Superoxide anions enhance platelet adhesion and aggregation

• Published in: British journal of pharmacology Vol. 97; no. 4; pp. 1145 - 1150
• Main Authors: Salvemini, Daniela, Nucci, Gilberto, Sneddon, John M., Vane, John R.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.08.1989; Nature Publishing
• Subjects: Adenine - metabolism; Biological and medical sciences; Blood. Blood coagulation. Reticuloendothelial system; Catalase - pharmacology; Humans; In Vitro Techniques; Mannitol - pharmacology; Medical sciences; oxygen; Pharmacology. Drug treatments; Platelet Adhesiveness - drug effects; Platelet Aggregation - drug effects; Platelet Aggregation Inhibitors; Pyrogallol - pharmacology; Superoxide Dismutase - pharmacology; Superoxides - pharmacology; Thrombin - pharmacology; Aggregation; Human; Hyperoxides; Platelet; Volunteer; Single dose; Superoxide dismutase; Normal; Adhesion; In vitro; Biological activity; Free radical
• ISSN: 0007-1188; 1476-5381
• DOI: 10.1111/j.1476-5381.1989.tb12572.x

1 Superoxide dismutase (SOD, 60 u ml−1) or ferricytochrome c (70 μm) significantly inhibited thrombin‐stimulated platelet adhesion to gelatin‐coated plastic, whereas catalase (1000 u ml−1) or mannitol (1 mm) had no effect. 2 The platelet aggregation induced by low concentrations of thrombin (causing less than 45% maximal change in light transmission) was inhibited by SOD. Catalase or mannitol had no effect on platelet aggregation. 3 Pyrogallol (an O2− generator) enhanced both platelet adhesion to gelatin‐coated plastic and platelet aggregation induced by thrombin; this enhancement was neutralized by SOD. 4 These results indicate that O2− increase both platelet adhesion and aggregation, whereas other free radicals such as hydrogen peroxide or hydroxyl radicals are not involved.