence of ophthalmic β-adrenoceptor antagonists and other antiglaucoma drugs on stimulated lipid peroxidation in rat brain homogenates. METHODS: Lipid peroxidation in rat brain homogenates was stimulated by iron/ascorbate or sodium nitroprusside. Lipid peroxidation was assessed by the formation of thiobarbituric acid reactive species (TBARS). RESULTS: Of the antiglaucoma drugs tested (brimonidine, carteolol, dorzolamide, latanoprost, levobetaxolol, levobunolol, metipranolol, pilocarpine, timolol, travoprost and unoprostone), only metipranolol and its active metabolite, desacetylmetipranolol, were found to significantly reduce iron/ascorbate-induced lipid peroxidation in rat brain homogenates with IC50 values of 6.9 and 1.1 M, respectively. Metipranolol and desacetylmetipranolol also concentration-dependently inhibited sodium nitroprusside-stimulated lipid peroxidation in rat brain homogenates, displaying IC50 values of 25.1 and 2.6 M, respectively. CONCLUSIONS: These data indicate that metipranolol and desacetylmetipranolol exhibit remarkable antioxidant properties, with an effect not dissimilar from the reference antioxidant trolox.
Dr. N.N. Osborne, Nuffield Laboratory of Ophthalmology, University of Oxford, Walton Street, Oxford, OX2 6AW, UK Email: neville.osborne@eye.ox.ac.uk
Classification:
11.3.4 Betablocker (Part of: 11 Medical treatment > 11.3 Adrenergic drugs)