The Experts below are selected from a list of 33 Experts worldwide ranked by ideXlab platform
Boris Janistyn - One of the best experts on this subject based on the ideXlab platform.
Evidence for conversion of arachidonic Acid to hydroxyIcosatetraenoic Acids by a cell-free homogenate from maize seedlingsPhytochemistry, 1990Co-Authors: Boris JanistynAbstract:
Abstract The conversion of arachidonic Acid to the hydroxyIcosatetraenoic Acids 5-HETE, [5( S )-hydroxy-6,8,11,14,-Icosatetraenoic Acid], 12-HETE, [12( S )-hydroxy-5,8,10,14-Icosatetraenoic Acid] and 15-HETE, [15( S )-hydroxy-5,8,11,13-Icosatetraenoic Acid] by a 10 000 g cell-free supernatant of a Zea mays seedlings homogenate is described. For metabolic pathway detection [1- 14 C] arachidonic Acid was added. The hydroxyIcosatetraenoic Acids were isolated by TLC and HPLC and purified to constant specific radioactivity against authentic [ 3 H]-labelled 5-HETE, 12-HETE and 15-HETE by co-chromatography.
Sakayu Shimizu - One of the best experts on this subject based on the ideXlab platform.
Journal of Japan Oil Chemists Society, 1995Co-Authors: Sakayu ShimizuAbstract:
Mycelia of a fungus Mortierella alpina 1S-4 and the mutants derived from it are new and rich sources of C20 polyunsaturated fatty Acids (PUFAs) of pharmacologically and dietary importance. M. alpina 1S-4 producs a unique triacylglycerol with high n-6 PUFA content. The mycelial content of arachidonic Acid reaches 274 mg/g dry mycelia (4.3 g/L) on cultivation of the fungus in a medium containing glucose and yeast extract. The value accounts nearly 70 % of the total fatty Acids in the extracted oil. Mutants defective in A 5 desaturase are potent produces of dihomo-γ-linolenic Acid (4.1 g/L). A Al2 desaturase-defective-mutant produces an oil containing only n-9 PUFAs. The mycelial Mead Acid content is 141 mg/g dry mycelia (1.9 g/L). An oil rich in n-3 PUFAs can be produced by the same mutant when grown in a medium containing linseed oil. The content of total n-3 PUFAs (i.e., α-linolenic Acid+8, 11, 14, 17-cis-Icosatetraenoic Acid+5, 8, 11, 14, 17-cis-icosapentaenoic Acid) is nearly 50 % in total mycelial fatty Acid. The enzyme systems for the biosynthesis of PUFAs in the Mortierella fungi is also discussed.
Selective Production of Polyunsaturated Fatty Acids by the Fungus Mortierella alpina 1 S-4 and Its MutantsJournal of Japan Oil Chemists Society, 1993Co-Authors: Sakayu Shimizu, Hiroshi Kawashima, Saeree JareonkitmongkolAbstract:
Mycelia of a fungus Mortierella alpina 1 S-4, which was isolated from soil, and the mutants derived from it were found to be new and rich sources of C20 polyunsaturated fatty Acids (PUFAs) of pharmacological and dietary importance. M alpina 1 S-4 produced a unique triacylglycerol oil with high ω 6 PUFA content. The mycelial content of arachidonic Acid reached 274 mg/g dry mycelia (4.3 g/L) on cultivation of the fungus in a medium containing glucose and yeast extract. The value accounted nearly 70 % of the total fatty Acids in the extracted oil. The same fungus produced dihomo-γ-linolenic Acid (DGLA, 2.17 g/L) when grown with sesamin, a specific inhibitor of Δ5 desaturase. A mutant defective in 5 desaturase also produced DGLA (4.1 g/L). Another mutant which is defective in Δ12 desaturase produced anoil containing only ω 9 PUFAs. The mycelial mead Acid content reached 141 mg/g dry mycelia (1.9 g/L). An oil rich inω3 PUFAs was produced by the same mutant when grown in a medium containing linseed oil.The content of total co 3 PUFAs (i. e., a ?linolenic Acid + cis-8, cis-11, cis-14, cis-17-Icosatetraenoic Acid + cis-5, cis-8, cis-11, cis-14, cis-17-icosapentaenoic Acid) reached nearly 50 % in total mycelial fatty Acid.
Bernd W. Spur - One of the best experts on this subject based on the ideXlab platform.
Structure/activity relationship of leukotriene B4 and its structural analogues in chemotactic, lysosomal‐enzyme release and receptor‐binding assaysFEBS Journal, 1993Co-Authors: Olukayode Soyombo, Bernd W. SpurAbstract:
The biological activities of chemically synthesized leukotriene B4 and eight structural analogues have been studied using chemotaxis, lysosomal-enzyme release and receptor-binding assays on human neutrophils. The results show that increasing the number of double bonds between C14 and C20, having triple bonds at C6 or C14, substitution of the primary carboxyl group at C1, changing the geometry of the double bond at C6 from the cis to trans configuration and changing the chirality of the hydroxyl group at C12 from the R to the S configuration result in substantial loss of both biological activity and the capacity to bind to the LTB4 recognition site in parallel. We suggest that the functional epitopes of 5S, 12R-dihydroxy-6, 14-cis-8, 10-trans-Icosatetraenoic Acid (LTB4) are either the same, or reside in the same domain as the binding site for the LTB4 receptor. Development of LTB4 antagonists to the high-affinity LTB4 receptor, based on the structure of LTB4, is unlikely to be successful.
Jens-michael Schröder - One of the best experts on this subject based on the ideXlab platform.
Chemotactic 5-oxo-Icosatetraenoic Acids activate a unique pattern of neutrophil responses. Analysis of phospholipid metabolism, intracellular Ca2+ transients, actin reorganization, superoxide-anion production and receptor up-regulation.FEBS Journal, 1996Co-Authors: Johannes Norgauer, Michael Barbisch, Wolfgang Czech, Johanna Pareigis, Uwe Schwenk, Jens-michael SchröderAbstract:
Neutrophil cell responses and signal pathways elicted by the chemotactic arachidonic Acid metabolites (6E, 8Z, 11Z, 14Z)-5-oxo-Icosatetraenoic Acid and (6E, 8Z, 11Z, 13E)-5-oxo-15-hydroxy-Icosatetraenoic Acid were studied and compared with those of other chemotaxins. Polyphosphoinositol lipid analysis revealed activation of phosphatidylinositol-bisphosphate 3-kinase by both agonists. Experiments with Fura-2 in the presence of EGTA indicated Ca2+ mobilization from intracellular stores by both 5-oxo-icosanoids. A transient actin response and production of small amounts of superoxide anions upon stimulation with both agents was detected. The changes induced by 5-oxo-icosanoids were more moderate and transient than those obtained by other chemotaxins. Desensitization studies indicated cross-desensitization between both 5-oxo-icosanoids, but no interference with the response of other chemotaxins. All cell responses elicted by 5-oxo-icosanoids were inhibited by pertussis toxin suggesting involvement of G-proteins, a common activation mechanism for all known potent chemotaxins. In contrast to other chemotaxins, 5-oxo-icosanoids at concentrations 500-fold higher than the ED50 of other functions did not induce up-regulation of CD11b and N-formyl-peptide receptors at the cell surface, and failed to potentiate N-formyl-peptide-induced superoxide anion production. These results indicate that 5-oxo-icosanoids trigger a unique pattern of neutrophil responses.
Walter Fiers - One of the best experts on this subject based on the ideXlab platform.
Tumour-necrosis-factor-mediated cytotoxicity is correlated with phospholipase-A2 activity, but not with arachidonic Acid release per seFEBS Journal, 1991Co-Authors: Philip Noel Suffys, Rudi Beyaert, Dirk De Valck, Bart Vanhaesebroeck, Walter FiersAbstract:
L929, a murine fibrosarcoma cell line highly sensitive to the anti-proliferative and cytotoxic action of tumour necrosis factor (TNF), was used as a target cell in our studies. We [Suffys et al. (1987) Biochem. Biophys. Res. Commun. 149, 735–743], as well as others, have previously provided evidence that a phospholipase (PL), most probably a PL-A2-type enzyme, is likely to be involved in TNF-mediated cell killing. We now further document this conclusion and provide suggestive evidence that the enzyme activity specifically involved in TNF cytotoxicity differs from activities associated with the eventual cell death process itself or with non-toxic serum treatment. We also show that the 5,8,11,14-Icosatetraenoic Acid (arachidonic Acid, 4Ach) released by PL, and possibly metabolized, is unlikely to be a key mediator of the TNF-mediated cytotoxicity. These conclusions are based on the following experimental findings. 1 TNF treatment of cells, prelabelled for 24 h with [3H]4Ach or [14C]3Ach (3Ach ≡ 5,8,11-icosatrienoic Acid) resulted in an early, time-dependent and concentration-dependent release of radioactivity in the supernatant preceding actual cell death. The extent of this response was moderate, albeit reproducible and significant. Analysis of the total lipid fraction from cells plus supernatant revealed that only release of arachidonic Acid from phospholipids, but not its metabolization was induced by TNF. However, the release of less unsaturated fatty Acids, such as linoleic Acid (Lin) or palmitic Acid (Pam), was not affected during the first hours after TNF addition. 2 An L929 subclone, selected for resistance to TNF toxicity, was found to be defective in TNF-induced 4Ach liberation. 3 Interleukin-1 (IL1) was not cytotoxic for L929 and did not induce release of 4Ach. 4 Release of 4Ach was not restricted to TNF; the addition of serum to the cells also induced release of fatty Acids into the medium. In this case, however, there was no specificity, as all fatty Acids tested, including Lin and Pam, were released. 5 Inhibition of PL-A2 activity by appropriate drugs markedly diminished TNF-induced 4Ach release and resulted also in a strong decrease in TNF-induced cytotoxicity. 6 Other drugs, including serine protease inhibitors, which strongly inhibit TNF-induced cytotoxicity, also decreased the TNF-induced 4Ach release, whereas LiCl potentiated both TNF-mediated effects. 7 Protection of cells against TNF toxicity by means of various inhibitors was not counteracted by addition of exogenous fatty Acids, including 4Ach. 8 We could not detect an increase in the amount of free inositol or any inositol phosphate after TNF treatment of cells, prelabelled with myo-[3H]inositol. This indicates that the phosphatidylinositol-specific PL-C is not involved in the TNF-induced fatty Acid release. 9 Neither were we able to observe a decrease in fatty Acid incorporation into phospholipids during TNF treatment. This excludes a decrease in acyltransferase activity as the reason for increased levels of free fatty Acid. The above observations strongly suggest that an activated PL-A2 is involved in TNF-mediated cell killing. The limited extent of TNF-specific fatty Acid release, the relative specificity for 4Ach of this early response which is not shared by serum treatment, and the characteristic drug-resistance profile of this activity, all argue for the involvement of a particular PL-A2 species. Moreover, our data also suggest that 4Ach itself and its metabolites do not play a key role in TNF cytotoxicity.