Abstract
The traditional view of the regulation of eicosanoid synthesis holds that agonists such as growth factors, differentiation factors, and cytokines activate receptor-coupled phospholipases before eicosanoid synthesis can occur (1,5). One of the consequences of receptor-mediated activation of phospholipases is the release of unesterified arachidonic acid (AA) (eicosatetraenoic acid, 20:4 ω6) from cellular phospholipid stores and the generation of other second messengers (1,5,6). The phospholipase-released AA is believed to be the major substrate for eicosanoid biosynthesis in animal cells because the constitutive free intracellular AA concentration has been estimated to be low (13). Unesterified AA, either experimentally provided to cultured cells as free AA/albumin complexes or released from cellular phospholipids upon agonist-dependent phospholipase activation, can be metabolized by a variety of distinct and highly regulated pathways within the AA cascade. These include the 5-lipoxygenase (EC 1.13.11.12) pathway that gives rise to the leukotrienes (LTs) (reviewed in 16,17) and the cyclooxygenase/prostaglandin (PG) H synthase (EC 1.14.99.1) pathway that gives rise to the PGs and thromboxane (reviewed in 13).
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Habenicht, A.J.R., Salbach, P., Janßen-Timmen, U. (1993). LDL Receptor-Dependent Polyunsaturated Fatty Acid Transport and Metabolism. In: Schettler, G., Greten, H., Habenicht, A.J.R. (eds) Cellular Metabolism of the Arterial Wall and Central Nervous System. Sitzungsberichte der Heidelberger Akademie der Wissenschaften, vol 1993/94 / 1993/1. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84949-7_11
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