ABSTRACT
This chapter investigates the role of lipoxygenase products in the thrombin-induced third mechanism of platelet aggregation. Activated blood platelets convert endogenous, free arachidonic acid via the cyclooxygenase or the lipoxygenase pathways into thromboxanes or 12-hydroxy acids, respectively. The role of the cyclooxygenase products in platelet functioning is clearly established, but the role of the lipoxygenase products is less clear. In the myeloproliferative syndrome platelet lipoxygenase-deficiency has been reported to occur at a high incidence. The myeloproliferative syndrome consists of four main types of disease: polycythemia vera, myelofibrosis, essential thrombocythemia, and chronic myeloid leukemia. The arachidonic acid-induced platelet cyclooxygenase activity, measured by malondialdehyde (MDA) production, was only slightly reduced in three patients and all patients had normal thrombin-induced MDA production. The 12-hydroxy-5,8,10-heptadecatrienoic acid and 12-hydroxy-5,8,10,14-eicosatetraenoic acid measurement of the patients was repeated on the role of the lipoxygenase products in platelet aggregation in platelet-poor plasma.
