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In the ASPItest arachidonic acid is added to the saline-diluted blood sample. Arachidonic acid is converted to prostaglandin H2 (PGH2) by cyclooxygenase-1 (COX1), and PGH2 is then converted to thromboxane A2 (TXA2) by thromboxane synthase. TXA2 increases platelet aggregation, promotes degranulation and stimulates platelet activation.
Arachidonic acid for signaling purposes appears to be derived by the action of group IVA cytosolic phospholipase A 2 (cPLA 2, 85 kDa), whereas inflammatory arachidonic acid is generated by the action of a low-molecular-weight secretory PLA 2 (sPLA 2, 14-18 kDa). [8] Arachidonic acid is a precursor to a wide range of eicosanoids:
Thromboxane A 2 (TXA 2) is generated from prostaglandin H 2 by thromboxane-A synthase in a metabolic reaction which generates approximately equal amounts of 12-hydroxyheptadecatrienoic acid (12-HHT). Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H 2 , and therefore TXA 2 .
They release arachidonic acid from membrane phospholipids. Arachidonic acid is both a signaling molecule and the precursor for the synthesis of other signaling molecules termed eicosanoids. These include leukotrienes and prostaglandins. Some eicosanoids are synthesized from diacylglycerol, released from the lipid bilayer by phospholipase C (see ...
The catalytic mechanism involves the insertion of an oxygen moiety at a specific position in the arachidonic acid backbone. [ citation needed ] The lipoxygenase pathway is active in leukocytes and other immunocompetent cells, including mast cells , eosinophils , neutrophils , monocytes , and basophils .
The binding of agonists such as thrombin, epinephrine, or collagen, to platelet surface receptors can trigger the activation of phospholipase C to catalyze the release of arachidonic acid from two major membrane phospholipids, phosphatidylinositol and phosphatidylcholine.