Carbocisteine can scavenge reactive oxygen species in vitro

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Background and objectiveReactive oxygen species (ROS) play an important role in the pathogenesis of various respiratory diseases. Carbocisteine, a mucoregulatory drug, is used in the treatment of several disease states but little information is available about its scavenger effects on ROS. The present study was designed to examine the scavenger effects of carbocisteine on ROS.MethodsThe oxidation-reduction potential of carbocisteine was measured, and its scavenger effects on hypochlorous acid (HOCl), hydrogen peroxide (H2O2), hydroxyl radical (OH) and peroxynitrite (ONOO-) were examined in cell-free conditions. The effects of carbocisteine on ROS generated from rat neutrophils, intracellular oxidative stress and release of inflammatory cytokines (IL-8 and IL-6) from IL-1β-induced airway epithelial cells, NCI-H292 cells, were investigated.ResultsCarbocisteine provided a reducing stage and showed scavenger effects on H2O2, HOCl, OH and ONOO- in cell-free conditions. Carbocisteine inhibited ROS generation from rat neutrophils, intracellular oxidative stress and release of IL-8 and IL-6 from NCI-H292 cells. N-acetyl-L-cysteine, a radical scavenger, also inhibited these events related to ROS as well as carbocisteine.ConclusionsThese results suggest that carbocisteine could exert anti-inflammatory and anti-oxidant effects through directly scavenging ROS in addition to its previously known mucoregulatory effect.

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