Author/Authors :
Timirci-Kahraman, Özlem Istanbul Üniversitesi - Deneysel Tip Arastirma Enstitüsü - Moleküler Tip Anabilim Dali, Turkey , Küçükhüseyin, Özlem Istanbul Üniversitesi - Deneysel Tip Arastirma Enstitüsü - Moleküler Tip Anabilim Dali, Turkey , Toptas, Bahar Istanbul Üniversitesi - Deneysel Tip Arastirma Enstitüsü - Moleküler Tip Anabilim Dali, Turkey , Isbir, Turgay Yeditepe Üniversitesi - Tip Fakültesi - Tibbi Biyoloji Anabilim Dali, Turkey
Abstract :
Since the discovery of the central role of cyclooxygenase (COX) in the metabolism of arachidonic acid, vascular biologists have been exposed with the duality of this system. Essentially, one substrate (arachidonic acid) converted by one enzyme (COX) yields end products (endoperoxides) that obtain only very briefly before being metabolized to more stable prostanoids by a group of specific synthases that were primarily believed to be tissue specific. For example, thrombocytes include mainly the synthase that produces thromboxane A2 (proaggregatory and vasoconstrictor substance), though endothelial cells contain mainly the enzyme that produces prostacyclin (antiaggregatory and vasodilator substance). The overproduction of thromboxane A2 by thrombocytes induces to thrombosis. Endothelial cells lean against vascular occlusion by producing prostacyclin. This duality of the metabolism of arachidonic acid has ruled over our thinking about atherothrombosis for decades. Based on the review of these studies, we will discuss association between cyclooxygenase enzyme and endothelial dysfunction.
