Thymoquinone (TQ) is a nutrient with anticarcinogenic activity by stimulating suicidal death of tumor cells. Moreover, TQ triggers suicidal death of erythrocytes or eryptosis, an effect at least partially due to increase in cytosolic Ca²⁺ activity and ceramide formation. The present experiments explored, whether TQ influences apoptosis of blood platelets. Cell membrane scrambling was determined utilizing annexin V-binding to phosphatidylserine-exposing platelets, cytosolic Ca²⁺ activity utilizing Fluo3 fluorescence, caspase activity utilizing immunofluorescence and Western blotting of active caspase 3 and inactive procaspase 3, mitochondrial potential utilizing DiOC6 fluorescence, and ceramide formation by flow cytometric analysis of ceramide binding antibodies. As a result, a 30 min exposure to thymoquinone (>= 5 mM) was followed by annexin V binding, paralleled by caspase activation, increase of cytosolic Ca²⁺ activity, mitochondrial depolarization and ceramide formation. Nominal absence of extracellular Ca²⁺ blunted but did not fully abolish the TQ-induced activation of caspase 3. In conclusion, thymoquinone triggers suicidal death of blood platelets, an effect paralleled by increase of cytosolic Ca²⁺ activity, ceramide formation, mitochondrial depolarisation and caspase 3 activation and partially dependent on stimulation of Ca²⁺ entry.