Synthesis from arachidonic acid of potential prostaglandin precursors

Baldwin, Jack E.; Davies, D. I.; Hughes, L. J.; Gutteridge, N. J. A.

doi:10.1039/p19790000115

Cited by 28 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…12(S) -and 15(5)-hydroxyarachidonoylethanolamide [12(S) -and 15(5) -HAEA] were synthesized from the imidazoles of the corresponding hydroxyeicosatetraenoic acids. 12(5) -Hydroxyeicosatetraenoic acid [12(S)-HETE; Biomole, Plymouth Meeting, PA, U.S.A.] and 15(5) -HETE (synthesized by the method of Baldwin et al, 1979) were dissolved in dry methylene chloride and cooled to 0°C and 1.2 equivalents of carbonyldiimidazole was added to the solution. The mixture was stirred for 60 mm, then cooled to -20°C.A solution of ethanolamine (5 equivalents) in methylene chloride was added slowly.…”

Section: Methodsmentioning

confidence: 99%

Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Hillard

Edgemond

Jarrahian

et al. 1997

Journal of Neurochemistry

317

266

View full text Add to dashboard Cite

Neurochem. 69, 631 -638 (1997).N-Arachidonoylethanolamine (AEA; also called anandamide) has been isolated from brain and shown to bind and activate the brain cannabinoid receptor (Devane et al., 1992). Exogenously administered AEA mimics many of the effects of z9-tetrahydrocannabinol (z9-THC), including the production of hypothermia, decreased spontaneous activity and analgesia in rodents (Fride and Mechoulam, 1993), inhibition of adenylyl cyclase (Vogel et al., 1993), and decreased opening of voltage-operated calcium channels (Mache et al., 1993). Recent studies have demonstrated that AEA is released from neurons in primary culture in response to increased intracellular calcium (DiMarzo et al., 1994), which supports the hypothesis that AEA functions in the brain as a signaling molecule.AEA is rapidly catabolized by brain membranes to arachidonic acid and ethanolamine through the action of an amidohydrolase that is selective for fatty acyl amides (Deutsch and Chin, 1993;Desarnaud et al., 1995;Hillard et al., 1995a;Cravatt et al., 1996). Although AEA amidohydrolase activity is high in crude membrane preparations from brain, it is quite low in tissue preparations that are enriched in plasma membranes (Hillard et al., 1995a). These results suggest that AEA released into the extracellular space is not inactivated by hydrolysis to arachidonic acid. The present experiments explore an alternative mechanism for AEA inactivation, specifically, cellular reuptake of AEA. DiMarzo and coworkers (1994) have reported that cortical neurons in primary culture accumulate AEA in a saturable manner. These investigators further reported that AEA accumulationwas rapid, was temperature sensitive, and was not inhibited by either arachidonic acid or N-palmitoylethanolamine. With the studies reported here, we describe and characterize a similar transport process for AEA in cerebellar granule cells. AEA transport is saturable, temperature dependent, specific, and inhibited by phloretin. The uptake process has the characteristics of facilitated diffusion, that is, it is reversible and not dependent on cellular ATP. These results suggest, first, that AEA distribution between intracellular and extracellular compartments in cerebellar granule cells is dependent on facilitated diffusion and, second, that AEA permeability across

show abstract

Section: Methodsmentioning

confidence: 99%

Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Hillard

Edgemond

Jarrahian

et al. 1997

Journal of Neurochemistry

317

266

View full text Add to dashboard Cite

show abstract

“…Synthesis of monohydroxy fatty acids 15-HETE and 13-HODD were prepared by incubating arachidonic acid and linoleic acid, respectively, with soybean lipoxidase according to one of the methods of Baldwin et al (1979). Briefly, fatty acid (100 mg) and enzyme (15 mg) were incubated at room temperature in 0.05 M sodium borate buffer, pH 9.0, containing a minimal quantity of aqueous ammonia (sp.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of ionophore‐stimulated leukotriene B₄ production in human leucocytes by monohydroxy fatty acids

Camp

Fincham

1985

British J Pharmacology

View full text Add to dashboard Cite

1 Leukotriene B4 (LTB4) release by calcium ionophore-stimulated human leucocytes was measured by use of selective solvent partition of reaction mixtures and an agarose microdroplet chemokinesis assay, and the inhibitory effects of four monohydroxy fatty acids were determined. 2 1 5-Hydroxy-eicosatetraenoic acid (I 5-HETE) was the most effective inhibitor of LTB4 production with an approximate ICm value of 6pLM and 99% inhibition at 501 M, whereas 13-hydroxyoctadecadienoic acid (I 3-HODD) and 12-HETE were weaker inhibitors with approximate IC50 values of 32 fiM and 23 tM, and 59% and 68% inhibition at 50 pM, respectively. 3 We suggest that 1 3-HODD and 1 2-HETE, which are present in large amounts in the lesions of the skin disease psoriasis, may act as endogenous modulators of 5-lipoxygenase activity in skin.

show abstract

“…Authentic LTB, was a generous gift from Dr J. Rokach , Merck-Frosst, Quebec, Canada. 1 5-hydroxy-5,8,11,13-eicosatetraenoic acid ( 15-HETE) was synthesized by incubation of arachidonic acid with soybean lipoxygenase according to a modification of a method previously described (2). After extraction of lipids, 15-HETE was purified by RP-HPLC and the identity and purity of 15-HETE were confirmed by direct mass spectrometry (1 1).…”

Section: Reagentsmentioning

confidence: 99%

Proliferation of adherent synovial fluid cell cultures is modified by eicosanoids

Andreasen

Hansen

Fogh

et al. 1990

APMIS

View full text Add to dashboard Cite

T. Proliferation of adherent synovial fluid cell cultures is modified by eicosanoids. APMIS 98: 605-608, 1990.Synovial fluid cells obtained from a carragheenan-induced chronic arthritis in the juvenile dog knee were allowed to adhere and proliferate in culture flasks. After twelve days secondary cultures were made and either 10-'M leukotriene B, (LTB,), 25 pM 15-hydroxy-eicosatetraenoic acid (1 SHETE), or both, were added and the cells were cultured for another 6 days. LTB, is generated via the 5-lipoxygenase pathway of arachidonic acid metabolism and stimulates a number of phagocyte functions. Compared to control cells LTB, increased proliferation in 9 out of 10 cell cultures (p < 0.05). The 15-lipoxygenase product, 15-HETE, is not proinflammatory and is an endogenous inhibitor of 5-lipoxygenase. Addition of 15-HETE decreased proliferation of cell cultures by 23% (p < 0.01). It is speculated that LTB, in addition to its effect on phagocytes may play a role in synovial hyperproliferation observed in arthritis.

show abstract

Synthesis from arachidonic acid of potential prostaglandin precursors

Cited by 28 publications

References 0 publications

Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Inhibition of ionophore‐stimulated leukotriene B₄ production in human leucocytes by monohydroxy fatty acids

Proliferation of adherent synovial fluid cell cultures is modified by eicosanoids

Contact Info

Product

Resources

About

Synthesis from arachidonic acid of potential prostaglandin precursors

Cited by 28 publications

References 0 publications

Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Accumulation of N‐Arachidonoylethanolamine (Anandamide) into Cerebellar Granule Cells Occurs via Facilitated Diffusion

Inhibition of ionophore‐stimulated leukotriene B4 production in human leucocytes by monohydroxy fatty acids

Proliferation of adherent synovial fluid cell cultures is modified by eicosanoids

Contact Info

Product

Resources

About

Inhibition of ionophore‐stimulated leukotriene B₄ production in human leucocytes by monohydroxy fatty acids