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Background  Aspirin is one of the most widely used non-steroidal anti-inflammatory drugs (NSAIDs). It is also a commonly used anti-platelet drug, which inhibits the formation of the platelet activator, thromboxane A 2  (TxA 2 ) via inhibition of cyclooxygenase-1 (COX-1). However, the presence of a patient subset that fails to respond to aspirin despite reduced TxA 2  concentrations suggests that the effect of aspirin might be more complex than exclusive COX-1 inhibition.    Methods  In this study we evaluated the impact of  in vivo  oral administration of a standard anti-platelet dose (75 mg) of aspirin in healthy volunteers on the acute impact of  in vitro  collagen-mediated platelet aggregation and generation of platelet-derived TxA 2  and the 12-lipoxygenase (LOX) metabolite 12-hydroxyeicosatetraenoic acid (12-HETE). The eicosanoids were quantified using liquid chromatography-tandem mass spectrometry (LC-MS/MS).    Results  Low-dose aspirin administration not only inhibited TxA 2  generation but also decreased the production of 12-HETE. Furthermore, a significant correlation was observed between the levels of 12-HETE and collagen-induced platelet aggregation. Pre-treatment of platelets with the 12-LOX inhibitor, baicalein, prior to activation attenuated platelet aggregation.    Conclusions  These findings support a role for 12-HETE as a pro-aggregatory eicosanoid in platelet function and suggest a role for 12-HETE in variable sensitivity to aspirin. The study also highlights a potentially important mechanism by which aspirin impacts upon eicosanoid generation.

12-hydroxyeicosatetraenoic acid is associated with variability in aspirin-induced platelet inhibition