The concentration of 12‐hydroxyeicosatetraenoic acid (12‐HETE) formed in rat platelets aggregated by collagen suspension increased continuously during a 115‐min incubation period, whereas the concentration of TXB₂ or PGF_2α reached the maximum within 3 min and stayed at the plateau for the remaining incubation period. These data indicate that platelet lipoxygenase is not completely inactivated as is cyclooxygenase by the oxidizing agent. Platelets of essential fatty acid deficient (EFAD) rats resuspended in plasma of control rats produced more 12‐HETE than platelet‐rich plasma (PRP) of EFAD rats, whereas platelets of control rats resuspended in plasma of EFAD rats formed less 12‐HETE than PRP of control rats. However, the concentration of TXB₂ or PGF_2α produced was not changed in both cases implying that platelet cyclooxygenase preferentially utilizes arachidonic acid (AA) derived from platelet lipids. Radioactivity of phosphatidylcholine (2‐arachidonyl‐1‐¹⁴C) suspended in the plasma of PRP was incorporated into 12‐HETE but not to TXB₂, indicating again that only lipoxygenase can utilize AA derived from plasma phospholipids. The significance of this observation is that the effects of platelet lipoxygenase products, although their physiological roles are not known, would be much more persistent than cyclooxygenase products after platelets are stimulated or aggregated in vivo.