Eicosanoids最新文献

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Prolactin secretion in anterior pituitary cells: effect of eicosanoids. 垂体前叶细胞催乳素分泌:类二十烷酸的作用。
Eicosanoids Pub Date : 1992-01-01
J R Cashman, K W Snowdowne
{"title":"Prolactin secretion in anterior pituitary cells: effect of eicosanoids.","authors":"J R Cashman,&nbsp;K W Snowdowne","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Ovariectomized Fischer 344 rats were implanted with silastic capsules containing estradiol for approximately 4 weeks to increase the number of lactotrophs in the anterior pituitary gland. Anterior pituitary cells were enzymatically dispersed and cultured for 1 day and challenged with eicosanoids or other prolactin (PRL) secretagogues. The isolated pituitary cells from estradiol-pretreated animals exhibited an increase in the ability to secrete PRL in the presence of maximally effective concentrations of thyrotropin releasing hormone (TRH), arachidonic acid or 5,6-epoxyeicosatrienoic acid (5,6-EET). Anterior pituitary cells from estradiol-pretreated animals also showed an increased activity of cytochrome P-450. The possible involvement of cytochrome P-450 in PRL secretion from anterior pituitary animal cells isolated from animals pretreated with estradiol was shown by the fact that these anterior pituitary cells increased the synthesis of 5,6-EET, a potent PRL releasing agent. TRH and 5,6-EET increased the mobilization of both cyclic AMP and cytoplasmic calcium to about the same extent. The data suggest that cytochrome P-450 is important in the release of PRL from anterior pituitary cells isolated from estradiol-pretreated Fischer 344 rats and that a product of cytochrome P-450-catalyzed epoxidation of arachidonic acid, 5,6-EET, plays a significant role in the release of PRL.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 3-4","pages":"153-61"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12511498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Comparison of bioanalytical determinations of Iloprost, a chemically stable PGI2 mimetic, by conventional radioimmunoassay (RIA) and scintillation proximity assay (SPA). 传统放射免疫法(RIA)和闪烁接近法(SPA)测定化学稳定的PGI2模拟物伊洛前列素的比较。
Eicosanoids Pub Date : 1992-01-01
M Hildebrand, T Louton, A Schütt
{"title":"Comparison of bioanalytical determinations of Iloprost, a chemically stable PGI2 mimetic, by conventional radioimmunoassay (RIA) and scintillation proximity assay (SPA).","authors":"M Hildebrand,&nbsp;T Louton,&nbsp;A Schütt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The scintillation proximity assay is a novel variant of classical radioimmunoassay. It can be performed as a single tube measurement because the separation of bound and unbound tracer fraction is avoided. In principle, microbeads are coated with anti-species antibodies that can couple with the respective antiserum used for RIA. By means of special cores, light emission takes place if labelled, antiserum-bound tracer is coupled to the anti-species antibody on the fluomicrosphere surface. In the present report, the novel assay was compared to a validated RIA for the bioanalysis of the PGI2 mimetic, Iloprost. Extraction recovery of Iloprost was approximately 90% at pH less than or equal to 4. The detection limit of the novel assay was 2-4 pg/sample, corresponding to 10-20 pg/ml plasma (if 0.2 ml plasma was used). Coefficients of variations were 9, 7 and 6% (within-day, n = 5) and 30, 11 and 10% (day-to-day, n = 10) at 50, 100 and 200 pg/ml. RIA and SPA levels of Iloprost measured in human plasma samples (n = 428) were similar. The SPA method exhibits both a similar specificity and detection limit to RIA and will be used for further analyses.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 1","pages":"5-8"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12557422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Prostaglandin photoaffinity probes: synthesis and binding affinity of aryl azide-substituted C-1 esters of prostaglandin F2 alpha. 前列腺素光亲和探针:前列腺素F2 α的芳基叠氮取代C-1酯的合成和结合亲和性。
Eicosanoids Pub Date : 1992-01-01
M Golinski, M Heine, D J Orlicky, T A Fitz, D S Watt
{"title":"Prostaglandin photoaffinity probes: synthesis and binding affinity of aryl azide-substituted C-1 esters of prostaglandin F2 alpha.","authors":"M Golinski,&nbsp;M Heine,&nbsp;D J Orlicky,&nbsp;T A Fitz,&nbsp;D S Watt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In seeking prostaglandin F2 alpha (PGF2 alpha) photoaffinity probes possessing both an efficient, photoactive cross-linking substituent and a radiolabel of high specific activity, the synthesis and binding affinity of PGF2 alpha C-1 esters in which the alcohol component possessed either an aryl azide or a perfluorinated aryl azide was investigated. These derivatives showed great promise due to their ability to compete for the binding of [3H]-PGF2 alpha in both a luteal membrane binding assay and in a whole luteal cell binding assay. Identification of the C-1 site in PGF2 alpha as a site for modification of the PGF2 alpha molecule with photoactive alcohol derivatives represented a logical step toward the goal of developing a useful PGF2 alpha photoaffinity probe.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 2","pages":"99-107"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12619688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Annexins and phospholipase A2 inhibition. 膜联蛋白和磷脂酶A2抑制。
Eicosanoids Pub Date : 1992-01-01
W J Buhl
{"title":"Annexins and phospholipase A2 inhibition.","authors":"W J Buhl","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Annexins of human placenta have been purified and characterized. In addition to annexins I to VI and II complex, two novel species of 45 and 68 kDa were obtained. Annexins V and II are most abundant. Phospholipase A2 inhibitory activity of annexin V is low in contrast to that of annexins I to VI, and it is best for annexin II complex. In vitro, annexins bind to liposomes to extents which depend on the type of phospholipid used. This induces liposome aggregation whereby Mix, PI, and PC liposomes preferably aggregate. This hinders PLA2 from its access to the substate. Our data suggest that substrate-depletion by annexins is rather the result of liposome cross-bridging than pure liposome surface coating.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 Suppl ","pages":"S26-8"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12619690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Diet-induced atherosclerosis in rabbits alters vascular prostacyclin release. 饮食诱导的动脉粥样硬化改变血管前列环素释放。
Eicosanoids Pub Date : 1992-01-01
J Brunkwall, E Mattsson, D Bergqvist
{"title":"Diet-induced atherosclerosis in rabbits alters vascular prostacyclin release.","authors":"J Brunkwall,&nbsp;E Mattsson,&nbsp;D Bergqvist","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Atherosclerosis is complicated by thrombosis and it has been suggested that a decreased prostacyclin and/or an increased thromboxane release from the vascular wall could play a part in this process. There are few reports dealing with determinations of prostanoid release from physiologically perfused normal and atherosclerotic vessel walls or from perfused atherosclerotic hearts. Therefore, fourteen rabbits were given 2% cholesterol added to the diet for 26 weeks, which led to atherosclerosis, verified by scanning electron microscopy. Five animals died, and in the surviving nine, as well as from ten healthy rabbits, the aorta was excised. The vessels were perfused with pulsatile flow at physiologic pressure five times for fifteen minutes with the addition of arachidonic acid to the last perfusate. Prostacyclin and thromboxane were determined as their stable degradation products 6-keto-PGF1 alpha and TxB2 by radio-immuno assay. Atherosclerotic and normal animals had the same initial release of prostacyclin but in the atherosclerotic animals the release did not decline with time as it did in the normal animals. The response to arachidonic acid was also higher in the atherosclerotic group. The release of thromboxane was not altered in the atherosclerotic group compared to the control group. It is concluded that prostacyclin release from aortas is altered in rabbits with diet-induced atherosclerosis compared to normal rabbit aortas, but that vascular thromboxane production is not.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 3-4","pages":"197-202"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12467468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of prostanoids in pediatric diseases employing mass spectrometric techniques. 利用质谱技术研究前列腺素在儿科疾病中的作用。
Eicosanoids Pub Date : 1992-01-01
H W Seyberth, H Schweer, B Tönshoff, A Leonhardt
{"title":"The role of prostanoids in pediatric diseases employing mass spectrometric techniques.","authors":"H W Seyberth,&nbsp;H Schweer,&nbsp;B Tönshoff,&nbsp;A Leonhardt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well renal as systemic prostanoid activity under clinical conditions. Children with renal diseases with systemic involvement, such as Bartter syndrome, renal diabetes insipidus, postobstructive hydronephrosis, and acute renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated. In contrast, systemic vascular diseases without renal involvement, such as Henoch-Schönlein purpura and persistent pulmonary hypertension in the newborn, are associated only with increased systemic prostanoid activity indicated by elevated excretion rates of prostanoid metabolites, whereas excretion rates of primary metabolites are in the normal range.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 Suppl ","pages":"S4-6"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12619695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of leukotriene D4 in septic shock models. 白三烯D4在感染性休克模型中的作用。
Eicosanoids Pub Date : 1992-01-01
T Hartung, G Tiegs, A Wendel
{"title":"The role of leukotriene D4 in septic shock models.","authors":"T Hartung,&nbsp;G Tiegs,&nbsp;A Wendel","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Septic shock is a major complication during the treatment of intense care patients. A similar pathologic state can be experimentally induced in rodents by application of endotoxins. There is circumstantial as well as direct evidence for a participation of leukotriene D4 in this experimental multiorgan failure. Due to liver-specific sensitivation by galactosamine endotoxin-induced multiorgan failure can be experimentally transposed to a single organ, i.e. hepatic failure. Data presented here show a participation of the eicosanoid leukotriene D4 in either model of sepsis. We have recently described a cellular system modelling endotoxin-induced hepatic failure. In this system based on the coculture of hepatocytes and nonparenchymal liver cells leukotriene D4 is required for the development of cytotoxicity. It is concluded that the three models share pivotal mechanistic principles and might be used complementary to each other in order to study underlying molecular events.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 Suppl ","pages":"S42-4"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12619696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The role of eicosanoids in reproduction. 类二十烷酸在生殖中的作用。
Eicosanoids Pub Date : 1992-01-01 DOI: 10.1002/9783527613625.CH8
H. P. Zahradnik, W. Schäfer, J. Neulen, B. Wetzka, T. Gaillard, J. Tielsch, F. Casper
{"title":"The role of eicosanoids in reproduction.","authors":"H. P. Zahradnik, W. Schäfer, J. Neulen, B. Wetzka, T. Gaillard, J. Tielsch, F. Casper","doi":"10.1002/9783527613625.CH8","DOIUrl":"https://doi.org/10.1002/9783527613625.CH8","url":null,"abstract":"The central role of eicosanoids in reproduction was studied in areas of important clinical interest. First, their involvement in pregnancy-induced hypertension was investigated. Urine of normotensive and hypertensive pregnant women was analysed for 6-keto-PGF1 alpha, TXB2 and PGE2 by HPLC/RIA. PGE2 and 6-keto-PGF1 alpha excretion was markedly reduced in the preeclamptic subgroup of hypertensive patients during the last two trimesters. A reduced urinary excretion of 6-keto-PGF1 alpha, TXB2 and PGE2 was also found in a hypertension animal model (rat). Further, tissue cultures of human placentas, deciduas and fetal membranes from hypertensive pregnancies displayed a reduced prostaglandin production. Secondly, in the same in-vitro model the central role of PGE2 of fetal membrane origin for the beginning or parturition was shown. Thirdly, concerning endometrial function, the enhancement of PGF2 alpha and PGE2 formation in secretory endometrial cells by estradiol-17 beta and progesterone was documented. Fourthly, lipoxygenase product content in peritoneal fluid of endometriotic patients did not differ from controls.","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"26 1","pages":"S56-9"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77968272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 8
LDL receptor-dependent polyunsaturated fatty acid transport and metabolism. LDL受体依赖性多不饱和脂肪酸的转运和代谢。
Eicosanoids Pub Date : 1992-01-01 DOI: 10.1007/978-3-642-84949-7_11
A. Habenicht, P. Salbach, U. Janssen‐Timmen
{"title":"LDL receptor-dependent polyunsaturated fatty acid transport and metabolism.","authors":"A. Habenicht, P. Salbach, U. Janssen‐Timmen","doi":"10.1007/978-3-642-84949-7_11","DOIUrl":"https://doi.org/10.1007/978-3-642-84949-7_11","url":null,"abstract":"","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"38 1","pages":"S29-31"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81543087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 10
PGD2 and its mimetic ZK 110.841 are potent inhibitors of receptor-mediated activation of human neutrophils. PGD2及其类似物ZK 110.841是受体介导的人中性粒细胞活化的有效抑制剂。
Eicosanoids Pub Date : 1991-01-01
P Ney, K Schrör
{"title":"PGD2 and its mimetic ZK 110.841 are potent inhibitors of receptor-mediated activation of human neutrophils.","authors":"P Ney,&nbsp;K Schrör","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The action of PGD2 and its mimetic ZK 110.841 ((5Z,13E)-(9R,11R,15S)-9-chloro-15-cyclohexyl-11,15- dihydroxy-16,17,18,19, 20-pentanor-5,13-prostadienoic acid) was compared to PGE1 in vitro on superoxide anion generation, degranulation, leukotriene (LT) B4 release and Ca++ fluxes in human polymorphonuclear leukocytes (PMN). All compounds were potent inhibitors of formyl-methionyl-leucyl-phenylalanine (FMLP)- and platelet-activating factor (PAF)-induced superoxide anion generation, beta-glucuronidase release and Ca++ influx. The PAF-induced release of LTB4 in the presence of 10 mumoles/l arachidonic acid was significantly attenuated by these prostaglandins. This inhibition of PMN function was paralleled by an increase in cellular cAMP levels. The molar potency of the prostaglandins used was comparable, although the D-type compounds appeared slightly more potent in some PMN function tests. None of the substances affected PMN activation induced by the calcium inophore calcimycin (A23187). The data demonstrate an effective inhibition of receptor-mediated (FMLP, PAF) PMN activation by PGD2 and its mimetic ZK 110.841, suggesting either an inhibitory PGD2 receptor on human PMN or action of PGD2 at the PGE receptor. PGD2 is a labile compound in vivo and is rapidly metabolized into a number of products with different biological properties. Since ZK 110.841 lacks this instability, this compound may serve as an important tool to classify PGD2-mediated reactions.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"4 1","pages":"21-8"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12813653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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