And some more on Mead acid:
Suppression of allergies patent - http://tinyurl.com/2lxb9x
Biochim Biophys Acta. 2005 Dec 30;1738(1-3):19-28. Epub 2005
Effects of arachidonic acid analogs on FcepsilonRI-mediated activation of mast cells.
Nakano N, Nakao A, Uchida T, Shirasaka N, Yoshizumi H, Okumura K, Tsuboi R, Ogawa H.
Atopy (Allergy) Research Center, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Polyunsaturated fatty acids (PUFAs) such as arachidonic acid (AA) have been shown to modulate a number of inflammatory disorders. Mast cells play a critical role in the initiation and maintenance of inflammatory responses. However, the effects of PUFAs on mast cell functions have not been fully addressed. We here-in examined the effects of PUFAs on the high affinity IgE receptor (FcepsilonRI)-mediated mast cell activation using RBL-2H3 cells, a rat mast cell line, that were cultured in the medium containing palmitic acid (PA), AA, or the AA analogs mead acid (MA) and eicosapentaenoic acid (EPA). In AA-supplemented cells, the FcepsilonRI-mediated beta-hexosamidase and TNF-alpha release, calcium (Ca(2+)) influx, and some protein tyrosine phosphorylations including Syk and linker for activation of T cells (LAT) were enhanced, whereas, in MA- or PA-supplemented cells, they were not changed when compared with cells cultured in control medium. In EPA-supplemented cells, the enhancements of beta-hexosamidase release and protein tyrosine phosphorylations were observed. Furthermore, in AA- or EPA-supplemented cells, FcepsilonRI-mediated intracellular production of reactive oxygen species (ROS) that is required for the tyrosine phosphorylation of LAT and Ca(2+) influx were enhanced when compared with the other cells. Thus, preincubation of AA or EPA augmented FcepsilonRI-mediated degranulation in mast cells by affecting early events of FcepsilonRI signal transduction, which might be associated with the change of fatty acid composition of the cell membrane and enhanced production of ROS. The results suggest that some PUFAs can modulate FcepsilonRI-mediated mast cell activation and might affect FcepsilonRI/mast cell-mediated inflammation, such as allergic reaction.
PMID: 16403671
Biochim Biophys Acta. 1995 Oct 26;1259(1):82-8.
Studies on the metabolism of [1-14C]5.8.11-eicosatrienoic (Mead) acid in rat hepatocytes.
Retterstøl K, Woldseth B, Christophersen BO.
Institute of Clinical Biochemistry, University of Oslo, Rikshospitalet, Norway.
The oxidation, esterification and formation of chain elongated and desaturated products of [1-14C]5,8,11-eicosatrienoic (Mead) acid was studied. Liver cells from essentially fatty acid deficient (EFAD) and control rats were used. The metabolism of [1-14C]20:4, n-6 and [1-14C]20:5, n-3 were studied under the same experimental conditions. More 20:3, n-9 than 20:4, n-6 and 20:5, n-3 was oxidised both in EFAD and control cells. 20:3, n-9 was elongated to [14C]22:3, n-9 in both cell types and significant amounts of [14C]22:4, n-9 were formed in EFAD cells. Less 20:3, n-9 was esterified in phospholipids and more in triacylglycerol than observed with 20:4, n-6 and 20:5, n-3 in both cell types. 20:3, n-9 was mainly esterified in phosphatidylcholine and little was esterified in phosphatidylethanolamine compared to 20:4, n-6 and 20:5, n-3. In comparison, 20:3, n-9 was rather efficiently esterified in phosphatidylinositol as 18:0-20:3. [14C]22:4, n-9 formed from 20:3, n-9 in EFAD hepatocytes was esterified in triacylglycerol, not in phospholipids, unlike [14C]22:5, n-6 and [14C]22:6, n-3 which were mainly esterified in phospholipids.
PMID: 7492619
Here we are getting a PGE2-like activity from Mead acid!
FEBS Lett. 1985 Feb 11;181(1):53-6.
Prostaglandin E2-like activity of 20:3n-9 platelet lipoxygenase end-product.
Lagarde M, Burtin M, Rigaud M, Sprecher H, Dechavanne M, Renaud S.
5,8,11-Icosatrienoic acid (20:3n-9), a fatty acid associated with platelet hyperactivity, was oxygenated by platelet lipoxygenase. The end-product of this pathway was purified by high-performance liquid chromatography (HPLC) and characterized as 12-hydroxy-5,8,10-icosatrienoic acid [12-OH-20:3(5,8,10)] by capillary gas-liquid mass spectrometry. When tested upon platelet aggregation, 12-OH-20:3(5,8,10) exhibited a biphasic effect. At low concentrations (below 5 X 10(-7) M) it potentiated aggregation but inhibited it at higher levels, a pattern similar to that obtained with prostaglandin E2. However, since the amounts of 12-OH-20:3(5,8,10) generated under thrombin stimulation are in the range of concentrations with potentiating effects, it seems that the 12-OH derivative is responsible for the hyperaggrebility of 20:3n-9-rich platelets.
PMID: 3918886
Toxicol Appl Pharmacol. 1993 May;120(1):72-9.
Essential fatty acid deficiency in cultured human keratinocytes attenuates toxicity due to lipid peroxidation.
Wey HE, Pyron L, Woolery M.
Centers for Disease Control, National Institute for Occupational Safety and Health, Division of Biomedical and Behavioral Science, Cellular Toxicology Section, Cincinnati, Ohio 45226.
Human keratinocytes are commonly grown in culture with a serum-free medium. Under these conditions, keratinocytes become essential fatty acid deficient (EFAD), as determined by gas chromatographic analysis of cell phospholipid fatty acid composition. Exposure of EFAD keratinocytes for 2 hr to concentrations of t-butyl hydroperoxide (tBHP) up to 2 mM did not result in toxicity assessed by lactate dehydrogenase (LDH) release and only a small indication of lipid peroxidation assessed by the release of thiobarbituric acid-reactive substances (TBARS). Addition of 10 microM linoleic acid (LA) to serum-free medium alleviated the EFAD condition by increasing the phospholipid content of LA and its elongation and desaturation products, arachidonic acid and docosatetraenoic acid. Exposure of LA-supplemented keratinocytes to tBHP resulted in significant LDH (at 1 and 2 mM tBHP) and TBARS (tBHP concentration dependent) release. TBARS release was also significantly elevated in unexposed LA-supplemented keratinocytes (basal release). Co-supplementation with the antioxidant, alpha-tocopherol succinate (TS) prevented tBHP (1 mM)-induced LDH release in LA-supplemented cultures. TS supplementation also attenuated the effect of tBHP on TBARS release, but when compared to TS-supplemented EFAD cultures, LA supplementation still led to increased tBHP-induced TBARS release. Keratinocyte cultures are potentially useful as an alternative to animals in toxicology research and testing. It is important, however, that the cell model provide a response to toxic insult similar to that experienced in vivo. Our results suggest that fatty acid and antioxidant nutrition of cultured keratinocytes are important parameters in mediating the toxic effects of lipid peroxidation.
PMID: 8511784
Most of the Mead acid biochemistry studies have been done by the Sprecher group and can be searched in Medline by:
"Sprecher H"[Author] Mead |
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