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Biomedical subjects

G Durand

Publications and source records attributed to G Durand.

At least 109 records · Page 6Linked to original sources
PubMed1995

Trace determination of herbicides in estuarine waters by liquid chromatography-high-flow pneumatically assisted electrospray mass spectrometry.

High-flow pneumatically assisted electrospray (ESP) was applied to the characterization of triazine (atrazine, simazine, ametryne, cyanazine, deethylatrazine and deisopropylatrazine), phenylurea (chlortoluron++, isoproturon, diuron, linuron and diflubenzuron) and other priority herbicides (alachlor, metolachlor). In LC-ESP-MS the [M+Na]+ ion was used as the base peak in most cases, with the exception of chlorotriazines, which showed [M+H]+ as the base peak. When LC-TSP-MS was used, [M+H]+ was the base peak for many of the pesticides, with the exception of linuron and diflubenzuron, which showed [M+NH4]+ as the base peak. The ESP results were compared with those obtained with thermospray (TSP). LC-TSP-MS offered greater sensitivity for triazines than phenylurea herbicides, whereas the use of LC-ESP-MS offered an enhancement in sensitivity for phenylurea herbicides. As regards the fragmentation obtained using both techniques, ESP offered a considerable amount of structural information for the different chlorotriazines studied when the extraction voltage was increased from 20 to 40 V. Liquid-liquid extraction with dichloromethane was used for the trace enrichment of the different herbicides in estaurine water samples from the Elorn river (France). The presence of the different triazine metabolites, atrazine, simazine, metolachlor, isoproturon and diuron was confirmed by both LC-MS techniques.

Chromatography, High Pressure Liquid↗
PubMed1995

Effect of low levels of dietary fish oil on fatty acid desaturation and tissue fatty acids in obese and lean rats.

The effect of very low levels of dietary long-chain n-3 fatty acids on delta 6 desaturation of linoleic acid (18:2n-6) and alpha-linolenic acid (18:3n-3), and on delta 5 desaturation of dihomo-gamma-linolenic acid (20:3n-6), in liver microsomes and its influence on tissue fatty acids were examined in obese and lean Zucker rats and in Wistar rats. Animals fed for 12 wk a balanced diet containing ca. 200 mg of long-chain polyunsaturated n-3 fatty acids per 100 g of diet were compared to those fed the same amount of alpha-linolenic acid. Low amounts of long-chain n-3 fatty acids greatly inhibited delta 6 desaturation of 18:2n-6 and delta 5 desaturation of 20:3n-6, while delta 6 desaturation of 18:3n-3 was not inhibited in Zucker rats and was even stimulated in Wistar rats. Inhibition of the biosynthesis of long-chain n-6 fatty acids was reflected in a decrease in arachidonic acid (20:4n-6) content of serum lipids when fasting, and also in the phospholipid fatty acids of liver microsomes. On the contrary, heart and kidney phospholipids did not develop any decrease in 20:4n-6 during fish oil ingestion. Docosahexaenoic acid (22:6n-3), present in the dietary fish oil, was increased in serum lipids and in liver microsome, heart, and kidney phospholipids.

Animals↗
PubMed1995

Time-course study of adipose tissue fatty acid composition during mammary tumor growth in rats with controlled fat intake.

Previous work in breast cancer patients has indicated an inverse relationship between the risk of relapse and the alpha-linolenic acid (18:3n-3) level in adipose breast tissue. To determine whether low alpha-linolenic levels in patients with aggressive breast cancer resulted from lower 18:3n-3 dietary intake and/or increased metabolism of stored 18:3n-3, we analyzed the fatty acid composition of mammary adipose tissue during tumor growth in a rat model of mammary carcinogenesis. Rats were fed a diet containing 10% fat as rapeseed oil (in which 9% of total fatty acids is 18:3n-3). one-half of the rats received an injection of nitrosomethylurea (NMU) to initiate mammary tumors. In control and NMU-treated groups, three to five animals were sacrificed every three weeks during the five-month experimental time. tumor growth was followed by weekly palpation of the animals and by the measure of total tumor mass and number in sacrificed rats. Mammary tumor and adipose tissues were sampled in sacrificed rats. We found that although mammary adipose tissue fatty acid profile changed throughout the experiment, there was no difference in fatty acid profile between control and NMU-treated rats of the same age. In the NMU-treated group, 18:3n-3 level remained identical throughout the experimental period, irrespective of tumor burden. These data show that, in this model, mammary tumor growth does not modify stored fatty acid levels, including 18:3n-3. this suggests that decreased 18:3n-3 level in patients with poor prognosis is not a consequence of tumor burden but more likely depends on decreased dietary intake.

Adipose Tissue↗
PubMed1995

Dietary polyunsaturated fatty acids and aging modulate glutathione-related antioxidants in rat liver.

The effects of dietary polyunsaturated fatty acids (PUFA) on the age-dependent changes in liver glutathione antioxidant system were investigated in male Wistar rats fed diets supplying either balanced amounts of linoleic acid and alpha-linolenic acids (control) or deficient in alpha-linolenic acid [n-3) deficient]. The animals were studied at the age of 6 or 24 mo. Glutathione antioxidative metabolism was markedly affected by aging. Cytosolic concentration of reduced glutathione (GSH) was lower (P < 0.01), whereas that of oxidized glutathione (GSSG) as well as the GSSG:GSH ratio were greater (P<0.001) in the 24-mo-old as compared with the 6-mo-old rats, regardless of the diet. Glutathione peroxidase activities were lower (P < 0.001) in 24-mo-old rats, though more markedly in those fed the control diet. The lipid composition of rat liver microsomal membranes was strongly modified by both diet and aging. The age-related changes mainly involved the polyunsaturated fatty acids. These results suggest that the nature of dietary PUFA and not only their degree of unsaturation affects the cellular glutathione-dependent antioxidant system and thus may modify the age-related changes in metabolic reactions.

Aging↗
PubMed1995

Effect of early dietary deficiency in polyunsaturated fatty acids on two lectin binding sites in the small intestine of postweanling rats.

This study was designed to determine whether dietary lipids influence the development of intestinal cell glycosylation, in relationship to diet-induced changes in phospholipid fatty acid composition. The ability of two different lectins, wheat germ agglutinin (WGA) and Maackia amurensis agglutinin (MAA), to combine specifically with particular carbohydrate residues was used to investigate the surface characteristics of epithelial cells of rats fed different dietary lipids from birth to 6 weeks of age. Diets contained 5% (weight) peanut oil (PO), rich in n-6 fatty acids; salmon oil (SO), rich in n-3 fatty acids; hydrogenated palm oil (HPO), deficient in both n-6 and n-3 fatty acids or a PO and rapeseed oil (RO) mixture (PRO), the control diet. Pieces of jejunal and ileal villi were excised from postweanling rats and prepared for lectin histochemical study. Concurrently, epithelial cells were removed from jejunal and ileal segments for determining their phospholipid fatty acid compositions. Polyunsaturated fatty acid (PUFA) deficiency was evidenced in the HPO group by the appearance of eicosatrienoic acid (20:3n-9) in both jejunal and ileal phospholipids, which paralleled the decrease in arachidonic acid content. Accretion of 18:1n-9 and 20:3n-9 in cell phospholipids of group HPO was not sufficient to match the unsaturation level in rats fed nonhydrogenated vegetable oils (PRO, PO) or fish oil (SO). The lectin histochemical study showed that WGA strongly labelled the brush border membrane microvilli whereas binding of MAA was specific to goblet cells and mucus. Regardless of the type of diet, WGA binding was weaker in the ileum than in the jejunum. In comparison to all other groups, WGA-labelling of villi was less intense in the jejunum and disappeared almost completely in the ileum of HPO-fed rats. Although SO- and PO-fed rats had, respectively, very low and high ratios of n-6 to n-3 in their intestinal phospholipids, binding of WGA in both groups was not markedly different from that in the control (PRO). MAA-labelling was very intense in jejunal and ileal villi of n-3-fed (SO) rats, whereas it was strongly attenuated in the n-3- and n-6 deficient (HPO) group. These results suggest that intestinal glycosyltransferase activities involved in cell differentiation were altered relative to the overall unsaturation index of dietary fatty acids. Alterations of epithelial glycosylation mainly resulted from a drop in total n-6 and n-3 fatty acids, although it may be speculated that there is a specific effect of n-3 fatty acids.

Animals↗
PubMed1995

Comparison of recovery of previously depressed hepatic delta 6 desaturase activity in adult and old rats.

The ability to recover hepatic delta 6 desaturase (delta 6D) activity with linoleic acid as substrate was compared in adult and old rats. Male rats fed a diet deficient in alpha-linolenic acid were used either at 6 or 21 months. From these two ages onward, animals were fed a diet containing 10% fish oil for 3 months to reduce delta 6D activity. After this period, some of the animals were killed. The other animals were returned to the original diet deficient in alpha-linolenic acid. Fatty acid composition in liver and brain and hepatic delta 6D activity were analysed 3 and 7 days after the change in diet. When rats were fed the diet containing 10% fish oil, delta 6D activity was lower than in those fed the diet deficient in alpha-linolenic acid. The liver fatty acid composition was altered with disappearance of 22:5 n-6 and a decrease in 18:2 n-6, 20:4 n-6 and 22:4 n-6 accompanied by an increase in 20:5 n-3, 22:5 n-3 and 22:6 n-3. When rats were re-fed the original diet, delta 6D activity returned after 3 days to its initial level in the 9-month-old rats; in 24-month-old animals, recuperation was incomplete. The level of 20:4 n-6 and 18:2 n-6 increased in the liver concurrently with a decrease in levels of 20:5 n-3, 22:5 n-3 and 22:6 n-3. In both age groups, the brain fatty acid profile remained unchanged 7 days after returning to the diet deficient in alpha-linolenic acid.

Aging↗
PubMed1995

[Pulmonary embolism: contribution of spiral x-ray computed tomography].

PURPOSE: Spiral computed tomography was compared retrospectively with digital subtraction pulmonary angiography (PA) in 45 patients suspected of having acute or chronic pulmonary embolism. MATERIALS AND METHODS: 45 patients in whom the presence of acute or chronic pulmonary embolism was suspected underwent examination by spiral CT and PA. Diagnosis of pulmonary embolism was based on the direct visualization of intraluminal clots. The study of the agreement between the two methods was based on the Kappa test. In 35 cases, pulmonary emboli were proved. Acute pulmonary emboli were present in 28 cases and chronic in 7 cases. RESULTS: Spiral computed tomography represents an excellent way to detect acute pulmonary embolism. In the chronic form, spiral CT is better than PA to detect intraluminal clots. However, Spiral CT can fail to detect small embole in the peripheral arterial bed. In the 10 patients without pulmonary embolism, the spiral CT proved diagnosis pulmonary oedema (n = 3), lymphangitic carcinoma (n = 4), pleural effusion (n = 3). CONCLUSION: This study suggest that the spiral CT examination is accurate for diagnosis of pulmonary embolism specifically in case of suspected important embolism. The advantages of spiral CT are multiple (non invasive, wide diagnosis spectrum). However, may be a limitation to is use is insufficient distal thrombi detection. This eventuality (5 to 10% in the Pioped study) justify the practice of pulmonary angiography. Spiral CT improvements should reduce this insufficiency in the next future.

Acute Disease↗
PubMed1994

Riluzole and experimental parkinsonism: antagonism of MPTP-induced decrease in central dopamine levels in mice.

We have investigated whether riluzole, a compound that interferes with glutamatergic (GLUergic) transmission, would protect central dopaminergic (DAergic) neurones from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced toxicity in the striatum in mice. MPTP decreased DA, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels. Riluzole protected against the MPTP-induced decrease in DA levels. The utilization of DA ([DOPAC+HVA]/DA) was increased after MPTP treatment, but returned to control values in mice given riluzole in combination with MPTP. Riluzole did not confer protection by inhibiting either monoamine oxidase type B activity or DA uptake. Possible mechanisms involved in the protective action of riluzole are discussed. Our results show that riluzole antagonizes the DAergic neurotoxicity of MPTP, a pro-parkinsonian neurotoxin, in mice.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1994

Transcriptional regulation of rat alpha 1-acid glycoprotein gene by phenobarbital.

Phenobarbital induces gene transcription of both cytochrome P450IIB (the barbiturate-inducible cytochrome P450 in mammals) and alpha 1-acid glycoprotein, one of the major acute-phase proteins in rats and humans. Analysis of the 5'-regulatory sequences of cytochrome P450IIB and alpha 1-acid glycoprotein genes in rats revealed the presence of a consensus sequence of 10 base pairs, termed the phenobarbital-responsive element or Barbie box, located in a region extending from positions -136 to -127 from the transcription start site of the alpha 1-acid glycoprotein gene. A 17-base pair oligonucleotide probe specific for alpha 1-acid glycoprotein and including the consensus sequence showed, in mobility shift assays, slight binding to liver nuclear protein from untreated animals. This binding was strongly and specifically increased with protein extracts from phenobarbital-treated rats. Transfection of rat primary hepatocytes with the pAGPcat construct induced basal expression of chloramphenicol acetyltransferase activity, which was increased by phenobarbital and dexamethasone treatment of cells. Induction of chloramphenicol acetyltransferase activity by phenobarbital was abolished when hepatocytes were transfected by constructs with a mutation or deletion of the Barbie box sequence. These results strongly suggest that the Barbie box sequence is involved in alpha 1-acid glycoprotein gene regulation by phenobarbital.

Animals↗
PubMed1994

Induction of rat alpha-1-acid glycoprotein by phenobarbital is independent of a general acute-phase response.

Phenobarbital (PB) induces transcription of the alpha 1-acid glycoprotein (AGP) gene, one of the major positive acute-phase proteins, the expression of which is controlled by a specific combination of glucocorticoids and cytokines. This raises questions as to the involvement of glucocorticoids and cytokine pathways in the PB-mediated effect on AGP gene expression. We found that the pattern of whole-serum proteins in PB-treated rats differed markedly from that observed during a typical acute inflammatory response (in turpentine-treated rats): levels of some positive acute-phase proteins (APP) increased slightly (alpha 1-acid glycoprotein, haptoglobin, hemopexin and T-kininogen), while levels of alpha 2 macroglobulin, the most sensitive marker of the acute-phase reaction, decreased. Among the negative APP, neither albumin nor prealbumin decreased while CBG increased. The cytokines involved in AGP gene regulation (mainly IL1, IL6 and TNF alpha) do not therefore seem to mediate the effect of PB on acute-phase protein expression. Glucocorticoid involvement is also ruled out by the observed enhancement of the effect of PB on AGP expression in adrenalectomized animals. Our results suggest that phenobarbital acts on AGP expression by a mechanism independent of the inflammatory pathway.

Acute-Phase Reaction↗
PubMed1994

Secretion of alpha 1-antitrypsin by alveolar epithelial cells.

We have investigated the ability of alveolar epithelial cells (human A549 cell line and rat type-II pneumocytes) to produce alpha 1-antitrypsin (AAT). Northern blot analysis demonstrated the presence of an AAT-specific mRNA transcript in A549 cells. Unstimulated A549 cells secreted immunoreactive AAT at a rate of 0.51 +/- 0.04 ng/10(6) cells/h, with a modified glycosylation compared to serum AAT. AAT formed a complex with neutrophil elastase. Rat type-II pneumocytes secreted immunoreactive AAT. Our results suggest that alveolar epithelial cells could participate in antiprotease defense within the lung through local AAT production.

Amidohydrolases↗
PubMed1994

Differential secretion of alpha 1-acid glycoprotein occurs in the Golgi complex of isolated rat hepatocytes. Evidence of partial retention in the Golgi.

Using weakly basic amines, we investigated the step at which the secretion kinetics of concanavalin-A-retained and nonretained alpha 1-acid glycoprotein glycoforms diverge in isolated rat hepatocytes. Both chloroquine and primaquine, whose action on protein secretion is targeted to terminal domains of the Golgi apparatus, cancelled the kinetic difference without influencing carbohydrate chain sialylation. To test for a possible interaction of alpha 1-acid glycoprotein with Golgi membranes, we also permeabilized control and primaquine-treated hepatocytes, as well as purified Golgi preparations, with saponin. In each case, we found that alpha 1-acid glycoprotein was associated with Golgi membranes, the association being more marked in primaquine-treated cells than in control cells. Membrane-bound alpha 1-acid glycoprotein appeared to be preferentially retained on concanavalin A. Such retention could account for the divergent secretion kinetics of alpha 1-acid glycoprotein glycoforms.

Animals↗
PubMed1994

Phenobarbital induction of alpha 1-acid glycoprotein in primary rat hepatocyte cultures.

The serum level of rat alpha 1-acid glycoprotein is significantly increased by treatment with phenobarbital, and in vivo studies have shown that phenobarbital seems to act mainly at the transcriptional level. To show the direct mediating effect of phenobarbital on alpha 1-acid glycoprotein gene expression, we investigated the ability of primary cultured rat hepatocytes to respond to in vitro phenobarbital administration. Phenobarbital increased both alpha 1 acid glycoprotein secretion and corresponding mRNA levels in primary rat hepatocytes cultured on matrigel. Used in combination with interleukin-1, interleukin-6 and dexamethasone, phenobarbital had an additive or synergistic effect on alpha 1-acid glycoprotein synthesis. These results show that (a) phenobarbital acts directly on hepatocytes by increasing alpha 1-acid glycoprotein gene expression and (b) this effect is mediated by a specific mechanism independent of pathways involved in alpha 1-acid glycoprotein induction by interleukin-1, interleukin-6 and glucocorticoids.

Animals↗
PubMed1994

Alteration in membrane lipid order and composition in metabolically hyperactive fatty rat adipocytes.

We have previously shown that adipose cells from young genetically obese Zucker rats are characterized by very high metabolic activity together with an increase in a wide range of membrane-mediated functions. The aim of the present study was to examine whether the physical properties of the membranes and the composition of the membrane lipids were altered in these cells. Plasma membranes and two intracellular membrane fractions were prepared by differential ultracentrifugation from inguinal adipose cells of 30-day-old obese (fa/fa) and lean (Fa/fa) littermates. The lipid order as measured by steady-state fluorescence polarization of diphenylhexatriene used as probe was markedly decreased in the plasma membranes of obese rat adipose cells. Consistent with this, the cholesterol-to-phospholipid ratio was significantly decreased, and the degree of unsaturation of the phospholipid fatty acids was significantly increased. In intracellular membranes, none of these parameters were altered by the different genotype. In fat cells from obese rats, both plasma and intracellular membranes exhibited a 2-fold decrease in the ratios of n-6/n-3 fatty acids mainly due to an enrichment in docosahexaenoic acid (22:6n-3). The data show that the fatty genotype is a determinant of membrane lipid order and composition in adipose cells. The alterations reported here for young obese Zucker rat adipocytes might be related to the metabolic hyperactivity of these cells.

Adipose Tissue↗
PubMed1994

Effect of dietary n-3 and n-6 polyunsaturated fatty acids on lipid-metabolizing enzymes in obese rat liver.

This study was designed to examine whether n-3 and n-6 polyunsaturated fatty acids at a very low dietary level (about 0.2%) would alter liver activities in respect to fatty acid oxidation. Obese Zucker rats were used because of their low level of fatty acid oxidation, which would make increases easier to detect. Zucker rats were fed diets containing different oil mixtures (5%, w/w) with the same ratio of n-6/n-3 fatty acids supplied either as fish oil or arachidonic acid concentrate. Decreased hepatic triacylglycerol levels were observed only with the diet containing fish oil. In mitochondrial outer membranes, which support carnitine palmitoyltransferase I activity, cholesterol content was similar for all diets, while the percentage of 22:6n-3 and 20:4n-6 in phospholipids was enhanced about by 6 and 3% with the diets containing fish oil and arachidonic acid, respectively. With the fish oil diet, the only difference found in activities related to fatty acid oxidation was the lower sensitivity of carnitine palmitoyltransferase I to malonyl-CoA inhibition. With the diet containing arachidonic acid, peroxisomal fatty acid oxidation and carnitine palmitoyltransferase I activity were markedly depressed. Compared with the control diet, the diets enriched in fish oil and in arachidonic acid gave rise to a higher specific activity of aryl-ester hydrolase in microsomal fractions. We suggest that slight changes in composition of n-3 or n-6 polyunsaturated fatty acids in mitochondrial outer membranes may alter carnitine palmitoyltransferase I activity.

Animals↗