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At least 1,099 records · Page 61Linked to original sources
PubMed1993

Kinetic mechanism of ketoreductase activity of prostaglandin F synthase from bovine lung.

The kinetic mechanism of ketoreductase activity of bovine lung prostaglandin F synthase, expressed in E. coli, was investigated. Data on initial velocity and radioisotope exchange between [3H]prostaglandin D2 and 9 alpha,11 beta-prostaglandin F2 suggest that the enzyme obeys the ping-pong mechanism. Using a fluorescence technique we obtained a binding constant of 3 microM for NADPH. This is in close correlation with the kinetically determined intrinsic Michaelis constant for NADPH. Activation energy of the redox process was determined from the temperature dependence of maximal velocities for nitrobenzaldehyde and menadione and was found to be 119 and 96 kJ/mol, respectively.

Acetophenones↗
PubMed1994

Elongation factor-2 kinase: effective inhibition by the novel protein kinase inhibitor rottlerin and relative insensitivity towards staurosporine.

The elongation factor-2 (eEF-2) is selectively phosphorylated by the eEF-2 kinase (calmodulin-dependent kinase III). This phosphorylation can be inhibited by calmodulin antagonists, such as CGS 9343B (IC50 = 4 microM). The novel protein kinase inhibitor rottlerin is shown to suppress eEF-2 phosphorylation with an IC50 of 5.3 microM. By contrast, the eEF-2 kinase is rather resistant towards the potent but non-selective protein kinase inhibitor staurosporine (IC50 > 50 microM) and thus can be differentiated from most other protein kinases that are suppressed by staurosporine in the nM range.

Acetophenones↗
PubMed1994

Phospholipase A2 enhances [3H]AMPA binding to a putative homomeric GluR-B receptor in the rat spinal cord.

[3H]AMPA and [3H]kainate binding to rat spinal cord was localised most densely in the substantia gelatinosa of the dorsal horn. Phospholipase A2 elicited a dose-dependent increase in specific [3H]AMPA binding but not in [3H]kainate binding. The enhancement of [3H]AMPA binding was blocked by bromophenacyl bromide and at 0 degree C and was not mimicked by arachidonic acid. Since GluR-B is the only AMPA receptor subunit detectable in the rat spinal cord, and recombinant homomeric GluR-B assemblies do not bind [3H]kainate, these results suggest phospholipase A2 may modulate [3H]AMPA binding to putative homomeric GluR-B receptors.

Acetophenones↗
PubMed1996

Regulation of intracellular pH by phospholipase A2 and protein kinase C upon neutrophil adhesion to solid substrata.

Adhesion to solid substrata has been shown to increase intracellular pH (pH(i)) of fibroblasts and of other cells (FEBS Lett. (1988) 234, 449-450; Proc. Natl. Acad. Sci. USA (1989) 86, 4525-4529; J. Biol. Chem. (1990) 265, 1327-1332; Exp. Cell Res. (1992) 200, 211-214; FEBS Lett. (1995) 374, 17-20). We have found that the inhibitors of PLA2, 4-bromophenacyl bromide and manoalide, completely blocked the increase of pH(i) and spreading of neutrophils upon adhesion to solid substrata. Inhibition of phospholipase C with neomycin or removal of extracellular Ca2+ affects neither neutrophil spreading nor their pH(i). Inhibition of PKC with H-7 or staurosporin increased pH(i). PMA, an activator of PKC, dramatically decreased pH(i) but did not impair the spreading of neutrophils. The effect of arachidonic acid, a product of PLA2 activity, on neutrophil pH(i) and spreading was similar to that of PMA. H-7, an inhibitor of PKC, partially blocked the effect of arachidonic acid (AA) on pH(i). BW755C, an inhibitor of AA metabolism by cyclooxygenase or lipoxygenase, affected neither the pH(i) nor cell spreading. We propose that the increase of pH(i) upon neutrophil adhesion is mediated by PLA2 activity, while PKC decreased pH(i). AA produced by PLA2 activates PKC, thus forming a feedback regulation of pH(i).

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Phospholipase D is involved in cytosolic phospholipase A2-dependent selective release of arachidonic acid by fMLP-stimulated rat neutrophils.

When rat polymorphonuclear neutrophils (PMN) were treated with N-formyl-Met-Leu-Phe (fMLP), the release of arachidonic acid in preference to other fatty acids was observed. Levels of arachidonic acid reached a plateau within 5 min, and were accompanied by an approximately 4-fold increase in in vitro phospholipase (PL) A2 and PLD activities in PMN lysates. Treatment of PMN with ethanol (an inhibitor of PLD-mediated phosphatidic acid formation), propranolol (a phosphatidic acid phosphatase inhibitor), or 4-bromophenacylbromide (a PLA2 inhibitor), each suppressed fMLP-stimulated arachidonate release. Treatment with RHC-80267 (a diacylglycerol lipase inhibitor), however, had no such effect. The cytosolic PLA2 (cPLA2) inhibitor, arachidonoyl trifluoromethyl ketone, suppressed PLA2 activity in PMN homogenates and arachidonate release by fMLP-treated PMN. These results suggest that fMLP-elicited arachidonate release is mediated by cPLA2 but not diacylglycerol lipase, and that the activation of cPLA2 is downstream of the PLD-dependent signaling pathway.

Acetophenones↗
PubMed1989

Isolation and characterization of the major phospholipase A2 from the venom of Trimeresurus purpureomaculatus (shore pit viper).

1. The major phospholipase A2 (PLA-DE4) of the venom of Trimeresurus purpureomaculatus (shore pit viper) has been purified to electrophoretic homogeneity. 2. The isoelectric point of the purified enzyme was determined to be 4.20, and the mol. wt was 31,700 as estimated by Sephadex G-75 gel filtration chromatography; and 14,000 as estimated by SDS-polyacrylamide gel electrophoresis. The purified enzyme hydrolyzed phosphatidylcholine (PC) faster than phosphatidylethanolamine (PE), whereas phosphatidylserine (PS) was not hydrolyzed at all (PC greater than PE greater than PS =0). However, in reaction system consisted of mixtures of PC and PS, phosphatidylserine was effectively hydrolyzed by the enzyme. 4. The phospholipase A2 exhibited edema-forming activity but not hemolytic, hemorrhagic or anticoagulant activities. It was not lethal to mice at a dosage of 10 micrograms/g by i.v. route.

Acetophenones↗
PubMed1990

Purification and characterization of two acidic phospholipase A2 enzymes from king cobra (Ophiophagus hannah) snake venom.

1. The two major phospholipase A2 enzymes (OHPLA-DE1 and OHPLA-DE2) of king cobra (Ophiophagus hannah) venom have been purified to electrophoretic homogeneity. 2. The isoelectric points of OHPLA-DE1 and OHPLA-DE2 were 3.81 and 3.89, respectively and the Mws were 14,000 and 15,000, respectively, as estimated by Sephadex G-75 gel filtration chromatography; and 14,000 as estimated by SDS-PAGE. 3. The enzymes were not lethal to mice at a dosage of 10 micrograms/g body wt by i.v. route. Both phospholipase A2 enzymes, however, exhibited moderate edema-inducing and anti-coagulant activities. 4. Bromophenacylation of the enzymes reduced the enzymatic activity drastically but did not affect the edema-inducing activity of the enzymes.

Acetophenones↗
PubMed1991

Identification of aromatic moieties and mycosamine in antifungal heptaenes with high-performance liquid chromatography, high-performance liquid chromatography-mass spectrometry and gas chromatography-mass spectrometry.

A high-performance liquid chromatographic (HPLC) method for the determination of the aromaticity of heptaene polyene antibiotics has been developed. The released aromatic moiety of the heptaene polyenes aureofungin, candicidin, candimycin, hamycin and trichomycin was assayed after alkaline hydrolysis. The presence of p-aminoacetophenone (PAAP) and N-methyl-p-aminoacetophenone (N-methyl-PAAP) in the hydrolysates was determined by HPLC, HPLC-mass spectrometry (HPLC-MS) and gas chromatography-MS (GC-MS). Candicidin and hamycin contained only the PAAP residue; aureofungin contained both PAAP and N-methyl-PAAP. Trichomycin contained PAAP and also some unknown component of molecular weight 179. The aromatic nature of the individual components of the heptaene complex was demonstrated using radioactivity flow detection for the determination of the incorporation of [14C]-p-aminobenzoic acid to individual candicidin components. Ammonia chemical ionization MS was successfully used for the GC-MS identification of the acetylated mycosamine moiety of heptaenes.

4-Aminobenzoic Acid↗
PubMed1983

Solubilization and characterization of a neutral-active, calcium-dependent, phospholipase A2 from rabbit heart and isolated chick embryo myocytes.

Homogenates of rabbit heart hydrolyzed the phospholipids of autoclaved E. coli maximally at pH 7.0 with 5.0 mM added CaCl2; EDTA was a potent inhibitor. More than 70% of the homogenate phospholipase A activity was sedimented at 100 000 x g. Homogenates dialyzed to pH 3.0 had a similar pH optima, but required less than 1.0 mM added CaCl2 for optimal activity. Sulfuric acid extraction of whole heart, and other rabbit organs, solubilized a calcium-dependent phospholipase A that was maximally active at pHs 7.0 to 7.5. Myocardial extracts were as active (approx. 60 nmol/h/mg) as acid extracts from rabbit lung, liver and kidney. Phospholipase(s) A with similar properties were solubilized by acid extraction of 12-day-old chick embryo myocytes (10 nmol/h/mg). Regardless of origin, the phospholipases A were absolutely specific for release of fatty acid from the 2-acyl position of phospholipids. Activity was inhibited by (i) pretreatment with p-bromo-phenacylbromide; (ii) the anesthetics, dibucaine and chlorpromazine; and (iii) the nonsteroidal antiinflammatory agents, indomethacin, ibuprofen and meclofenamate. Aspirin and dexamethasone had little or no effect on enzymic activity.

Acetophenones↗
PubMed1987

Characterization of Agrobacterium tumefaciens virulence proteins induced by the plant factor acetosyringone.

The Ti plasmid virulence (vir) loci encode functions essential for the transfer of the T-DNA element from Agrobacterium tumefaciens to plant cells. The expression of these loci is specifically signaled by plant phenolics such as acetosyringone. Here, we characterize the protein products that are induced in Agrobacterium grown in the presence of acetosyringone. More than 10 to 15 proteins are induced in strains harboring different Ti plasmids. Two general classes of acetosyringone-induced proteins are observed, encoded either within or outside the vir region. Synthesis of both classes of proteins requires acetosyringone and the products of the vir regulatory genes A and G. Those proteins encoded outside the vir region define a novel category of proteins, the virulence-related proteins, which are both chromosomally and Ti plasmid-encoded. The molecular weight and subcellular localization of several pTiA6 vir-induced proteins are identified. The most abundant induced protein has a molecular weight of 65,000, and is the single product of the virE locus; this protein distributes into both cell envelope and soluble fractions. Three proteins with molecular weights of approximately 33,000, 80,000 and 25,000 fractionate with the cell envelope and are encoded by genes within the 5' half of the virB locus. The envelope localization of the virB proteins suggests that they play a role in directing T-DNA transfer events that occur at the bacterial surface.

Acetophenones↗
PubMed1988

Crystal structure of bovine pancreatic phospholipase A2 covalently inhibited by p-bromo-phenacyl-bromide.

Bovine pancreatic phospholipase A2 covalently inhibited by p-bromo-phenacyl-bromide was crystallized from 50% (v/v) 2-methyl-2,4-pentanediol. The space group was P3(1)21 with cell dimensions a = b = 46.73 A and c = 102.5 A (1 A = 0.1 nm). Diffraction data were collected by oscillation photography from one single crystal of dimensions 0.2 mm x 0.2 mm x 0.2 mm. The crystal structure was determined to a resolution of 2.5 A by crystallographic refinement of a starting model, which consisted of native bovine pancreatic phospholipase A2 positioned and oriented in the P3(1)21 cell as in the bovine pro-phospholipase A2. The crystallographic R-factor decreased from 0.378 to 0.197 after 70 refinement cycles. For the greater part the three-dimensional structure was very similar to that of native phospholipase. The inhibitor group shows up clearly. However, as in solution, there is no calcium ion bound any more in the active site, and this causes a significant conformational change in the loop from residue 59 to 73. This loop is remote from the calcium binding site. Interestingly, this is the same loop that also shows different conformations in other phospholipase A2 molecules. The inhibitor molecule has hydrophobic interactions with Phe5 and Cys45. Rational design of specific and potent inhibitors of phospholipase A2 catalysis is discussed on the basis of the present three-dimensional structure.

Acetophenones↗
PubMed1987

Leukotrienes as common intermediates in the cyclic AMP dependent and independent pathways in adrenal steroidogenesis.

Aldosterone secretion from adrenal glomerulosa cells can be stimulated by angiotensin II (AII), extracellular potassium and adrenocorticotropin (ACTH). Since the mitochondria can recognize factors generated by AII (cyclic-AMP-independent) and ACTH (cyclic AMP dependent), it is reasonable to postulate the existence of a common intermediate in spite of a different signal transduction mechanism. We have evaluated this hypothesis by stimulation of mitochondria from glomerulosa gland with fractions isolated from glomerulosa gland stimulated with AII or from fasciculata gland stimulated with ACTH; the same fractions were tested using mitochondria from fasciculata cells. Postmitochondrial fractions (PMTS) obtained after incubation of adrenal zona glomerulosa with or without AII (10(-7) M) or ACTH (10(-10) M), were able to increase net progesterone synthesis 5-fold in mitochondria isolated from non-stimulated rat zona glomerulosa. In addition, AII in zona glomerulosa produced in vitro steroidogenic fractions that were able to stimulate mitochondria from zona fasciculata cells. Inhibitors of arachidonic acid release and metabolism blocked corticosterone production in fasciculata cells stimulated with ACTH. This concept is supported by the experiment in which bromophenacylbromide and nordihydroguaiaretic acid also blocked the formation of an activated PMTS. In fact, non-activated PMTS, in the presence of exogenous arachidonic acid AA, behaved as an activated PMTS from ACTH stimulated cells. We suggest that the mechanisms of action of ACTH and AII involve an increase in the release of AA and an activation of the enzyme system which converts AA in leukotriene products.

Acetophenones↗
PubMed1987

Effects of leukotrienes B4, C4, and D4 on rat mesenteric microcirculation.

Arachidonic acid is metabolized to leukotriene (LT) B4, C4, D4, and E4 by lipoxygenase. LTB4 is a chemotactic agent while LTC4 and LTD4 stimulate smooth muscle fibers to contract. Mesenteric vessels have the capacity to release leukotrienes. The possibility that leukotrienes might be responsible for or contribute to mesenteric ischemia during mesenteric low flow, embolism, and thrombosis prompted us to investigate their action on mesenteric vessels. LTB4, C4, and D4 were applied topically on small bowel mesentery of 22 Sprague-Dawley rats in sequentially increasing concentrations. Mesenteric arterioles with diameters of 8-20 microns were observed through a microscope and vessel diameters were measured using a video shear monitor. LTB4 had no effect on diameter, but doses as low as 3 X 10(-8) M induced white blood cell adherence to venular endothelium, reflecting the potent chemotactic properties of this compound. LTC4 and D4 had no effect on systemic blood pressure or white blood cell adherence. Applications of 6.4 X 10(-9), 3.2 X 10(-8), and 6.4 X 10(-8) M LTC4 decreased mesenteric arteriolar diameter to 85.3* +/- 4.7% (mean +/- SD), 75.7* +/- 7.5%, and 66.8* +/- 6.1% of baseline, and 4 X 10(-9), 2 X 10(-8), and 4 X 10(-8) M LTD4 decreased diameter to 84.9* +/- 6.1%, 75.1* +/- 4.2%, and 64.1* +/- 5% of baseline, respectively (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetophenones↗
PubMed1990

LY171883 preserves mesenteric perfusion in porcine endotoxic shock.

Superior mesenteric arterial perfusion (Q) decreases and gut intramucosal hydrogen ion concentration, [H+], increases in resuscitated normodynamic endotoxic pigs. The present study tested the hypothesis that these adverse phenomena can be prevented by pretreatment with LY171883, a specific leukotriene (LT) D4/E4 receptor antagonist. Pentobarbital-anesthetized pigs (14-18 kg) were instrumented to permit measurement of Q (ultrasonic flow probe) and [H+] (tonometer). Mesenteric O2 delivery (DO2) and consumption (VO2) were calculated from the O2 contents of arterial and superior mesenteric venous blood. At t = -20 min, groups (N = 6) of pigs were pretreated witH LY171883 (10 mg/kg) or vehicle. At t = 0 min, the pigs were infused over 20 min with lipopolysaccharide (LPS; 150 micrograms/kg) and resuscitated for 2 hr with saline (1.2 ml/kg min). Irrespective of treatment group, mean arterial pressure and systemic vascular resistance index decreased significantly after infusion of LPS. In general, cardiac index (CI) was well preserved, although in controls at t = 20, 100, and 120 min, CI decreased significantly with respect to the t = 0 min value. Normal mesenteric Q and DO2 were maintained in the LY171883 group, whereas, in controls, these parameters decreased significantly. Mesenteric VO2 increased transiently but significantly in controls; this phenomenon was abrograted by the LT receptor antagonist. In controls, intramucosal [H+] increased by almost threefold; this adverse effect was significantly ameliorated by LY171883. These data suggest that decreased mesenteric Q and increased intramucosal [H+] may be mediated by LT in this porcine endotoxic shock model.

Acetophenones↗
PubMed1991

Leukotriene C4 induces mesenteric hypoperfusion and intestinal intramural acidosis in pigs.

We examined the effect of intravenous infusion of graded doses of authentic leukotriene (LT) C4 on several physiological variables in pentobarbital-anesthetized immature swine. Mesenteric blood flow (Qsma) was measured using an ultrasonic flow probe and ileal intramucosal hydrogen ion concentration ([H+]I) was estimated tonometrically. Three groups were studied. Pigs in Group I (n = 6) were infused beginning at t = 0 min with increasing doses (0.03-1.0 microgram/kg-min) of LTC4, each dose being administered for 10 min. Pigs in Group II (n = 6) were infused with LTC4 as above, but were pre- and post-treated with a specific sulfidopeptide LT receptor antagonist, LY203647 (30 mg/kg bolus and then 10 mg/kg-hr) beginning at t = -20 min. Pigs in Group III (n = 4) received only normal saline (5 ml/kg-h). Infusing LTC4 significantly decreased Qsma and mesenteric oxygen uptake and significantly increased ileal [H+]I. These changes were prevented by LY203647. These data support the idea that sulfido-peptide LT are capable of causing mesenteric ischemia and that this phenomenon can be blocked by LY203647.

Acetophenones↗