WordNet

street name for lysergic acid diethylamide (同)back breaker, battery-acid, dose, dot, Elvis, loony toons, Lucy in the sky with diamonds, pane, superman, window pane, Zen
any of various water-soluble compounds having a sour taste and capable of turning litmus red and reacting with a base to form a salt
having the characteristics of an acid; "an acid reaction"

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酸性の / 酸味のある,すっぱい(sour) / (言葉・態度などが)厳しい,しんらつな / 酸 / すっぱいもの / 《俗》=LSD

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/04/04 01:29:02」(JST)

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Chemical structure of 14,15-epoxyeicosatrienoic acid.

The Epoxyeicosatrienoic acids or EETs are signaling molecules formed by the action of Cytochrome P450 epoxygenase on 20-carbon essential fatty acids, such as arachidonic acid, from which it is produced by the enzyme epoxygenase. ^[1]

These nonclassic eicosanoids act as short-range hormones, (i.e. they are autocrine and paracrine mediators) of the cardiovascular system and kidney. They produce vasorelaxation as well as anti-inflammatory and pro-fibrinolytic effects.^[2] EETs are metabolized by the soluble epoxide hydrolase to the corresponding vicinal diol, or dihydroxyeicosatrienoic acids (DHETs), which are biologically less active.

Biological effects

Generally, EETs cause:

Calcium release from intracellular stores^[1]
Increased sodium-hydrogen antiporter activity^[1]
Increased cell proliferation^[1]
Decreased cyclooxygenase activity^[1]

Other effects are specific to certain cells or locations:

EETs are cardioprotective after ischemic heart attack and reperfusion.^[3]
They act in the corpus cavernosum to maintain penile erection.^[4]
Specific epoxidation of EET sites produces endogenous PPARα agonists.^[5]
Decreased release of somatostatin, insulin and glucagon from endocrine cells.^[1]
Vasodilation and angiogenesis in blood vessels.^[1]
Increased risk of tumor adhesion on endothelial cells^[1]
Decreased platelet aggregation^[1]

References

^ ^a ^b ^c ^d ^e ^f ^g ^h ⁱ Walter F., PhD. Boron (2003). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. p. 108. ISBN 1-4160-2328-3.
^ Spector AA, Fang X, Snyder GD, Weintraub NL (January 2004). "Epoxyeicosatrienoic acids (EETs): metabolism and biochemical function". Prog Lipid Res 43 (1): 55–90. doi:10.1016/S0163-7827(03)00049-3. PMID 14636671.
^ Nithipatikom K, Moore JM, Isbell MA, Falck JR, Gross GJ (August 2006). "Epoxyeicosatrienoic acids in cardioprotection: ischemic versus reperfusion injury". Am. J. Physiol. Heart Circ. Physiol. 291 (2): H537–42. doi:10.1152/ajpheart.00071.2006. PMID 16473964.
^ Jin L, Foss CE, Zhao X et al. (March 2006). "Cytochrome P450 epoxygenases provide a novel mechanism for penile erection". FASEB J. 20 (3): 539–41. doi:10.1096/fj.05-4341fje. PMID 16415108.
^ Ng VY, Huang Y, Reddy LM, Falck JR, Lin ET, Kroetz DL (July 2007). "Cytochrome P450 eicosanoids are activators of peroxisome proliferator-activated receptor alpha". Drug Metab Dispos 37 (7): 1126–34. doi:10.1124/dmd.106.013839. PMID 17431031.

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English Journal

Isolation and characterization of Xenopus soluble epoxide hydrolase.

Purba ER1, Oguro A1, Imaoka S2.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Jul;1841(7):954-62. doi: 10.1016/j.bbalip.2014.03.010. Epub 2014 Mar 28.
Soluble epoxide hydrolase (sEH) contributes to cell growth, but the contribution of sEH to embryonic development is not well understood. In this study, Xenopus sEH cDNA was isolated from embryos of Xenopus laevis. The Xenopus sEH was expressed in Escherichia coli and was purified. The epoxide hydrol
PMID 24681163

Protection from hypertension in mice by the Mediterranean diet is mediated by nitro fatty acid inhibition of soluble epoxide hydrolase.

Charles RL1, Rudyk O1, Prysyazhna O1, Kamynina A1, Yang J2, Morisseau C2, Hammock BD2, Freeman BA3, Eaton P4.
Proceedings of the National Academy of Sciences of the United States of America.Proc Natl Acad Sci U S A.2014 May 19. pii: 201402965. [Epub ahead of print]
Soluble epoxide hydrolase (sEH) is inhibited by electrophilic lipids by their adduction to Cys521 proximal to its catalytic center. This inhibition prevents hydrolysis of the enzymes' epoxyeicosatrienoic acid (EET) substrates, so they accumulate inducing vasodilation to lower blood pressure (BP). We
PMID 24843165

Role of Transient Receptor Potential Vanilloid 4 activation in indomethacin-induced intestinal damage.

Yamawaki H1, Mihara H, Suzuki N, Nishizono H, Uchida K, Watanabe S, Tominaga M, Sugiyama T.
American journal of physiology. Gastrointestinal and liver physiology.Am J Physiol Gastrointest Liver Physiol.2014 May 1. [Epub ahead of print]
Gastrointestinal ulcers and bleeding are serious complications of non-steroidal anti-inflammatory drug (NSAID) use. While administration of antibiotics and Toll-like receptor 4 knockdown mitigate NSAID-induced enteropathy, the molecular mechanism of these effects is poorly understood. Intestinal hyp
PMID 24789205

Japanese Journal

Mechanism Underlying Endothelium-Dependent Relaxation by 2-Methylthio-ADP in Monkey Cerebral Artery

Geddawy Ayman,Shimosato Takashi,Tawa Masashi,Imamura Takeshi,Okamura Tomio
Journal of Pharmacological Sciences advpub(0), 1009090448, 2010
… 10 μM) induced concentration-dependent relaxation that was abolished by removal of endothelium but was not influenced by either carboxy PTIO or 18α-glycyrrhetinic acid. … Relaxation induced by 2MeSADP was inhibited by arachidonyl trifluoromethyl ketone, ketoconazole, and 14,15-epoxyeicosa-5(Z)-enoic acid. … Furthermore, phospholipase A2, cytochrome P450–derived epoxyeicosatrienoic acids and Ca2+-activated K+ channels appear to be involved in the relaxation. …
NAID 130000336310