Beta-2-Agonists Have Antioxidant Function in vitro

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Abstract
β2-Agonists are known to have anti-inflammatory efficacy. In this context, β2-agonists are also capable of inhibiting oxidant production of cultured inflammatory cells. As the mechanisms of this function still remain speculative, the purpose of this study was to quantify the efficacy of β2-agonists in vitro to inhibit superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH•) and hypochlorous acid (HOCl). We tested the following antiasthma drugs: ipratropium bromide, salbutamol (salbutamol base), fenoterol (fenoterol hydrobromide), terbutaline (terbutaline sulfate), isoproterenol, prednisolone (prednisolone hydrogensuccinate), beclomethasone (beclomethasone dipropionate) and theophylline (theophylline sulfate). Antioxidant function was quantified by using the following assay systems: O2- (ferricytochrome c + xanthine/xanthine oxidase), H2O2 (phenol red + 5·• 10-6M H2O2 OH• (deoxyribose assay) and HOCl (HOCl/OCl- in luminol-dependent chemiluminescence). At 10-4M, the anti- H2O2 and anti- O2- capacity was as follows: salbutamol/terbutaline 2-agonists (10-4M) tested reduced HOCl activity by > 50% (p • reduction (10-30%) by the β2-agonists is regarded as an nonspecific effect, due to the high concentrations needed (10-3M). Corticosteroids and theophylline had no antioxidant effect. These results demonstrate the different redox potentials of different phenol types within the molecular structure of the β2-agonists. The good antioxidative function of isoproterenol is related to ortho formation of the phenol ring, whereas fenoterol has two phenol rings which can be oxidized. A direct oxidant scavenger function may explain the ability of β2-agonists to reduce the oxidant production of inflammatory cells in vitro.

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