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Biomedical subjects

E Gelpí

Publications and source records attributed to E Gelpí.

At least 19 recordsLinked to original sources
PubMed1992

In vivo transformation of arachidonic acid into 12-hydroxy-5,8,10,14-eicosatetraenoic acid by human nasal mucosa.

A method for the determination of 12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE) by gas chromatography-mass spectrometry (GC-MS) in samples obtained from healthy subjects by nasal lavage is presented. HETEs were extracted from samples obtained by nasal lavage using C18 solid-phase cartridges. The purification of 12-HETE and 5-HETE was carried out in two consecutive steps of purification by reversed-phase high-performance liquid chromatography. Methylated and trimethylsilylated fractions were separated by GC-MS with electron-impact ionization. The production of 12-HETE by human nasal mucosa was confirmed by GC-MS.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Gas chromatographic/mass spectrometric analysis of high-performance liquid chromatographic fractions reflecting arachidonic acid metabolism in mouse peritoneal macrophages.

Mouse peritoneal macrophages are used as a model for studies undertaken around the oxidative metabolism of arachidonic acid elicited by xenobiotics (N-phenyllinoleamide, related to the toxic oil syndrome, has been used as an example). A high-performance liquid chromatographic method for cyclo- and lipoxygenase metabolite fractionation has been developed. Gas chromatographic/mass spectrometric analysis of the high-performance liquid chromatographic fractions thus obtained show that the major products detected in the incubates correspond to three principal structures: monohydroxy acids (12-hydroxyeicosatetraenoic acid being the major component), epoxyhydroxy acids and trihydroxy acids. Other minor compounds such as 12-hydroxyheptadecatrienoic acid, various dihydroxy acids and prostaglandins were also detected. Cells pre-exposed to N-phenyllinoleamide show selectively enhanced levels of 6-keto prostaglandin F1 alpha, as measured by both gas chromatography/mass spectrometry and radioimmunoassay of the corresponding high-performance liquid chromatographic fraction.

Anilides↗
PubMed1992

Human and experimental studies on renal eicosanoid response to long-term cadmium exposure.

In order to assess the effects of long-term exposure to cadmium (Cd) on the renal metabolism of eicosanoids, the urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), and thromboxane B2 (TXB2) was determined in 37 workers exposed to Cd and in female Sprague-Dawley rats given 100 ppm Cd in drinking water for 10 months. Urinary output of sodium and calcium was also determined. The Cd-exposed workers showed an increased urinary concentration of 6-keto-PGF1 alpha, PGE2, sodium, and calcium. The rise of 6-keto-PGF1 alpha was related to Cd levels in blood and weakly correlated with urinary sodium. Calcium in urine was not related to the concentration of the metal in blood and urine. A slight elevation in urinary TXB2 was also observed in workers with blood Cd higher than 5 micrograms/liter. After 10 months of exposure to Cd, female Sprague-Dawley rats presented an enhanced urinary excretion of albumin, transferrin, beta 2-microglobulin, sodium, and PGE2 in urine. The latter was significantly correlated with albuminuria and transferrinuria. In conclusion the results show that chronic exposure to Cd induces changes in the urinary excretion of some eicosanoids. The possible relation of these changes to Cd-induced kidney dysfunction are discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Altered systemic and tissue prostacyclin in cerulein induced acute pancreatitis in rats.

Prostacyclin metabolism in rat acute pancreatitis was evaluated by measuring the tissue levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and the urinary excretion of 2, 3-dinor 6-keto-PGF1 alpha. Acute pancreatitis was induced by i.v. cerulein perfusion and was confirmed by the pancreas enzyme changes and the histological findings. Significantly enhanced tissue and urinary prostacyclin levels were found in acute pancreatitis rats, when compared to the controls. Concomitantly, an enhanced tissue phospholipase A2 (PLA2) activity was also found. These data show the importance of 2, 3-dinor PGF1 alpha as an inflammatory marker in cerulein-induced pancreatitis.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Influence of N-phenyllinoleamide from toxic oil samples on the lipoxygenase metabolism of exogenous arachidonic acid in mouse peritoneal macrophages.

N-phenyllinoleamide (NPLA) is a useful marker for adulterated oil samples associated with cases of toxic oil syndrome (TOS). To date, NPLA has not reproduced the human poisoning episode in experimental animal models and, thus, its pathological role in the syndrome remains controversial. The present report describes the effect of NPLA on the lipoxygenase metabolism of exogenous arachidonic acid (AA) in mouse peritoneal macrophages (MPM). Results show that MPM cells exposed to 1mM NPLA for 2 h, when subsequently incubated with exogenous 3H-AA, undergo a significant increase in the biosynthesis of 3H-12-hydroxyeicosatetraenoic acid (3H-12-HETE) whereas levels of 3H-15-HETE are relatively stable. These data indicate that NPLA selectively potentiates the lipoxygenase metabolism of exogenous AA, supporting the possible implication of lipid peroxidative processes in the ethiopathology of TOS, although the relatively high NPLA concentration required 'in vitro' makes it unlikely that this xenobiotic could be directly related to human toxicity.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1992

Release of peptide leukotriene into nasal secretions after local instillation of aspirin in aspirin-sensitive asthmatic patients.

Although the mechanism of aspirin-induced asthma and rhinitis is unknown, it has been suggested that adverse nasal and bronchial reactions are caused by an increased production of lipoxygenase products. In examining this hypothesis we have measured the release of peptide leukotrienes (PeptLTs), 15-HETE, and prostaglandins in nasal fluids obtained by nasal lavages after instillation of acetylsalycilic acid (ASA) and placebo (saline). Ten ASA-sensitive asthmatics, 10 ASA-insensitive asthmatics, and seven healthy subjects were challenged in a double-blind study with normal saline and 12 mg of ASA. Twelve mg were administered based on the results of a previous study that showed that this dose caused minor to moderate symptoms in ASA-sensitive patients. PeptLTs, LTB4, 15-HETE, PGE2, PGF2 alpha, and PGD2 were measured by radioimmunoassay methods. Significant levels of PeptLTs were detected in sensitive asthmatic patients 60 min after nasal challenge. This change was associated with a significant increase in symptoms. No increase in PeptLTs levels were found, however, in either insensitive patients or healthy subjects. Inhibition of PGE2 and PGF2 alpha release was detected in the three groups after ASA administration. ASA also inhibited PGD2 release in insensitive asthmatic patients but not in both sensitive patients and healthy subjects. These results suggest that an abnormal release of PeptLTs in ASA-sensitive asthmatic patients contributes to nasal and bronchial adverse reactions. The lack of effects on PGD2 release suggests that mast cells from ASA-insensitive patients are more sensitive to ASA than those from sensitive asthmatic patients and healthy subjects.

Administration, Intranasal↗
PubMed1991

Cyclooxygenase and lipoxygenase arachidonic acid metabolism by monocytes from human immune deficiency virus-infected drug users.

Prostaglandin E2, thromboxane B2 and leukotriene B4 monocyte production have been determined in human immune deficiency virus (HIV)-infected drug users (n = 36) and healthy subjects (n = 29). Eicosanoids were extracted from the incubates using C18 solid-phase cartridges and determined by radioimmunoassay. An enhanced production of prostaglandin E2 and thromboxane B2 was detected in monocytes from HIV-positive drug users whether or not they had been previously stimulated with zymosan. Concomitant leukotriene B4 increases were not observed. The results reported in this paper indicate that altered cyclooxygenase arachidonic acid metabolism in monocytes from HIV-infected drug users is associated with the severe cellular immunodysfunction characteristic of AIDS. In contrast, leukotriene B4 does not seem to play a role in AIDS-associated immunosuppression.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Characteristic fragmentation of thromboxane B2 in thermospray high-performance liquid chromatography-mass spectrometry.

Cyclo- and lipo-oxygenase metabolites of arachidonic acid have been reported to have very simple thermospray mass spectra. However, thromboxane B2 (TXB) in ammonium acetate-methanol and at interface temperatures below the point of total vaporization shows a mass spectral pattern characterized by abundant ions at low masses. The more abundant TXB fragment ions have been characterized as adducts from four principal fragments with molecular masses of 156, 170, 196 and 326. Positive- and negative-ion mass spectra, and mass spectra obtained with an alternative thermospray buffer (butylammonium acetate) support the molecular masses of these fragments. A tentative assignment of the fragments can be made by comparison of the thermospray mass spectra of TXB, 2,3-dinor-TXB and some of their methyl ester and methyl oxime derivatives. Interface temperature and solvent composition effects on the fragmentation, as well as in the electron-capture processes observed when working in the filament-on mode, are discussed. Fragmentation mechanisms can be related to those observed for monosaccharides, and imply retro-Diels-Alder as well as retroaldolic condensation-type rearrangements.

Buffers↗
PubMed1991

Tissular prostanoid release, phospholipase A2 activity, and lipid peroxidation in pancreas transplantation.

Free radical species have been implicated as important agents in ischemia-reperfusion injury associated to transplantation procedures. This study was carried out to investigate the possible relationship between phospholipase A2 activity (PLA2), lipoperoxidation, and the changes in arachidonic acid metabolism during ischemia reperfusion injury in pancreas transplantation, as well as the effect of a free radical scavenger such as superoxide dismutase on these changes. For this purpose male Lewis rat groups (n = 7) were classified as follows: group I--control; group II--syngenic pancreas transplantation after 15 min preservation in Collins solution at 4 degrees C; group III--syngenic pancreas transplantation after 18 hr preservation in the same conditions; group IV--same as III but with administration of SOD (i.v.) immediately before revascularization in the recipient rat. The results indicate that significant increases in PLA2 activity and lipoperoxide levels occur concomitantly with an increase of thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) in pancreatic tissue after pancreas transplantation. The counteracting effect of a free radical scavenger such as SOD supports the role of oxygen free radicals (OFR) mediating activation of PLA2 and subsequent formation of eicosanoids in pancreas transplantation.

Animals↗
PubMed1990

Simultaneous reversed-phase extraction of lipoxygenase and cyclooxygenase metabolites of arachidonic acid in nasal secretions: methodological aspects.

An improved analytical method for the simultaneous solid-phase extraction of arachidonic acid metabolites in biological samples is described. The major aim of the work was to define the cause of the different recoveries reported in the literature for leukotrienes and hydroxyeicosatetraenoic acids. We used nasal lavages to carry out a comparative study of solid-phase extraction parameters of practical importance in securing good recoveries of leukotrienes and hydroxyeicosatetraenoic acids from biological samples. We evaluated the influence of the pH of the sample, the pH of the water used to wash the extraction cartridge before elution of the adsorbed analytes, the comparative behaviour of commercially available octadecyl adsorbents and the influence of the concentration-evaporation step on final recoveries. Data thus obtained show that there is no significant difference in results when the samples and the water used to wash the cartridge before analyte elution are adjusted to pH values ranging between 4.0 and 7.4. Below pH 4.0, losses may be significant. Furthermore, recoveries can be very much dependent on the type of solid-phase cartridge material and on the eluent evaporation method, especially with regard to aqueous phase removal.

Arachidonic Acid↗
PubMed1990

Rapid non-enzymatic HPLC determination of total MHPG in human plasma.

We have previously reported a method for the determination of total 3-methoxy-4-hydroxy phenylethylene glycol (MHPG) in brain, based on a simple acid-catalyzed hydrolysis. Now we extend this procedure to the determination of plasma total MHPG. The method involves the deproteinization of plasma with perchloric acid, followed by 3 minutes of an acid-catalyzed step. The hydrolysates are injected into the HPLC system, using a formic acid/methanol eluent with fluorimetric detection. Sample detection limit is below 1 ng MHPG/mL of plasma. This procedure has been used for the determination of plasma total MHPG from 109 healthy individuals of both sexes. Mean value was: 5.4 + 2.3 ng total MHPG/mL of plasma (means +/- S.D., N = 109). No sex differences were observed, and a slight correlation with age (r = 0.24, p less than 0.02) has been found. Plasma-free MHPG was also determined in a subgroup of 15 randomly chosen individuals (3.0 +/- 1.2 ng free MHPG/mL plasma, means +/- S.D.). A significant correlation was obtained with plasma total MHPG (r = 0.77, p less than 0.001, N = 15). The main advantage of the present method lays in its simplicity, since no enzymatic hydrolysis or extraction procedures are needed, being its reliability fully proven through 109 plasma total MHPG determinations.

Chromatography, High Pressure Liquid↗
PubMed1990

Prostaglandin E2 and thromboxane B2 levels in rats subjected to pancreas transplantation.

This work undertakes the study of changes in urinary, plasmatic and tissue levels of Thromboxane B2 (TXB2) as well as in tissue Prostaglandin E2 (PGE2) after pancreas transplantation and the effect of superoxide dismutase (SOD) on these changes. For this purpose, streptozotocine induced diabetic rats were subjected to pancreas transplantation. Experimental groups were classified as follows: Group I: Control; Group II: Animals subjected to 15 min of pancreas arterial flow occlusion followed by reperfusion; Group III: Syngenic pancreas transplantation after 12 hours of organ preservation; Group IV: Same as III, but with additional SOD (13 mg/kg) pretreatment. The results indicate that significant increases of PGE2 and TXB2 levels occur as a consequence of the surgical removal, preservation and implantation of the organ. For TXB2 these increases, immediate in plasma and tissue, are not detected in urine until 24 hours after transplantation of the pancreas. The release of TXB2 and PGE2 was effectively prevented in the SOD treated group supporting the role of oxygen free radicals and lipid peroxidation in the processes of ischemia-reperfusion associated to transplantation of the pancreas.

Animals↗
PubMed1990

Cyclooxygenase products of metabolism of arachidonic acid in mouse macrophages exposed to N-phenyllinoleamide from toxic oil samples.

N-phenyllinoleamide (NPLA), one of the major extraneous constituents of Spanish toxic oil samples, appears to enhance the cyclooxygenase metabolic pathway of arachidonic acid by peritoneal mouse macrophages. Results reported herein show an increased biosynthesis of 6-oxo-PGF1 alpha and TXB2 by macrophages exposed to NPLA. However, light and electron microscopy failed to show cellular alterations in macrophages incubated with NPLA for two hours at 27 degrees C. These data suggest a possible involvement of cyclooxygenase arachidonic acid metabolism in the etiopathogenesis of the Spanish Toxic Oil Syndrome.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Recovery of nasal prostaglandin production after inhibition by aspirin.

We have investigated the duration of the inhibitory effects of aspirin in eight healthy volunteers after oral administration of a single 500 mg dose. Prostaglandin E2, D2 and leukotriene C4 levels in nasal lavage fluid were measured by radioimmunoassay without purification by high performance liquid chromatography. The inhibitory effects of aspirin on eicosanoid synthesis were maximum between 1 h to 24 h, showing total recovery within 3-5 days. LTC4 synthesis was not modified by aspirin.

Adult↗