thromboxanes


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Related to thromboxanes: Eicosanoids, Leukotrienes

throm·box·anes

(throm-boks'ānz),
A group of compounds, included in the eicosanoids, formally based on thromboxane, but with the terminal COOH group present; biochemically related to the prostaglandins and formed from them through a series of steps involving the formation of an endoperoxide (an O-O bridge between carbons 9 and 11 in the prostaglandins) by a cyclooxygenase, followed by a rearrangement (catalyzed by thromboxane synthase) that inserts one of the two oxygen atoms between carbons 11 and 12, leaving the other still bridging carbons 9 and 11. Thromboxanes are so named from their influence on platelet aggregation and the formation of the oxygen-containing six-membered ring (pyran or oxane). Like the prostaglandins, individual thromboxanes (abbreviated TX) are designated by letters (A, B, C, etc.) and subscripts indicating structural features.
Farlex Partner Medical Dictionary © Farlex 2012

throm·box·anes

(throm-bok'sānz)
A group of compounds, included in the eicosanoids, formally based on thromboxane, but with the terminal COOH group present; biochemically related to the prostaglandins and formed from them. Thromboxanes are so named from their influence on platelet aggregation and the formation of the oxygen-containing six-membered ring (pyran or oxane). Like the prostaglandins, individual thromboxanes (abbreviated TX) are designated by letters (A, B, C, and onward) and subscripts indicating structural features.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

thromboxanes

Substances similar to the prostaglandins that promote blood clotting. Aspirin in small doses reduces the production of thromboxane by PLATELETS.
Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005
References in periodicals archive ?
These drugs inhibit the action of cyclooxygenase-2 that catalyzes the production of prostaglandins and thromboxanes, key mediators of inflammation, from arachidonic acid [33].
(12,13) The specific inhibition of COX-2 alters the balance between platelet-derived thromboxane [A.sub.2] ([TXA.sub.2]) and endothelium-derived [PGI.sub.2], leading to increases in the risk of thrombosis due to altered vascular tone.
Ullrich, "Prostacyclin and thromboxane synthases," Journal of Lipid Mediators and Cell Signalling, vol.
Arachidonic acid thromboxane pathway is an important platelet activation pathway (Figure 4).
Pharmacodynamic studies support the use of a lower dose of aspirin, finding that serum thromboxane is completely inhibited by a maintenance dose as low as 30 mg/d in healthy individuals and 50 mg/d for those with chronic stable angina.
Reduced levels of circulating thromboxane prevent platelet aggregation and vasoconstriction such that bleeding time is prolonged when patients are taking NSAIDs.
Licofelone also inhibits both cyclooxygenase (COX)-1 and COX-2, the enzymes that convert arachidonic acid into prostaglandins and thromboxanes, which means that the drug is a dual LOX-COX inhibitor.
Thromboxane mediates diapedesis after ischemia by activation of neutrophil adhesion receptors interacting with basally expressed intercellular adhesion molecule-1.
The fatty acids also may prevent renal damage by inhibiting inflammation and thromboxanes while allowing prostaglandin synthesis (Emancipator, 1998).
Arachidonic acid may also be converted to other pharmacologically active C20 compounds, e.g., leukotrienes, prostacyclin, and thromboxanes. All the above-mentioned compounds, including PGs, are known collectively as "eicosanoids." Another enzyme, lipoxygenase, can also convert arachidonic acid to PGs.
Some researchers are testing drugs that specifically inhibit the synthesis of thromboxanes, substances made by the body that cause vessels to constrict.
Eicosanoids consist of multiple subfamilies including prostaglandins, thromboxanes, leukotrienes, and derivatives of arachidonate [22].