AIMS: Serotonin (5-HT) is capable of reducing the oxidative burst of professional phagocytes. In this study, we investigated whether 5-HT mediates this modulation via 5-HT receptors (5-HTR) or whether this is due instead to 5-HT antioxidative properties. MAIN METHODS: The leukocytes or polymorphonuclear leukocytes (PMNL) were isolated from human blood, and their ability to produce reactive oxygen species (ROS) after 5-HT or its agonist treatment was tested by luminol-enhanced chemiluminescence (CL) analysis. KEY FINDINGS: It was found that 5-HTR(2) agonist DOI hydrochloride does not have any antioxidative properties, despite its ability to inhibit the CL response of activated human total leukocytes. On the other hand, DOI hydrochloride was unable to inhibit the CL response of activated human PMNL. It seems that the reduction of the oxidative burst of professional phagocytes was evoked by the activation of 5-HTR not on the neutrophil surface but on the surface of different leukocytes, which produced anti-inflammatory cytokines with NADPH oxidase activity modulating properties. SIGNIFICANCE: Platelets and activated PMNL are in tight contact at sites of inflammation. 5-HT released from platelets might have a protective function against PMNL-derived oxidative stress and oxidative damages.

Department of Free Radical Pathophysiology Institute of Biophysics v v i Academy of Sciences of the Czech Republic Královopolská 135 612 65 Brno Czech Republic

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Serotonin and its metabolites reduce oxidative stress in murine RAW264.7 macrophages and prevent inflammation