Complement-independent Ab-induced peroxide lysis of platelets requires 12-lipoxygenase and a platelet NADPH oxidase pathway
J. Clin. Invest. Michael Nardi, et al. 113:973 doi:10.1172/JCI20726 [Go to this article.]

Figure 4
Role of platelet 12-LO in anti–GPIIIa49–66–induced platelet fragmentation. (A) Lipoxygenase inhibitors: 5-, 8-, 11-eicosatriynoic acid (ETI), nordihydroguairetic acid (NDGA) (n = 4), and cinnamyl-3-, 4-dihydrocyanocinnamate (CDC) (n = 8) were added to gel-filtered human platelets 15 minutes prior to Ab, and percentage of fragmentation measurements were made after a 4-hour incubation. Cg, control IgG (25 μg/ml); Ci, control IgG plus inhibitor (25 μg/ml); 0, patient IgG without inhibitor (25 μg/ml). (B) Effect of 12-LO products, 12(S)-HETE and 12(S)-HPETE (n = 8), on platelet fragmentation. 12(R)-HETE is a nonlipoxygenase-derived stereosisomer (n = 3). (C) Comparison of Ab versus 12(S)-HETE–induced platelet fragmentation (typical of three experiments). (D) Effect of patient IgG (Pg) vs. control IgG (Cg) on platelet 12(S)-HETE production (typical of three experiments).