thromboxane

(redirected from Thromboxanes)
Also found in: Dictionary, Medical.
Related to Thromboxanes: Eicosanoids, Leukotrienes

thromboxane

[‚thräm′bäk‚sān]
(biochemistry)
Any member of a group of 20-carbon fatty acids related to the prostaglandins and derived mainly from arachidonic acid.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
The authors say, "Experimental studies have suggested a rebound effect after aspirin discontinuation, involving increased thromboxane levels possibly resulting from the pro-thrombotic effects of residual very low levels of aspirin." Does a rebound effect increase heart attack risk, even if a patient discontinues aspirin therapy for a short time because of surgery or other medical procedure?
Cyclooxygenases (COX) catalyze the production of prostaglandins and thromboxanes from arachidonic acid as depicted in Figure 4 [16].
(1) Prostanoids include what are sometimes referred to as the "classical" prostaglandins (PGs), such as PGD, PGE, and PGF (all of which have a prostanoic acid backbone), as well as prostacyclin ([PGI.sub.2]) and thromboxane. Specific prostanoids are designated by a letter that indicates the type of ring structure, followed by a number that indicates the number of double bonds in the hydrocarbon structure.
Thromboxane synthase (TXS) is a hemoprotein with feature of the cytochrome P-450 family which catalyzes prostaglandin endoperoxide into thromboxanes [39].
Phipps, "Human bone marrow megakaryocytes and platelets express PPARy, and PPARy agonists blunt platelet release of CD40 ligand and thromboxanes," Blood, vol.
(11) The aspirin-induced decrease in thromboxane production leads to a decline in platelet activation and aggregation, which accounts both for aspirin's beneficial cardiovascular effects and the associated risk of bleeding--aspirin's most common adverse effect.
Prostacyclin opposes the effects of thromboxane, a thrombogenic and atherogenic eicosanoid.
Both NSAIDs and COX-2s work by inhibiting the enzyme cyclo-oxygenase (COX) which in turn stops the production of prostaglandins (PGE2 and PGF2[alpha]) and thromboxanes from membrane phospholipids.
To the Editor: Chin and Commerford (1) suggest the imbalance between eicosanoids (prostacyclins and thromboxanes) as a possible cause for the observed increase in cardiovascular risk with the cyclo-oxygenase-2 (COX-2) inhibitors and traditional non-steroidal anti-inflammatory drugs (NSAIDs).
BERLIN -- A new type of NSAID that inhibits the production of leukotrienes, prostaglandins, and thromboxanes was as effective as and better tolerated than a standard NSAID or a selective cyclooxygenase inhibitor for the treatment of osteoarthritis in a pair of phase III studies.
Licofelone also inhibits both cydooxygenase (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.
(58,63) This process leads to an increase in circulating tissue levels of various cytokines, (177-180) leukotrienes, (181) thromboxanes, (182) platelet activating factor, (183) complement components, (184) elastases, and other enzymes, (185) and it causes the formation of additional ROS.