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PubMed1992

Prostaglandin D2 increases Cl secretion across canine tracheal epithelium through cyclo-oxygenase stimulation and cAMP production.

Prostaglandin (PG) D2 is one cyclo-oxygenase product of arachidonic acid metabolites that may play a role in the pathogenesis of asthma. To determine the effect of PGD2 on ion transport by airway epithelium and its mechanism of action, we measured bioelectric properties of canine cultured tracheal epithelium under short-circuit conditions in vitro. PGD2 (10(-7) M) increased short-circuit current (Isc) from 5.5 +/- 1.2 to 14.1 +/- 2.9 microA cm-2 (means +/- SE, P less than 0.01) when added to the mucosal solution, and to 22.2 +/- 3.8 microA cm-2 (P less than 0.001) when added to the submucosal solution, an effect that was accompanied by the corresponding increases in transepithelial potential difference and conductance. These effects were dose-dependent. The PGD2-induced increase in Isc was not altered by preincubation of cells with autonomic antagonists (phentolamine, propranolol, atropine), the lipoxygenase inhibitor AA-861, the protein kinase C inhibitor H-7, or the Na channel blocker amiloride, but it was inhibited by each of indomethacin, piroxicam, the Cl channel blocker diphenylamine-2-carboxylate, the Cl transport inhibitor furosemide, and Cl-free medium. Intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels were dose-dependently increased by PGD2. These results suggest that PGD2 may selectively stimulate airway epithelial Cl secretion via cyclo-oxygenase- and cAMP-dependent pathway.

Animals↗
PubMed1992

In-vitro evaluation of 5-lipoxygenase and cyclo-oxygenase inhibitors using bovine neutrophils and platelets and HPLC.

Inhibition of 5-lipoxygenase has been determined by monitoring the formation of leukotriene B4 and 5-hydroxyeicosatetraenoic acid in bovine polymorphonuclear leucocytes. For evaluating the inhibition of cyclo-oxygenase two different test systems are presented: the first uses 12-hydroxyheptadecatrienoic acid produced by bovine platelets as an indicator of the cyclo-oxygenase activity; the second test system monitors the prostaglandin E2 formation by bovine platelets. All arachidonic acid metabolites are quantified by reverse-phase HPLC with UV-detection.

Animals↗
PubMed1995

Cyclo-oxygenase mediation of endotoxin-induced fever, anterior and posterior pituitary hormone release, and hypothalamic c-Fos expression in the prepubertal pig.

Prepubertal pigs (n = 8) treated with bacterial endotoxin (20 micrograms lipopolysaccharide; LPS) exhibited a sustained (4 h) hyperthermia, increased plasma concentrations of cortisol, prolactin, growth hormone and vasopressin, but no change in adrenaline or noradrenaline levels was observed. All these effects were prevented or attenuated when the animals were pretreated intravenously with the cyclo-oxygenase inhibitor indomethacin (IND; 2 mg/kg). Similarly, in pigs (n = 3 per treatment) given IND, LPS or IND + LPS, parallel changes in the neuronal expression of c-Fos were observed in hypothalamic regions concerned with thermoregulation, neurohypophysial secretion, and the control of pituitary-adrenocortical function. The stimulatory action of LPS in the median preoptic, supraoptic and paraventricular nuclei was prevented by IND, whereas IND given alone was without effect. These findings suggest that inducible cyclo-oxygenase pathways are responsible for the febrile and neuroendocrine effects of endotoxin in this species.

Animals↗
PubMed1984

New type of oxygenase involved in the metabolism of propane and isobutane.

Nocardia paraffinicum (Rhodococcus rhodochrous), a hydrocarbon-degrading microorganism, was used in a study of propane and isobutane metabolism. The bacterium was able to utilize propane or isobutane as a sole source of carbon, and oxygen was found to be essential for its metabolism. Gas chromatographic analysis showed that n-propanol was the major compound recovered from the metabolism of propane by resting cells, although trace amounts of isopropanol and acetone were detected. When a mixture of propane and isobutane was used, drastic inhibition (72 to 88%) of hydrocarbon utilization by resting cells occurred. The ratio of hydrocarbon to oxygen consumed was found to be approximately 2:1 during the metabolism of propane or isobutane by resting cells when these substrates were provided individually to the organism. Gas chromatographic-mass spectrometric analysis of products formed from O(2) confirmed that the initial oxidative step in the metabolism of these substrates involved molecular oxygen. The proportion of the alcohol containing O was the same as that of O(2) in the gas mixture. Only a negligible amount of O was detected in the alcohol when H(2)O was incorporated into the system. The observed 2:1 ratio of hydrocarbon to oxygen consumption suggests that the oxygenase in N. paraffinicum, unlike the conventional mono- or dioxygenases, requires two hydrocarbon-binding sites for each of the oxygen-binding sites and is therefore an intermolecular dioxygenase. The newly described oxygenase, which catalyzes the reaction of two molecules of propane with one molecule of oxygen to yield two molecules of a C(3) alcohol, is proposed as the initial oxidation step of the hydrocarbon substrate.

Journal Article↗
PubMed1995

Purification and Properties of Component B of 2,4,5-Trichlorophenoxyacetate Oxygenase from Pseudomonas cepacia AC1100.

Pseudomonas cepacia AC1100 degrades 2,4,5-trichlorophenoxyacetate (2,4,5-T), an herbicide and chlorinated aromatic compound. Although some progress has been made in understanding 2,4,5-T degradation by AC1100 by molecular analysis, little is known about the biochemistry involved. Enzymatic activity converting 2,4,5-T to 2,4,5-trichlorophenol in the presence of NADH and O(inf2) was detected in cell extracts of AC1100. Phenyl agarose chromatography of the ammonium sulfate-fractionated cell extracts yielded no active single fractions, but the mixing of two fractions, named component A and component B, resulted in the recovery of enzyme activity. Component B was further purified to homogeneity by hydroxyapatite and DEAE chromatographies. Component B had a native molecular weight of 140,000, and it was composed of two 49-kDa (alpha)-subunits and two 24-kDa (beta)-subunits. Component B was red, and its spectrum in the visible region had maxima at 430 and 560 nm (shoulder), whereas upon reduction it had maxima at 420 (shoulder) and 530 nm. Each mole of (alpha)(beta) heterodimer contained 2.9 mol of iron and 2.1 mol of labile sulfide. These properties suggest strong similarities between component B and the terminal oxygenase components of the aromatic ring-hydroxylating dioxygenases. Component A was highly purified but not to homogeneity. The reconstituted 2,4,5-T oxygenase, consisting of components A and B, converted 2,4,5-T quantitatively into 2,4,5-trichlorophenol and glyoxylate with the coconsumption of NADH and O(inf2).

Journal Article↗
PubMed2006

A survey of inclusion of the time element when reporting adverse effects in randomised controlled trials of cyclo-oxygenase-2 and tumour necrosis factor alpha inhibitors.

BACKGROUND: The adequacy of reporting the time element in adverse effects in articles on randomised clinical trials of cyclo-oxygenase-2 and tumour necrosis factor (TNF)alpha antagonists was surveyed. METHODS: Prominent rheumatology and general/internal medicine journals were searched for all randomised controlled trials published about cyclo-oxygenase-2 and TNFalpha inhibitor use in rheumatological diseases up to November 2005. Reporting of time to the occurrence of the adverse effects, the use of patient years as the time frame of the reported adverse effects and the use of annual standard incidence ratios based on the surveillance, epidemiology and end-results (SEER) programme when reporting neoplasms as potential adverse effects of TNFalpha antagonists were specifically tabulated. RESULTS: Only 23 of 70 (33%) of all articles gave the specific time of onset of an adverse effect. Nine studies used patient years to report the adverse effects and six studies used annual standard incidence ratios, using SEER, as the comparator. CONCLUSION: In reporting of adverse effects in randomised clinical trials, a particularly neglected issue is the reporting of the time dimension of adverse effects.

Antirheumatic Agents↗
PubMed1979

The effects of low temperature acclimation of winter rye on catalytic properties of its ribulose bisphosphate carboxylase-oxygenase.

A comparison was made of the kinetics of the carboxylation reaction of bicarbonate-magnesium-activated ribulose biphosphate carboxylase-oxygenase purified from cold-hardened and unhardened winter rye (Secale cereale L. cv. Puma). The activity of the (NH4)2SO4-precipitated enzyme from hardened plants was stable at -20 degrees C for a month, whereas the form from unhardened plants was reversibly cold inactivated. The KmCO2 of the unhardened form increased more rapidly with decreasing pH below 8.2, but the estimated pKa of chemical groups associated with the active site was not affected by the cold hardening. The temperature dependencies of the KmCO2 of the two forms of the enzyme crossed at 10 degrees C with the effect that the catalysis of carboxylation by ribulose biphosphate carboxylase-oxygenase from Puma rye was most efficient in the temperature range to which the plants had been adapted.

Acclimatization↗
PubMed1989

Localization of cyclo-oxygenase and prostaglandin E2 in the secretory granule of the mast cell.

The application of anti-cyclo-oxygenase and anti-prostaglandin E2 immunoglobulins to A23187-stimulated rat connective tissue mast cells has permitted the localization of cyclooxygenase activity (prostaglandin H2 synthetase) and the site of prostaglandin E2 (PGE2) formation in the secretory granules. Because binding was carried out after stimulation but before dehydration and embedding, we have limited the loss of these antigens due to normal degradation and to aqueous and solvent washes. As this method permits labeling of exposed cell surfaces, only granules that have been exteriorized can be labeled. Contrary to what might have been expected, no labeling was associated with plasma membranes or with any portion of damaged cells. Antibodies to PGE2 were bound evenly over the surface of the granule matrix, whereas antibodies to cyclo-oxygenase appeared to be bound to strands of proteo-heparin projecting from the surface of the granule matrix. Where granule matrix had become unraveled and dispersed, label appeared to adhere throughout the ribbon-like proteo-heparin strands. These results support our previous conclusion that the secretory granule is the site of the arachidonic acid cascade during exocytosis.

Animals↗
PubMed2006

First-dose analgesic effect of the cyclo-oxygenase-2 selective inhibitor lumiracoxib in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled comparison with celecoxib [NCT00267215].

Cyclo-oxygenase-2 selective inhibitors are frequently used to manage osteoarthritis. We compared the analgesic efficacy of the novel cyclo-oxygenase-2 selective inhibitor lumiracoxib (Prexige) versus placebo and celecoxib in patients with knee osteoarthritis. This seven day, double-blind, placebo and active comparator controlled, parallel group study included 364 patients aged > or = 50 years with moderate-to-severe symptomatic knee osteoarthritis. Patients received lumiracoxib 400 mg/day (four times the recommended chronic dose in osteoarthritis; n = 144), placebo (n = 75), or celecoxib 200 mg twice daily (n = 145). The primary variable was actual pain intensity difference (100 mm visual-analogue scale) between baseline and the mean of three hour and five hour assessments after the first dose. Actual pain intensity difference, average and worst pain, pain relief and functional status (Western Ontario and McMaster Universities Osteoarthritis Index [WOMAC]) were measured over seven days. Patients also completed a global evaluation of treatment effect at study end or premature discontinuation. For the primary variable, the superiority of lumiracoxib versus placebo, the noninferiority of lumiracoxib versus celecoxib, and the superiority of lumiracoxib versus celecoxib were assessed by closed test procedure adjusting for multiplicity, thereby maintaining the overall 5% significance level. In addition, celecoxib was assessed versus placebo in a predefined exploratory manner to assess trial sensitivity. Lumiracoxib provided better analgesia than placebo 3-5 hours after the first dose (P = 0.004) through to study end. The estimated difference between lumiracoxib and celecoxib 3-5 hours after the first dose was not significant (P = 0.185). Celecoxib was not significantly different from placebo in this analysis (P = 0.069). At study end 13.9% of lumiracoxib-treated patients reported complete pain relief versus 5.5% and 5.3% of celecoxib and placebo recipients, respectively. WOMAC total and subscales improved for both active treatments versus placebo except for difficulty in performing daily activities, for which celecoxib just failed to achieve significance (P = 0.056). In the patient's global evaluation of treatment effect, 58.1% of patients receiving lumiracoxib rated treatment as 'excellent' or 'good', versus 48.6% of celecoxib and 25.3% of placebo patients. Lumiracoxib was well tolerated. The overall incidence of adverse events was similar across treatment groups.

Aged↗
PubMed2003

Cyclo-oxygenases and prostaglandins in acute inflammatory demyelination of the peripheral nerve.

OBJECTIVE: To investigate the expression of cyclo-oxygenases (COX), key enzymes in propagating inflammatory responses by converting arachidonic acid to prostaglandins, in inflammatory demyelinating disorders of the peripheral nervous system (PNS). METHODS: Expression and distribution of COX messenger RNA (mRNA) and protein were studied in sural nerve biopsies, serum, and CSF samples from patients with Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), or, for comparison, with vasculitic neuropathy (VN), which is a inflammatory nondemyelinating disorder, and noninflammatory neuropathies (NIN) using RT-PCR, immunohistochemistry, and immunoblotting. To confirm functional COX-2 activity, the expression of prostaglandin E(2) (PGE(2)) and prostaglandin F(2alpha) (PGF(2alpha)) was evaluated by ELISA ex vivo and in vitro. RESULTS: Whereas COX-1 expression was unaltered in all investigated groups, a significant upregulation of COX-2 mRNA was detected in sural nerves from patients with GBS, CIDP, or VN but not in control subjects with noninflammatory disorders. Macrophages were identified as its primary cellular source. Increased COX-2 protein levels were detectable in serum and CSF from all patients with GBS and, in smaller numbers only, in samples from patients with CIDP or VN but not from the NIN group studied. Moreover, increased levels of PGE(2) and PGF(2alpha) were measurable in sera from patients with GBS, CIDP, or VN and in cell culture supernatants from in vitro stimulated macrophages, indicative of COX-2 activity. CONCLUSIONS: Cyclo-oxygenase-2, expressed by macrophages, may generate prostaglandins during acute inflammatory demyelination of the peripheral nerve.

Acute Disease↗
PubMed2000

Colon cancer: a role for cyclo-oxygenase-2-specific nonsteroidal anti-inflammatory drugs.

Large bowel cancer is not only the third most frequent cancer in the world but is one of the most common human malignancies in Western countries, including North America. In recent years, multidisciplinary research in epidemiology, molecular biology, and laboratory animal model studies have contributed much to our understanding of the aetiology of this cancer; more importantly, it has enabled us to devise preventive strategies. Several epidemiological studies have detected a 40 to 50% decrease in risk of colorectal cancer in individuals who regularly use aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). Clinical trials with NSAIDs in patients with familial adenomatous polyposis have demonstrated that treatment with NSAIDs caused regression of pre-existing adenomas. Preclinical efficacy studies have provided scientifically sound evidence as to how NSAIDs act to retard, block, or reverse colonic carcinogenesis. Equally exciting are opportunities for effective chemoprevention with selective cyclo-oxygenase-2 inhibitors in a variety of animal models of colon cancer. Selective cyclo-oxygenase-2 inhibitors such as celecoxib have been proven to be effective chemopreventive agents against colonic carcinogenesis with minimal gastrointestinal toxicity. Our exploration of the multistep process of carcinogenesis has provided substantial insights into the mechanisms by which anti-inflammatory agents modulate these events. There is growing optimism for the view that realisation of preventive concepts in large bowel cancer will also serve as a model for preventing malignancies of the prostate and breast.

Animals↗
PubMed1979

Activation and regulation of ribulose bisphosphate carboxylase-oxygenase in the absence of small subunits.

Ribulose 1,5-bisphosphate carboxylase from Rhodospirillum rubrum requires CO2 and Mg2+ for activation of both CO2, both the carboxylase and oxygenase activities are stimulated by 6-phoshpo-D-gluconate, fructose 1,6-bisphosphate, 2-phosphoglycolate, 3-phosphoglycerate, NADPH, and fructose 6-phosphate. The carboxylase activity is not activated by ribose 5-phosphate. The substrate, ribulose bisphosphate, neither activates nor inhibits the CO2 and Mg2+ activation of this enzyme. Activation by CO2 and Mg2+ is rapid and results in increased susceptibility to active-site-directed protein modification reagents. Because the R. rubrum carboxylase-oxygenase is a dimer of large subunits and contains no small subunits, these results suggest that the effector binding sites of the higher plant enzyme may also be found on the large subunit.

Bicarbonates↗
PubMed1989

Characterization of platelet cytoplasmic Ca2+ mobilization in patients with congenital cyclo-oxygenase deficiency and with defective platelet aggregation to A23187.

Agonist-induced platelet cytoplasmic Ca2+ concentrations ([Ca2+]i) in patients with congenital cyclo-oxygenase deficiency (A) and with impaired aggregation to A23187 (B) were measured with aequorin in the presence or absence of extracellular Ca2+. The influence of TMB-8 or ONO3708 on agonist-induced [Ca2+]i in those platelets was also investigated. In Patient 1, there was a single aequorin luminescence peak in response to arachidonate, which was a thromboxane A2(TXA2) independent Ca2+ influx. The luminescence peak due to the formation of TXA2 was not detectable. The A23187-induced [Ca2+] i was decreased in the presence of extracellular Ca2+, but was within normal limits in the absence of extracellular Ca2+. A thrombin or STA2-induced elevation of [Ca2+] i was always within normal limits under any conditions. These results suggest that cyclo-oxygenase activity (CO activity) contributes to the A23187-induced Ca2+ influx, but does not contribute to the Ca2+ release from intracellular stores, and that the thrombin or STA2-induced Ca2+ influx and release do not depend on the CO activity. In Patient 2, the time lag from the addition of A23187 to the aequorin luminescence peak was found both in the presence and absence of extracellular Ca2+, which was more obvious in the latter. This A23187-induced elevation of [Ca2+] i disappeared after treatment of the platelets with TMB-8 in the absence of extracellular Ca2+, which is rarely seen in normal platelets. The most striking finding was that the thrombin-induced rise in [Ca2+] i in the absence of extracellular Ca2+ was not detectable. These findings might be closely related to abnormal platelet function in this patient.

Blood Platelet Disorders↗
PubMedDate not supplied

Placental mono-oxygenation: characteristics and partial purification of a hematin-activated human placental mono-oxygenase.

Human placental mono-oxygenase activities were markedly increased after additions of micromolar quantities of hematin to reaction vessels. The magnitude of the increases diminished with increasing (induced) levels of hematin-independent activity. The activating effect of hematin could be observed in unbroken cell preparations, in whole homogenates, and in various subcellular fractions. Highest hematin-dependent activity was measured in microsomal fractions of placental homogenates. With benzo(a)pyrene as substrate, response to the stimulatory effect of hematin in human placental preparations was not as profound as that observed in monkey or rabbit placentas but was more marked than the responses observed in placental preparations from rats or mice. Hematin-activated mono-oxygenase activity present in washed microsomal fractions of human placental homogenates could be solubilized with detergents, the most effective of which was Triton N-101. The solubilized activity also could be partially purified by polyethylene glycol fractionation. Attempts to further purify, however, resulted in loss of activity. All results were consistent with the hypothesis that the effect of hematin is mediated via reconstitution of hematin-free apocytochrome(s) P-450.

Animals↗
PubMedDate not supplied

Metabolism of alcohol and ketone by cytochrome P-450 oxygenase: fluoren-9-ol in equilibrium with fluoren-9-one.

Fluoren-9-ol and fluoren-9-one were used as model substrates to study microsomal metabolism of alcohols and carbonyl compounds. It was found that there was an oxidoreductase(s) present in the microsomal preparation that catalyzed interconversion of this alcohol and ketone using pyridine nucleotides as cofactors. The alcohol could also be oxygenated to the ketone by microsomes and NADPH. It required molecular oxygen. This oxygenation was inhibited by SKF 525-A and CO, suggesting the involvement of P-450 oxygenase. Using highly purified P-450 oxygenase components, it was shown that fluoren-9-ol was oxygenated by the complete system to fluoren-9-one. Exclusion of cytochrome P-450 or its reductase resulted in no oxygenation. Dilauroylglyceryl-3-phosphorylcholine was without effect on the reaction. Fluoren-9-one, on the other hand, was reduced to fluoren-9-ol by NADPH-cytochrome P-450 reductase and NADPH. It is suggested that other alcohols and carbonyl compounds are similarly metabolized.

Alcohols↗
PubMed1983

Aspirin can inhibit gastric mucosal cyclo-oxygenase without causing lesions in rat.

Dose-response relationships between aspirin-induced cyclo-oxygenase inhibition and gastric mucosal injury were studied in rats. Oral or parenteral aspirin, 25 mg/kg, inhibited prostaglandin generation by 87%-95% at 1, 3, and 6 h with no lesion formation. Aspirin, 100 mg/kg, inhibited prostaglandin generation by 95%-98% at 1, 3, and 6 h, but lesions were observed only when aspirin was given orally. Three-hour pretreatment with intraperitoneal aspirin, 12.5 mg/kg, did not enhance the mucosal injury caused by 10 mM acidified taurocholate, although prostaglandin generation was inhibited by 80%. Pretreatment with 25 mg/kg aspirin inhibited prostaglandin generation by 89% and was associated with significant mucosal injury by acidified taurocholate. We conclude that aspirin-induced 95% inhibition of gastric mucosal cyclo-oxygenase is not, by itself, sufficient to produce lesions and inhibition by greater than 80% is required to predispose the gastric mucosa to injury by otherwise mild irritants.

Administration, Oral↗
PubMed1983

The function of the small subunits of ribulose bisphosphate carboxylase-oxygenase.

When ribulose bisphosphate carboxylase-oxygenase from Synechococcus (strain RRIMP N1) was precipitated under mildly acidic conditions, most of its small subunits remained in solution. The precipitated enzyme readily redissolved at neutral pH and remained as an octamer of large subunits with some small subunits still attached. Optimum pH for this separation was 5.3 and disulfide-reducing reagents were not necessary. The fraction of small subunits removed by a single precipitation increased with increasing NaCl concentration. Catalytic activity of small subunit-depleted enzyme was linearly proportional to the fraction of small subunits remaining, while the carboxylase:oxygenase activity ratio and the affinity for CO2 remained constant. When isolated small subunits were added back to depleted enzyme preparations at neutral pH, reassociation occurred with return of catalytic activity. Under the usual assay conditions at pH 7.7, the binding constant of the small subunits was estimated to be about 10(-9) M. The small subunits also bound avidly to surfaces. However, loss of small subunits from the enzyme during the course of purification was minimal. The results are consistent with a simple model in which only those large subunits which have a small subunit bound to them are catalytically competent. Thus, an essential, even if indirect, role for the small subunits in catalysis is indicated.

Carboxy-Lyases↗
PubMed1998

Membrane translocation of 15-lipoxygenase in hematopoietic cells is calcium-dependent and activates the oxygenase activity of the enzyme.

Mammalian 15-lipoxygenases, which have been implicated in the differentiation of hematopoietic cells are commonly regarded as cytosolic enzymes. Studying the interaction of the purified rabbit reticulocyte 15-lipoxygenase with various types of biomembranes, we found that the enzyme binds to biomembranes when calcium is present in the incubation mixture. Under these conditions, an oxidation of the membrane lipids was observed. The membrane binding was reversible and led to an increase in the fatty acid oxygenase activity of the enzyme. To find out whether such a membrane binding also occurs in vivo, we investigated the intracellular localization of the enzyme in stimulated and resting hematopoietic cells by immunoelectron microscopy, cell fractionation studies and activity assays. In rabbit reticulocytes, the 15-lipoxygenase was localized in the cytosol, but also bound to intracellular membranes. This membrane binding was also reversible and the detection of specific lipoxygenase products in the membrane lipids indicated the in vivo activity of the enzyme on endogenous substrates. Immunoelectron microscopy showed that in interleukin-4 -treated monocytes, the 15-lipoxygenase was localized in the cytosol, but also at the inner side of the plasma membrane and at the cytosolic side of intracellular vesicles. Here again, cell fractionation studies confirmed the in vivo membrane binding of the enzyme. In human eosinophils, which constitutively express the 15-lipoxygenase, the membrane bound share of the enzyme was augmented when the cells were stimulated with calcium ionophore. Only under these conditions, specific lipoxygenase products were detected in the membrane lipids. These data suggest that in hematopoietic cells the cytosolic 15-lipoxygenase translocates reversibly to the cellular membranes. This translocation, which increases the fatty acid oxygenase activity of the enzyme, is calcium-dependent, but may not require a special docking protein.

Animals↗