Journal of Lipid Research, Vol 30, 1925-1932, Copyright © 1989 by Lipid Research, Inc.
Albumin redirects platelet eicosanoid metabolism toward 12(S)- hydroxyeicosatetraenoic acid
MJ Broekman, AM Eiroa and AJ Marcus
Department of Medicine, New York Veterans Administration Medical Center, NY 10010.
Albumin is a major determinant of eicosanoid formation, affecting autacoids
important in cell-cell interactions. We delineated three mechanisms by
which albumin controlled platelet eicosanoid formation: 1) Albumin diverted
free arachidonate toward 12-lipoxygenation. 2) Albumin enhanced release of
arachidonate from phospholipids. 3) Albumin inhibited incorporation of
arachidonate from the medium into platelet phospholipids.
12(S)-Hydroxyheptadecatrienoic acid (12-HHTrE) formation was reduced 70% by
albumin as compared to that formed in albumin-free medium. In sharp
contrast, formation of 12(S)-hydroxyeicosatetraenoic acid (12-HETE), the
platelet lipoxygenase product, was much less influenced by albumin.
Moreover, 12-HETE production in the presence of albumin was markedly
increased and prolonged after aspirin treatment. These data suggested that
albumin redirected released endogenous arachidonate from cyclooxygenase to
lipoxygenase. Therefore, the metabolic fate of arachidonate present in the
medium of stimulated platelets was studied by adding tracer
[3H]arachidonate 30 sec before thrombin. Albumin increased arachidonate
metabolism by lipoxygenase 7- fold as compared to albumin-free controls,
while cyclooxygenation increased 2.7-fold. Redirection of eicosanoid
metabolism by albumin toward lipoxygenase products constitutes a heretofore
undescribed and potentially important physiological role for albumin. In
vitro utilization of albumin may reflect in vivo events in thrombosis and
hemostasis more accurately than previous studies without albumin could
appreciate.
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