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Biomedical subjects

J J Moreno

Publications and source records attributed to J J Moreno.

54 records · Page 3Linked to original sources
PubMed1992

Effects of copper, iron and zinc on oedema formation induced by phospholipase A2.

1. Intradermal or subplantar injection of soluble snake venom phospholipase A2 (PLA2) evoked a brisk inflammatory response, with cutaneous vascular permeability increase and paw oedema. 2. These inflammatory processes are mainly the result of arachidonic acid cascade activation and mast cell degranulation. 3. Copper, iron and zinc have an inhibitory effect on vascular permeability increase and paw oedema induced by PLA2. 4. Copper and iron could have not only a direct effect on PLA2 but on enzymes of arachidonic acid cascade. 5. However, zinc have a moderate antiinflammatory activity. This effect could be the result to inhibit PLA2 induced mast cell degranulation.

Animals↗
PubMed1992

PLA2-induced oedema in rat skin and histamine release in rat mast cells. Evidence for involvement of lysophospholipids in the mechanism of action.

Injection of phospholipase A2 (PLA2) in the rat skin produced a significant rise in oedema, which was inhibited by the simultaneous coinjection of aristolochic acid (100 micrograms), mepacrine (100 micrograms) and p-bromophenacyl bromide (10 micrograms). Indomethacin, nordihydroguaiaretic acid and WEB 2086 were without inhibitory effect on this model, whereas dexamethasone (5 mg/kg, p.o.) and coinjection of chlorpheniramine (20 micrograms) inhibited the oedema formation by more than 60%. Dose-dependent histamine release by rat peritoneal cells was induced by PLA2 and by lysophosphatidylserine and this effect could be antagonized by aristolochic acid and mepacrine. Apomorphine, previously reported to be an antagonist at lysophospholipid receptors, was able to inhibit the histamine release by mast cells as well as the oedema formation in rat skin. Taken all together, these results suggest that lysophospholipids, produced by the action of PLA2, are the mediators for the histamine release in rat peritoneal cells and could play an important role in the early oedema development in rat skin after PLA2 administration.

Animals↗
PubMed1991

Effect of Mycobacterium butyricum on the hepatic cytochrome P-450 system of the mouse: influence of anti-inflammatory drug.

1. M. butyricum administration to rats induces arthritis and impairment in hepatic cytochrome P-450 activity. 2. This work was performed to verify if M. butyricum administrated to mice produces similar effects on cytochrome P-450 hepatic without involvement of articular lesions. 3. We also studied the role of arachidonate metabolites in the genesis and perpetuation of hepatic injury. 4. Intraperitoneal M. butyricum administration to mice increased sleeping time induced by pentobarbital and decreased both aminopyrine N-demethylase (AND) and aniline p-hydroxylase (APH) activities without producing articular inflammation. 5. Only preventative oral administration of indomethacin or dexamethasone during the week before M. butyricum injection avoided drug-metabolizing system alterations. 6. Our results suggest a possible link between arachidonate metabolites inhibited by indomethacin or dexamethasone and the genesis of cytochrome P-450 disfunction.

Aminopyrine N-Demethylase↗
PubMed1990

Urinary N-acetyl-beta-D-glucosaminidase as a marker of renal injury in adjuvant arthritis.

In the present study we have determined if renal damage occurs with adjuvant arthritis (AA). As a sensitive indicator of renal injury in tubular cells, urinary N-acetyl-beta-D-glucosaminidase (NAG) was measured at predetermined times after arthritis induction. Urinary protein, sodium and potassium excretion were also evaluated. NAG levels in arthritic animals were higher than those in healthy ones from day 12 after induction and the levels remained high during the study period. A significant positive correlation was noted between urinary NAG excretion and disease severity reflected by hind paw edema. Protein excretion also increased in arthritic animals but there was no correlation between urinary protein, NAG levels, and degree of inflammation. Changes in urine sodium and potassium levels did not reach statistical significance. Thus, we can conclude that some renal damage occurred in this experimental model of chronic inflammation.

Acetylglucosaminidase↗
PubMed1990

[Evaluation in our milieu of an ELISA method (ANDA-Tb) for the serological diagnosis of tuberculosis].

We have evaluated the new ELISA test (ANDA-Tb) for the serological diagnosis of tuberculosis in serum samples from 343 individuals: 160 were from blood donors, 152 from patients with nontuberculous diseases, most of them respiratory, and 31 from tuberculous patients diagnosed by positive culture. Using a cutoff value in 350 serounits we had a positive predictive value of 57% and a negative predictive value of 98% in blood donors, and 43% and 97%, respectively, in control patients. Sensitivity was 68%. There was a higher false positive rate in patients with respiratory diseases, particularly acute pneumonia. We conclude that this particular ELISA is very useful as a supportive test for the diagnosis of tuberculosis, with a lower specificity in hospital nontuberculous patients.

Antibodies, Bacterial↗
PubMed1989

Effects in vitro of copper and zinc on hepatic cytochrome P-450 activities.

1. In previous studies we have shown that hepatic copper and zinc increases and liver microsomal cytochrome P-450 activities greatly decreases in adjuvant arthritic rats. 2. In the present paper we study if the changes in copper and zinc could be related to depression of drug microsomal activity. Thus, the effect of in vitro addition of copper or zinc to microsomal fraction upon aminopyrine N-demethylase (AND) and aniline p-hydroxylase (APH) activity was measured. 3. Both metals produced an inhibition of enzyme activity. The reduction of AND and APH activities produced by copper (ID25 = 4.7 x 10(-5)M to AND; 1.05 x 10(-5)M to APH) was greater than that obtained with zinc (ID25 = 2.26 x 10(-4)M to AND; 3.3 x 10(-4)M to APH).

Aminopyrine N-Demethylase↗
PubMed1987

Serum sulfhydryl group levels in experimental chronic inflammation.

Serum sulfhydryl group concentration and protein fraction were determined in adjuvant arthritic rats, during six weeks. Significantly reduced sulfhydryl levels were found in arthritic rats from day 3 and these values remained decreased throughout the study period. Good correlation exists between serum sulfhydryl alterations and degree of inflammation measured as hind paw swelling, as well as between the former and changes in serum protein fractions.

Animals↗
PubMedDate not supplied

Effect of aristolochic acid on arachidonic acid cascade and in vivo models of inflammation.

Recently, it has been reported that aristolochic acid inhibits phospholipase A2 (PLA2) in vitro and also decrease either oedema induced by snake venom and human synovial fluid PLA2. The aim of this research was to study the antiinflammatory activity of aristolochic acid and to investigate the effect of the alkaloid on the enzymes involved in the release of eicosanoids. Our results demonstrate that aristolochic acid is able to inhibit inflammation induced by immunological, immune complexes, and nonimmunological agents such as carrageenan or croton oil. We suggest that one mechanism of the antiinflammatory activity of alkaloid may be by directly blocking PLA2 catalyzed release of arachidonic acid. Moreover, this study demonstrates that aristolochic acid could also inhibit other steps involved in eicosanoids release such as cyclooxygenase and lipooxygenase pathways.

Administration, Topical↗
PubMedDate not supplied

Effect of retinoids on dermal inflammation and on arachidonic acid mobilization and metabolism in murine 3T6 fibroblasts retinoids, arachidonate release and metabolism.

Retinoids have shown anti-inflammatory activity in some animal models and human diseases, although the mechanism by which retinoids elicit this activity is unknown. In this study, retinoids significantly attenuated, in a dose-dependent fashion, murine ear oedema induced by phorbol 12-myristate 13-acetate (PMA) or oxazolone. Dexamethasone inhibited both oedemas whereas ketoprofen reduced only that induced by PMA. PMA application or oxazolone-induced contact hypersensitivity markedly increased production of eicosanoids such as 6-keto-PGF1 alpha or LTB4. The anti-oedematous effects of retinoids were accompanied by inhibition of tissue eicosanoid levels. Besides, retinoids showed toxic effects on culture fibroblasts caused by an irritant effect on plasma membrane. However, when we used subtoxic doses, we demonstrated that retinoids in vitro could inhibited arachidonate mobilization and eicosanoid biosynthesis induced in fibroblast cultures by PMA, calcium ionophore A23187 or bradykinin. Thus, this paper reports the ability of retinoids to inhibit skin inflammatory processes induced by tumour promotors or immunological stimuli. Moreover, we have demonstrated that retinoids at non-cytotoxic doses may inhibit eicosanoid generation and arachidonic acid mobilization in 3T6 fibroblasts.

3T3 Cells↗
PubMedDate not supplied

Release of iron from ferritin by aqueous extracts of cigarette smoke.

This study demonstrates the ability of aqueous extracts of cigarette smoke to reduce iron and cause its release from ferritin. Superoxide dismutase (SOD) increases the rates of iron release with the less filtered smoke extracts, but has no effect on the rate of iron release caused by aqueous extracts of well-filtered gas-phase cigarette smoke. Faster rates of iron release are observed under anaerobic conditions, and the reducing power of the cigarette smoke extracts is prolonged when incubated in argon. Hydroquinone and catechol, two of the major polyhydroxybenzenes in cigarette smoke, increase in concentration in the smoke extracts as these are subjected to less filtration, and higher concentrations of polyhydroxybenzenes correlate with higher rates of iron release from ferritin. Concomitant with iron release, depletions of amino acids in ferritin are observed. Depletion of histidine is partially prevented by bathophenanthrolinedisulfonate and mannitol, while lysine and arginine depletions remain unaffected. These observations suggest that cigarette smoke components react directly with these amino acid residues in ferritin. Cigarette smoke induced release of iron could alter iron metabolism in the lungs of chronic smokers and contribute to the increase in the total oxidative burden on the lungs of smokers.

Aerobiosis↗
PubMedDate not supplied

Inactivation of alpha 1-proteinase inhibitor by peroxynitrite.

We here report the reactions of peroxynitrite (O=NOO-) with alpha 1-proteinase inhibitor (alpha 1PI) and with a synthetic decapeptide (MER10) containing the sequence of amino acids found in the active site of alpha 1PI (Pro-Met-Ser-Ile-Pro-Pro-Glu-Val-Lys-Phe). Peroxynitrite inactivates alpha 1PI at both pH 7.4 and 12.0. Thiourea and methionine protect alpha 1PI against inactivation by peroxynitrite, while mannitol and benzoate fail to afford effective protection. The major product isolated from the reaction between peroxynitrite and MER10 was analyzed by NMR, mass spectrometry, and amino acid analysis. These analyses indicate that peroxynitrite primarily oxidizes the methionine residue in the peptide. We detect neither smaller molecular weight peptides, which would indicate cleavage of MER10, nor hydroxylation or nitration of the phenylalanine residue. Our results suggest that peroxynitrite is capable of oxidizing methionine residues in proteins without the involvement of the hydroxyl radical or nitrogen dioxide. The implications of these observations on lung diseases attributed to cigarette smoke are discussed.

Amino Acid Sequence↗
PubMedDate not supplied

Peroxynitrite, a cloaked oxidant formed by nitric oxide and superoxide.

Peroxynitrite [oxoperoxonitrate(1-), ONOO-] may be formed in vivo from superoxide and nitric oxide. The anion is stable, but the acid (pKa = 6.8) decays to nitrate with a rate of 1.3 s-1 at 25 degrees C. The experimental activation parameters of this process are delta H++ = +18 +/- 1 kcal/mol, delta S++ = +3 +/- 2 cal/(mol.K), and delta G++ = +17 +/- 1 kcal/mol. Peroxynitrite (or its protonated form) oxidizes some compounds such as thiols and thioethers in a biomolecular reaction. The reactions with glutathione and cysteine have activation enthalpies of 10.9 and 9.7 kcal/mol, respectively, which are lower than that of the isomerization reaction. Peroxynitrite reacts with other compounds such as dimethyl sulfoxide and deoxyribose in a unimolecular reaction for which the activation of peroxynitrite is rate-limiting. In theory, activation could involve (1) heterolysis to OH- and NO2+ (delta rxn Gzero' = 13 kcal/mol at pH 7) or (2) homolysis to .OH and .NO2 (delta rxn Gzero = 21 kcal/mol), and these processes also could be involved in the isomerization to nitrate. However, thermodynamic and kinetic considerations indicate that neither process is feasible, although binding to metal ions may reduce the large activation energy associated with heterolysis. An intermediate closely related to the transition state for isomerization of ONOOH to HONO2 may be the strongly oxidizing intermediate responsible for hydroxyl radical-like oxidations mediated by ONOOH. Thus, peroxynitrite reacts with different compounds by at least two distinct mechanisms, and the hydroxyl radical is not involved in either.

Cysteine↗
PubMedDate not supplied

[Bacteremia caused by Bacteroides. An analysis of 50 episodes].

During the 32 months between October 1984 and May 1987 there were 72,800 admissions in our center; 31,523 blood cultures were undertaken and in 3,831 of them (11.5%) at least one significant organism was recovered; 6.7% of blood cultures yielded anaerobic bacteria, and 3.1% Bacteroides spp. In the 1,478 instances of bacteremia recorded during that period, the relative frequencies of bacteremia by anaerobic bacteria and by Bacteroides were 8.6% and 3.9%, respectively. In overall 50 Bacteroides bacteremias (47 due to Bacteroides fragilis and 3 to Bacteroides spp), 32 (64%) were hospital acquired and 14 (28%) postsurgical. Their most common source was the abdominal cavity (25, 50%), followed by the skin and soft tissues (7, 14%), feminine pelvis (4, 8%), miscellaneous (8, 16%), and unknown (7, 14%). Fifteen bacteremias (30%) were polymicrobial, 20 (40%) were associated with septic shock, and 15 (30%) with renal failure. Overall mortality rate was 52%, and that directly attributable to bacteremia was 32%. Poor prognostic predictors included the source from a perforated viscus, septic shock, renal failure or gastrointestinal hemorrhage, and the absence of adequate antimicrobial therapy.

Adolescent↗