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Biomedical subjects

C Bravo

Publications and source records attributed to C Bravo.

At least 55 records · Page 3Linked to original sources
PubMed1994

Identification of a 20-kDa protein with calcium uptake transport activity. Reconstitution in a membrane model.

This paper presents results of experiments designed to further purify the membrane system involved in mitochondrial calcium transport. A partially purified extract, which transported calcium with a specific activity of 1194 nmol 45Ca2+/mg protein/5 min, was used to obtain mouse hyperimmune serum. This serum inhibited calcium uptake both in mitoplasts and in vesicles reconstituted with mitochondrial proteins containing cytochrome oxidase. Western blot analysis of the semipurified fraction showed that the serum recognized specifically two antigens of 75 and 20 kDa. Both antibodies were purified by elution from the nitrocellulose sheets and their inhibition capacity was analyzed. The antibody that recognized the 20-kDa protein produced a higher degree of inhibition than the other one.

Animals↗
PubMed1994

Triphenyltin as inductor of mitochondrial membrane permeability transition.

The effect of triphenyltin on mitochondrial Ca2+ content was studied. It was found that this trialkyltin compound induces an increase in membrane permeability that leads to Ca2+ release, drop of the transmembrane potential, and efflux of matrix proteins. Interestingly, cyclosporin A was unable to inhibit triphenyltin-induced Ca2+ release. Based on these results it is proposed that the hyperpermeable state is produced by modification of 2.25 nmol of membrane thiol groups.

Animals↗
PubMed1994

On the role of ADP to increase the inhibitory effect of cyclosporin on mitochondrial membrane permeability transition.

This work reports an investigation which demonstrate that the addition of ADP is necessary to attain the protective effect of cyclosporin on the carboxyatractyloside-induced mitochondrial Ca2+ release. Evidence are presented which indicate that the effect of ADP is exerted by increasing the inhibitory action of cyclosporin on the enzyme cyclophilin.

Adenosine Diphosphate↗
PubMed1993

[Unilateral lung transplantation: the first 2 cases. Group of Lung Transplantation of the University General Hospital of the Vall d'Hebron].

Since 1983 unilateral lung transplantation has become a clinical reality. The initial experience of the Hospital General Universitario de la Vall d'Hebron is presented with the description of the two first unipulmonary transplants. The first was a 20 year-old woman with idiopathic pulmonary fibrosis in whom a left unipulmonary transplant was carried out and who, at present is at home following the 23rd postoperative month. The second case was a 27 year-old man with pneumoconiosis who, at 12 months following the left lung transplantation, carries on a normal life. Among the complications observed, the presence of pneumonitis by cytomegalovirus in both patients is of note. Stenosis and partial dehiscence of the bronchial suture in the first patient and isolation of syncitial respiratory virus in the second patient were also observed. The effort and integration into a normal life style of the second patient is excellent. In contrast, the first patient presents an important postoperative functional deterioration secondary to her complications. The present study demonstrates that unipulmonary transplantations is a reality in Spain which must be considered by all respiratory disease specialists in their daily clinical practise.

Adult↗
PubMed1993

Diagnostic value of bronchoalveolar lavage in peripheral lung cancer.

A prospective study has been performed to assess the value of the addition of bronchoalveolar lavage (BAL) to the routine bronchoscopic exploration with bronchial washing (BW) and postbronchoscopy sputum (PBS) procedures in the diagnosis of peripheral primary lung cancer not visible through bronchoscope when fluoroscopic guidance is not available. BW, BAL, and PBS were performed in 67 patients with suspected primary lung cancer by peripheral lung lesion on chest radiograph (39 nodules and 28 infiltrates) and nonendoscopically visible lesion. The sequence of procedures was in all cases BW, BAL, and post-bronchoalveolar lavage bronchoaspirate (PBBA). An attempt was made to collect early morning postbronchoscopy samples of sputum (PBS) on 3 consecutive days. BW and PBBA were collected in the same test tube, and the cytologic result was considered as BW diagnostic yield. If there were negative bronchoscopic results, either percutaneous fine-needle aspiration or open-lung biopsy were performed for diagnosis. Fifty-five patients were found to have malignant disease (23 adenocarcinomas, 22 squamous cell carcinomas, six small cell carcinomas, and four bronchioloalveolar cell carcinomas). BAL was positive in 18 of the 55 (33%) carcinomas, and it gave the only positive result in six (11%). BW was also positive in 18 of the 55 (33%), but it gave positive results in only 3 (5%). PBS was positive in 13 of the 43 (30%) patients from whom samples could be spontaneously obtained and were suitable for cytologic examination (not consisting of saliva), and gave the only positive result in three (7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Ionophoretic-like properties of ketorolac for calcium.

Ketorolac is an analgesic drug known to induce its therapeutic effect by inhibiting prostaglandin synthesis. In this work we introduce the nonsteroidal antialgesic drug as a compound with ionophoretic properties for calcium ions, showing that ketorolac induces mitochondrial Ca++ release. This reaction did not depend on an uncoupler-like action, because the drug does not collapse the internal negative membrane potential nor does it affect oxidative phosphorylation. In addition, it is shown that ketorolac ferries calcium ions into energized liposomes and has a hydrophobic phase with an affinity constant of 4 x 10(-3). The therapeutic action of ketorolac is related to its ionophoretic properties in addition to its well known inhibitory effect on the cyclooxygenase enzyme.

Animals↗
PubMed1991

[The hepatotoxicity of tuberculosis treatment].

BACKGROUND: The hepatic toxicity of antituberculous drugs used for the therapy of initial cases was evaluated, assessing the incidence and severity and its relation with each drug, age, other associated hepatic risks and the chronological time of therapy. METHODS: 1235 patients with tuberculosis were prospectively assessed with a protocol including periodical clinical and laboratory controls. RESULTS: Hepatic toxicity was found in overall 16.5%, with 3.5% of severe forms and need for a definitive change in therapy in 1.5%. Differences in toxicity between the 6-month and the 9-month schedules were not found. The most commonly incriminated drugs was isoniazid followed by pyrazinamide. All severe forms presented with symptoms, although some were nonspecific and insidious. Other associated hepatic risks implied an increased frequency of iatrogenic reactions. Age did not have a determining influence in severe forms, which predominantly developed within the first two months of therapy. CONCLUSIONS: Moderate, transient and asymptomatic increase in transaminase activity not requiring a change a therapy is common. Severe and dangerous forms are uncommon and predominate at the beginning of therapy and in persons with associated hepatic risk factors. Therefore, although the clinical controls should be maintained throughout treatment, laboratory controls should only be carried out during the first two months, except when symptoms are present or in patients with associated hepatic risk factors, where they should be more frequent and carried out throughout treatment.

Age Factors↗
PubMed1991

Inhibition of substrate oxidation in mitochondria by the peripheral-type benzodiazepine receptor ligand AHN 086.

The effects, of the benzodiazepines RO5-4864, AHN 086, PK 11195 and clonazepam on respiration of mitochondria from heart, kidney, and liver were studied. ADP-stimulated respiration of heart mitochondria was the most sensitive to inhibition by AHN 086; clonazepam was not inhibitory. Several respiratory chain segment activities of submitochondrial particles were insensitive to AHN 086, except for NADH oxidase which was partially inhibited. However, in contrast to submitochondrial particles, the succinate-cytochrome c oxidoreductase activity in intact mitochondria was inhibited by AHN 086, suggesting an effect at the substrate transport level. Phosphate-induced, succinate-dependent swelling was also inhibited by AHN 086 it was not affected by clonazepam. Uncoupled ATP hydrolysis was partially inhibited by RO5-4864, AHN 086, and clonazepam. It is suggested that there is an unspecific inhibition of NADH oxidase and ATP hydrolysis by these benzodiazepines and a specific inhibition on oxidizable substrate transport by the peripheral-type benzodiazepine AHN 086.

Adenosine Triphosphate↗
PubMed1991

Release of Ca2+ from heart and kidney mitochondria by peripheral-type benzodiazepine receptor ligands.

1. The effect of the benzodiazepines Ro5-4864, AHN 086 and clonazepam on the release of Ca2+ from rat heart and kidney mitochondria was studied. 2. The peripheral-type benzodiazepines Ro5-4864 and AHN 086 induced Ca2+ release which was blocked by Mg2+ whereas the central-type benzodiazepine clonazepam was ineffective. 3. An associated collapse of membrane potential and swelling were also induced by AHN 086 in the presence of Ca2+. 4. However, no oxidation of pyridine nucleotides or increased rate or respiration were observed. 5. Release of Sr2+ was induced by AHN 086 in the absence of inorganic phosphate but not in its presence. 6. These data are discussed in the context of the current hypotheses on the mechanism of mitochondrial Ca2+ release.

Animals↗
PubMed1989

Extensive Ca2+ release from energized mitochondria induced by disulfiram.

The effect of the alcohol-deterrent drug, disulfiram, on mitochondrial Ca2+ content was studied. Addition of this drug (20 microM) to mitochondria induces a complete loss of accumulated Ca2+. The calcium release is accompanied by a collapse of the transmembrane potential, mitochondrial swelling, and a diminution of the NAD(P)H/NAD(P) radio. These effects of disulfiram depend on Ca2+ accumulation; thus, ruthenium red reestablished the membrane delta psi and prevents the oxidation of pyridine nucleotides. The binding of disulfiram to the membrane sulfhydryls appeared to depend on the metabolic state of mitochondria, as well as on the mitochondrial configuration. In addition, it is shown that modification of 9 nmol -SH groups per mg protein suffices to induce the release of accumulated Ca2+.

Adenosine Diphosphate↗
PubMed1989

Induction of mitochondrial Ca2+ uptake by mersalyl.

1. The addition of mersalyl to aged mitochondria from rat kidneys, is followed by induction of an ATP-driven Ca2+ uptake which is sensitive to Ruthenium Red. 2. This Ca2+ influx requires Mg2+, albumin, and is accomplished by membrane energization. 3. The activation of Ca2+ uptake by the mercurial in the presence of ATP can be explained if it is assumed that the inorganic phosphate generated by ATPase activity, and trapped in the matrix by the thiol reagent, provides the negative potential which results in an electrophoresis cation influx.

Adenosine Triphosphate↗