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M Moret

Publications and source records attributed to M Moret.

10 recordsLinked to original sources
PubMed2002

Equation of state data for iron at pressures beyond 10 Mbar.

We present equation of state points for iron, in the pressure range 10-45 Mbar, the first obtained with laser-driven shock waves. The experiment has been performed with the high energy laser Phebus, optically smoothed with Kinoform phase plates. Our results double the set of existing experimental data at very high pressures showing good agreement with the predictions of the quotidian equation of state model and with previous results.

Journal Article↗
PubMed1999

[Re]

A chair conformation comparable to that observed for six-membered rings composed of tetrahedral carbon atoms is found for the cluster anion [Re(6)(µ-H)(5)(CO)(24)](-) (see picture; black spheres: Re, white spheres: µ-H; CO ligands omitted for clarity) in spite of the octahedral coordination at the Re centers. This is the first example of a carbonyl cluster exhibiting a cyclohexane-like geometry of the metallic framework.

Journal Article↗
PubMed1992

In vitro metabolism of bladder carcinogenic nitrosamines by rat liver and urothelial cells.

In order to establish the importance of the target organ in the activation of bladder carcinogens, we compared rat liver and urothelial cell alpha-hydroxylation activities using as substrates N-nitrosobutyl(4-hydroxybutyl)amine and its metabolite N-nitrosobutyl(3-carboxypropyl)amine, two potent urinary bladder carcinogens in animals. Previous studies have shown that the production of molecular nitrogen can serve as an indicator of nitrosamine alpha-hydroxylation. The use of doubly 15N-labelled nitrosamines and the gas chromatography-mass spectrometric detection of 15N2 formed gives a measurement of the extent of this metabolic step. Various amounts of 15N-labelled substrates were incubated for 60 min at 37 degrees C with rat liver S9 preparations or urothelial cell homogenates in the presence of a NADPH generating system. Both enzyme sources metabolized 15N-labelled N-nitrosobutyl(4-hydroxybutyl)amine and N-nitrosobutyl(3-carboxypropyl)amine through the alpha-hydroxylation pathway. Using hepatic S9 fractions, 15N2 production from 15N-labelled N-nitrosobutyl(4-hydroxybutyl)amine increased from 1.69 +/- 0.02 nmol/h per mg protein (mean +/- S.E.) to 5.78 +/- 0.5 with substrate concentrations ranging between 0.55 and 5.55 mM. 15N2 produced by urothelial cell homogenates was about 40-50% that of the liver S9. 15N-labelled N-nitrosobutyl(3-carboxypropyl)amine was also metabolized through the alpha-hydroxylation pathway both by hepatic S9 and urothelial cell homogenates, though to a lesser extent. 15N2 production was about 10-times less than from 15N-labelled N-nitrosobutyl(4-hydroxybutyl)amine, but again urothelial cell 15N2 production was about 40-50% that of the liver. Treatment with phenobarbital resulted in a 2.7-fold increase in the 15N2 produced from 15N-labelled N-nitrosobutyl(4-hydroxybutyl)amine by hepatic S9. No effect was observed with urothelial cell homogenates. Acetone treatment had no effect on 15N2 production from 15N-labelled N-nitrosobutyl(4-hydroxybutyl)amine by hepatic S9, but raised 15N2 production by urothelial cell homogenates 1.8 times. Although the liver has a greater capacity than the bladder for activating the 15N-labelled nitrosamines studied, the target organ can metabolize bladder carcinogens, thus increasing the possibility of a local toxic effect. Moreover, the distribution of P-450 isozymes might be different in the bladder and this could affect the metabolism of nitrosamines reportedly formed in the human bladder in some pathological conditions.

Acetone↗
PubMed1991

Renal and urinary lipid changes associated with an acutely induced renal papillary necrosis in rats.

A single dose of 2-bromoethanamine hydrobromide (BEA; 100 mg/kg body weight) given ip to male Wistar rats causes an acute renal papillary necrosis in 24 hr. Oil Red O (ORO) lipid staining is normally confined to the polyunsaturated lipid droplets of the medullary interstitial cells, but ORO-positive material was present in the endothelial cells of the vasa recta 7 hr after BEA treatment. At 24 hr (by which time papillary necrosis had developed), there were also markedly increased quantities of lipid in the cells of the collecting ducts and covering epithelia. At 48 hr totally necrosed areas stained heavily with ORO, and lipid deposits were particularly numerous in the hyperplastic urothelia adjacent to the necrosed region. Epithelial and endothelial accumulation of lipid material also extended into areas of the juxtamedulla and cortex, which appeared normal by routine haematoxylin and eosin staining. Lipid staining is more selective and sensitive for identifying papillary necrosis than routine histology, because neither hexachlorobutadiene-, aminoglycoside-, cis-platin- nor polybrene-induced lesions produce similar histochemical changes. This suggests that the capillary and epithelial deposits of lipid material are pathognomonic for the development of renal papillary necrosis. An increase in urinary triglycerides following BEA treatment supports the biochemical basis of these ORO changes as a neutral lipid accumulation.

Acute Disease↗
PubMed1991

N-Nitrosobutyl(4-hydroxybutyl)amine alpha-hydroxylation by rat liver and urothelial cell homogenates.

Determination of molecular nitrogen formed as a consequence of nitrosamine alpha-hydroxylation provides a useful means for studying the extent of activation of these compounds in target and nontarget organs and tissues. alpha-Hydroxylation in rat liver and urothelial cells was compared using as substrate doubly 15N-labelled N-nitrosobutyl(4-hydroxybutyl)amine (15N-NBHBA), a potent bladder carcinogen in rodents. Both enzyme sources metabolized 15N-NBHBA through the alpha-hydroxylation pathway. 15N2 production was dependent on the amount of substrate incubated. Vmax values for 15N2 production by urothelial cells and by liver postmitochondrial supernatant were 4.47 and 3.21 nmol/mg protein per h, respectively.

Animals↗
PubMed1990

Determination of O6-butylguanine in DNA by immunoaffinity extraction/gas chromatography-mass spectrometry.

A sensitive, specific, and rapid method for quantitating the minor adduct O6-butylguanine (O6BuG) in hydrolyzed DNA has been developed by combining immunoaffinity chromatography and high resolution gas chromatography-negative ion chemical ionization-mass spectrometry. Polyclonal antibodies raised against O6BuG were coupled to CNBr-activated Sepharose 4B and used for sample clean-up and extraction of the specific O6-alkylguanine. After addition of O6BuG and its deuterium labeled analogue (O6BuG-D7), used as internal standard, hydrolyzed DNA was applied on the immunoaffinity column and washed with water, and the immunoadsorbed butylated guanines were eluted with acetone/water cetome/water (95/5) before gas chromatographic derivatization. O6BuG and O6BuG-D7 were analyzed and quantitated by high resolution gas chromatography-negative ion chemical ionization-mass spectrometry as their pentafluorobenzyl-trimethylsilyl derivatives. Immunoaffinity column capacity and O6BuG recovery from this column were 1.53 nmol O6BuG/column and 62 +/- 5%, respectively. The method was applied to evaluate O6BuG levels in DNA butylated in vitro with 10 mM N-nitroso-Nr-butylurea or isolated from rats given an i.p. dose of 185 mg/kg N-nitroso-N-butylurea or N-nitrosodibutylamine. In the first case the level of modifications present in calf thymus DNA was 104 mumol O6BuG/mol guanine, and in the second case O6BuG in liver DNA was about 6 times higher after N-nitroso-N-butylurea (2.11 mumol O6BuG/mol guanine) than after N-nitrosodibutylamine (0.34 mumol O6BuG/mol guanine) treatment. These results indicate that O6BuG formed in vivo can be isolated and quantitated by this method, which may also be useful for studying DNA damage and repair mechanisms.

Animals↗
PubMed1990

Cytogenetic analysis of malignant mesothelioma.

Cytogenetic analyses of 40 confirmed malignant mesotheliomas (MMs) are reported. Pleural effusion cells were studied in 90% of the cases by direct method or after culture or both. Biopsy and ascites fluid were also analyzed in some patients. A normal karyotype was found in nine cases, and complex karyotypic abnormalities were observed in 30 cases. In one case, analyzable metaphases were not obtained. The chromosomal changes were all complex and heterogeneous; no consistent presumably specific abnormality was detected. Nevertheless, two main patterns of nonrandom abnormalities were observed: 1) loss of chromosomes 4 and 22, 9p, and 3p in the most of the abnormal cases and corresponding to a hypodiploid and/or hypotetraploid modal chromosome number; and 2) gain of chromosomes 7, 5, and 20 with deletion or rearrangement of 3p as well in the hyperdiploid cases, which were a minority in our series. These findings are discussed in view of other reported cytogenetic studies of MM, asbestos exposure, and possible mechanisms of malignant transformation.

Adult↗
PubMed1990

A novel variant of the bcr-abl fusion product in Philadelphia chromosome-positive acute lymphoblastic leukemia.

Two patients with Philadelphia chromosome-positive acute lymphoblastic leukemia showed novel variants of the chimeric bcr-abl mRNA. The bcr-abl breakpoint region on cDNA derived from the chimeric mRNA was amplified using the polymerase chain reaction (PCR). Sequence analysis of the breakpoint-containing fragment showed that in both patients exon a2 of the abl gene was deleted, giving rise to an in-frame joining at the mRNA level of 5' bcr sequences to the abl exon a3. These findings were confirmed by Southern blot analysis and cloning of chromosomal DNA. Protein studies showed a bcr-abl protein with heightened tyrosine kinase activity in blast cells of both patients: one of the P190 type, the other of the P210 type. The significance of these findings and the role of this new type of translocation in the disregulation of the abl gene are discussed.

Adult↗