eicosanoid


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ei·co·sa·noid

 (ī′kō-sə-noid′)
n.
Any of a group of substances that are derived from arachidonic acid, including leukotrienes, prostaglandins, and thromboxanes.

[eicosan(e), chemical name (Greek eikosi, twenty, from its twenty carbon atoms; see wīkm̥tī- in Indo-European roots + -ane) + -oid.]

eicosanoid

(aɪˈkəʊsəˌnɔɪd)
n
any of a group of compounds, including the leukotrienes and the prostglandins, which are produced by the oxygenation of essential fatty acids and which are involved in a range of physiological processes, including inflammation and immunity
References in periodicals archive ?
Inflammation is partially regulated through the eicosanoid pathway.
In fact, it has been shown that indapamide stimulates the synthesis of prostaglandin E2; in susceptible individuals, the presence of other contributing factors, such as an inborn error in eicosanoid metabolism or a clinical or subclinical infection, might lead to the local accumulation of prostaglandins during treatment with indapamide, causing vasodilation, increased vascular permeability, and ultimately ciliochoroidal effusion [2].
Banerjee, "Eicosanoid pathway in colorectal cancer: recent updates," World Journal of Gastroenterology, vol.
The results were expressed as the mean [+ or -] standard deviation (SD) of the cytokine and eicosanoid production.
(15,19-24) Most of these phenotypes are recapitulated in mice lacking one or more of the biosynthetic enzymes or receptors for PGs and LTs, lending strong support to the notion that c[PLA.sub.2][alpha] lies upstream of eicosanoid biosynthesis in many situations.
sativa inhibits eicosanoid generation in leukocytes and lipid peroxidation.
The Transcellular Biosynthesis of Eicosanoid Derivatives: Crossover Pathways.
Results: Cur treatment of acute Chagas mice enhanced survival and proved to hinder relevant inflammatory processes in the heart, including leukocyte recruitment, activation of the eicosanoid pathway and BNP overexpression, without modifying parasite burden in the organ.
Exhaled breath condensate eicosanoid levels associate with asthma and its severity.
Apart from Eicosanoid dependent mechanism, EFA also affects cellular signalling by making lipid rafts and altering gene expression by their effect on transcription factor and blockage of TNF [alpha] (Tumour Necrosis Factor), IL (Interleukin) and LT (Leukotriene), which is responsible for improved lacrimal secretion (Figure 2).
To this purpose, we studied the influence of physiological concentrations of C4 on HDAC activity, immune signalling pathways, the eicosanoid pathway, and cellular metabolism.