PubMed Health⌕ Search

Biomedical subjects

M Repetto

Publications and source records attributed to M Repetto.

At least 73 records · Page 4Linked to original sources
PubMed1992

Isolation of a zinc finger motif (ZNF75) mapping on chromosome Xq26.

We report here the partial characterization of a new human zinc finger (ZNF75) gene of the Kruppel type mapping to the long arm of the X chromosome. A cosmid clone was isolated from a library specific to the Xq24-qter region by hybridization to a degenerate oligonucleotide representing the link between two contigous fingers of the C2H2 type. The sequence of the pertinent cosmid fragments demonstrated five consecutive zinc finger motifs, all pertaining to the Kruppel family. A reading frame starting at least 75 amino acids before the first zinc finger and ending 11 amino acids after the last one was identified; comparison with other ZF genes suggests that this genomic fragment represents the carboxy-terminal exon of the gene. Homology of approximately 55% in the zinc finger region was detected with many zinc finger genes including mouse Zfp-35 and human ZFN7 cDNA clones. Mapping using a panel of sematic cell hybrids and chromosomal in situ hybridization localized the gene to Xq26, in a region not previously known to contain zinc finger genes.

Amino Acid Sequence↗
PubMed1992

Acute intoxication by endosulfan.

The authors report six patients with acute endosulfan intoxication. The symptoms of nausea, vomiting, headache, and dizziness began 2.7 +/- 0.5 h after ingestion; in four cases the patients had been hospitalized but were asymptomatic. All had severe metabolic acidosis with high anion gap and hyperglycemia; five of six had decreased blood platelets. Three patients had pulmonary aspiration, and five required mechanical ventilation. The one fatality followed acute renal failure, disseminated intravascular coagulation, thrombi in the pulmonary arteries and aorta, and cardiogenic shock. In this patient the blood endosulfan was 2.85 mg/L versus a mean of 0.48 mg/L in the survivors.

Accidents↗
PubMed1991

Inhibition of microsomal lipid peroxidation by alpha-tocopherol and alpha-tocopherol acetate.

1. The antioxidant effects of alpha-tocopherol and alpha-tocopherol acetate were assayed for the (a) oxygen uptake, (b) chemiluminescence and (c) malondialdehyde formation, of tert-butyl hydroperoxide-supplemented rat liver microsomes. 2. Oxygen uptake was inhibited 60% by both alpha-tocopherol and alpha-tocopherol acetate with the half-maximal effect at 5 nmol tocopherol/mg protein. Chemiluminescence and malondialdehyde formation were equally inhibited 35% by both tocopherols with half-maximal effects at 2 nmol tocopherol/mg protein. 3. The rate of O2 uptake by tocopherol-supplemented microsomes was dependent on O2 concentration. A 60% inhibition by 5 nmol tocopherol/mg protein at 0.2 mM O2 is decreased to 5% inhibition at 0.6 mM O2. 4. The inhibition of O2 uptake, chemiluminescence and malondialdehyde formation indicate that both alpha-tocopherol and alpha-tocopherol acetate have similar effects as free radical traps in the hydrophobic domain of biomembranes. The different inhibition observed at different O2 concentrations indicate competition between vitamin E and O2 by unoxygenated lipid radicals.

Animals↗
PubMed1991

Red blood cell and total blood acetylcholinesterase and plasma pseudocholinesterase in humans: observed variances.

Although acetylcholinesterase is the target molecule of organophosphate poisoning, it is not always assayed in clinical evaluations which include only the determination of plasma or serum cholinesterase. In this paper we present observations on workers exposed to, or poisoned by, ethylparathion. Acetylcholinesterase decreased earlier and more intensely than cholinesterase, with the suggestion of an initial increase of acetylcholinesterase activity in newly exposed, workers. A simplified standard Ellman assay of total acetylcholinesterase activity of hemolyzed total blood correlated with that of washed erythrocyte acetylcholinesterase. All results were standardized to both red blood cell and hemoglobin concentration. Normal values in a group of unexposed subjects were acetylcholinesterase: 1225 +/- 181 nU x 10/RBC and 39.30 +/- 5.05 U/g Hb for men, 1321 +/- 234 nU x 10/RBC and 42.57 +/- 6.85 U/g Hb for women. Differences between total and erythrocyte acetylcholinesterase were not statistically significant. Plasma cholinesterase appeared to be decreased in pregnancy and increased in anesthesia, liver and kidney disease and neuropathologic conditions attributed to metal poisoning while total acetylcholinesterase was unaffected. The determination of both cholinesterase and acetylcholinesterase assists the evaluation of individuals exposed to or poisoned by organophosphate, the differentiation of other conditions affecting cholinesterase and the recognition of genetically atypical cholinesterase.

Acetylcholinesterase↗
PubMed1991

Death following crude oil aspiration.

This is a report on three deaths following oil aspiration by workers in petrol tankers. Lung aspiration was demonstrated by the presence of a yellowish-brown material in the alveolar spaces, which was difficult to identify by optic microscopy. Volatile hydrocarbons from petroleum were identified in lung samples by gas chromatography/mass spectrometry.

Cause of Death↗
PubMed1990

[Wine as a source of lead contamination: study in the southern region of Sevilla].

To assess whether the wines from the south of Sevilla constitute a source of lead intoxication we have prospectively studied the blood levels of lead in 100 healthy controls, 100 patients with alcoholic and nonalcoholic hepatopathy and at the same time the lead content in 135 samples of water and in 176 samples of alcoholic drinks consumed by the above patients. The results demonstrate: 1) presence of normal amounts of lead (mean +/- SD = 62 +/- 5 micrograms/l) in 97 of wines analyzed; 2) a higher content of lead in wines from areas close to the highway A-4 (100 +/- 10 micrograms/l) than in those from more remote zones (42 +/- 3 micrograms/l, p less than 0.005); and 3) although the blood levels of lead in alcohol consumers are not at the toxic range (22.9 +/- 8.9 micrograms/l) are, however, significantly higher (p less than 0.0007) than in patients with no alcohol intake (16.8 +/- 9.9 micrograms/l) or in healthy persons (17.1 +/- 7.4 micrograms/l, p less than 0.0008). Blood levels of lead correlate with the condition of "usual drinker" but not with the amount of alcohol consumed, number of cigarettes, lead content of water and wine, nor with the existence of severe hepatopathy among the studied factors. Our results suggest that alcohol influences the lead metabolism and that the usual drinkers constitute a risk population for saturnism.

Alcoholism↗
PubMed1990

Teratogenic effect of the cholesterol synthesis inhibitor AY 9944 on rat embryos in vitro.

AY 9944 [trans-1,4-bis(2-chlorobenzylaminomethyl) cyclohexane dihydrochloride] is an amphiphilic cationic molecule. This chemical is an established inhibitor of cholesterol synthesis and is teratogenic in rats. The mechanisms of this teratogenicity remain to be clarified. This study used cultured rat whole embryos to ascertain whether AY 9944 had a direct effect on embryos, or whether its action was indirect, via the maternal cholesterol metabolism. Four experimental conditions were investigated: (A) controls; (B) 10 day untreated embryos were cultured in serum of treated rats; (C) 10 day untreated embryos were cultured in serum containing added AY 9944 (0-1,000 micrograms/ml); and (D) 10 day embryos from females treated on day 4 of gestation were cultured in normal serum. In group B there was no growth retardation; some slight nonspecific abnormalities were not significant. In group C, direct addition of AY 9944 to culture medium retarded growth and differentiation in a dose-dependent manner. No malformation was observed, but histological examinations showed numerous areas of cell necrosis, especially in the CNS. In group D, not only was growth retardation observed, but also characteristic malformations of AY 9944 teratogenesis, including pituitary agenesis. These results show that AY 9944 teratogenicity is initiated prior to day 10.

Abnormalities, Drug-Induced↗
PubMed1990

Autoinduction of rifabutin metabolism in man.

1. The pharmacokinetics of the antimycobacterial agent rifabutin were studied in healthy volunteers, following single (450 mg) and repeated (450 mg once daily for 10 days) oral administration. 2. After repeated administration, induction of metabolism was indicated by lower AUC and Cmin values, compared to the corresponding theoretical values. The elimination half-life was unchanged after repeated administration. 3. Induction of presystemic extrahepatic metabolism, which seems to be important in the availability of rifabutin, should be mainly responsible for the decrease in the AUC observed, while induced systemic clearance (if any) should be of minor importance. 4. Induction of presystemic extrahepatic metabolism after repeated administration has also been reported for rifampicin, an antibiotic agent with hepatic enzyme-inducing properties, which has a structure similar to rifabutin but a different pharmacokinetic profile.

Adult↗
PubMed1990

[Tobacco and arterial pressure (I.). The hormonal changes in a model of acute nicotine overload].

42 persons with normal blood pressure were studied. Only 31 of them were smokers. We did not find any differences in the basal blood pressure, heart rate, ACTH nor cortisol levels, but there were significant differences in the levels of biological markers of tobacco (cotinine and nicotine). When the smokers were induced to smoke 2 cigarettes which had 2.2 mg of nicotine, we observed an increase in the diastolic and systolic blood pressure as well as the heart rate, plasma levels of ACTH (basal: 21.61 +/- 12.52, 10 minutes: 28.06 +/- 21.01, p less than 0.05; 20 minutes: 26.06 +/- 18.56 ng/ml) and cortisol (basal: 14.56 +/- 3.84; 10 minutes: 14.60 +/- 4.7; 20 minutes: 16.55 +/- 6.61 ug/dl, p less than 0.01). At the same time, the nicotine and cotinine levels were significantly higher (p less than 0.0001) and correlated. Our results suggest that apart from the adrenergic response to tobacco exposure, nicotine can produce other hormonal changes which affect the regulating systems of blood pressure. Nicotine and cotinine are the election biological markers to monitor the response to passive or active tobacco smoke inhalation.

Adrenocorticotropic Hormone↗
PubMed1990

Study of delayed neurotoxicity caused by fatty acid anilides in hens.

We have observed that the oral administration of a single dose of a mixture of oleyl and linoleylanilides (80 mg/kg) in adult hens determines the apparition of delayed muscular neuropathy, which we have compared to that induced by metamidophos as a model of organophosphate-induced delayed neuropathy (OPIDN). We have compared the modifications produced by each of the 2 treatments on the enzymatic activity of neuropathy target esterase (NTE) measured in nervous tissue homogenates of brain, medulla and sciatic nerve. In addition we determined total esterases (TE), acetylcholine esterase (AchE) and serum creatine phosphate kinase (CPK). The organophosphate compound (OP) induced an initial reduction in the activity of NTE, TE and AchE which was reestablished 48 h later, except for brain TE which increased slowly during the latency period. This behaviour was accompanied by a permanent increase in the activity of serum CPK. Anilides induced a strong activation of AchE, NTE and TE (except brain TE) in the first 24-36 h. Normal levels were relatively quickly reestablished in brain (by 48 h) and slowly in medulla and sciatic nerve. But the AchE activity remained high throughout the whole period of latency. This activity level coincided with the AchE level observed at the onset of signs in animals dosed with OPs. CPK was also increased in sciatic nerve at 15 d but was depressed in serum throughout the whole latency period. Substances with chemical characteristics very different from OPs can induce a delayed neuropathy with modification of the activity of NTE.

Acetylcholinesterase↗
PubMed1990

In vitro modifications of rat NTE and other esterases by chemicals which induce delayed neurotoxicity in vivo.

A rat in vitro model has been developed which permits direct study of the biochemical mechanisms involved in delayed neurotoxicity induced by any chemical compound, not only organophosphates. Using rat brain homogenate, a parallel study on the activity of neurotoxic esterase (NTE) and total esterases (TE) compared the action of metamidophos, which is known to induce delayed neurotoxicity, and the synthetic fatty acid anilides, oleylanilide and linoleylanilide. Inhibition in the activity of NTE and TE, unrelated to the concentration and the incubation time assayed, was caused by metamidophos, while the anilides showed a 2-phase concentration-time dependent behaviour. This confirmed the results we previously obtained in vivo. In both cases the appearance of delayed neuropathy was related to modification of NTE activity. We concluded that phosphorylation of the enzyme may not be the only biochemical requirement for the development of delayed neurotoxicity syndromes in which modification of NTE is produced.

Anilides↗
PubMed1989

Lung embolism with liquid silicone.

A lung embolism was reported in a case involving death following repeated injections of liquid silicone for aesthetic reasons. The liquid extracted from the sites of injection was identified as methylsilicone using infrared spectrophotometry, and the presence of silicone in vacuoles in the lung was verified by scanning electron microscopy with energy dispersive X-ray analysis (EDXA). A study has been carried out with rats after intravenous and subcutaneous injections of methylsilicone.

Adult↗