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S Salmon

Publications and source records attributed to S Salmon.

At least 55 records · Page 3Linked to original sources
PubMed1990

[The modification of high density lipoproteins by malondialdehyde changes their interaction with J774 macrophages and decreases cholesterol cell efflux].

The treatment of HDL3 with malondialdehyde (MDA) results in an increase of the electrophoretic mobility of the particle and in aggregation of the apolipoprotein AI. The binding of MDA-treated-HDL3 to murine macrophages J774 is decreased, as compared to native HDL3. The cholesterol efflux is also markedly reduced. In view of the fact that MDA is produced following plaquette aggregation or oxidative stress, the eventual existence of MDA-modified-HOL in vivo might accelerate the appearance of atherosclerotic lesions by reducing cellular cholesterol efflux.

Animals↗
PubMed1989

Carbon disulfide modification and impaired catabolism of low density lipoprotein.

Carbon disulfide interacts in vitro with low density lipoprotein (LDL), resulting in an increased electrophoretic mobility of the particle, due to a decrease in free amino groups of apolipoprotein B-100. The processing of carbon disulfide-modified LDL through the apo B/E receptor pathway of cultured human fibroblasts is decreased as compared to that of native LDL, depending on the level of modification. Carbon disulfide-modified LDL is recognized and degraded by the scavenger pathway of macrophages, but to a lesser extent than acetylated LDL. Carbon disulfide modification decreases the ability of the LDL to down-regulate sterol synthesis and to stimulate cholesterol esterification in fibroblasts. Carbon disulfide-modified LDL markedly stimulates cholesteryl ester formation in macrophages, albeit to a lesser extent than acetylated LDL. These results indicate that after carbon disulfide modification the LDL catabolism is shifted to the scavenger pathway, and are consistent with the fact that carbon disulfide intoxication accelerates the appearance of atherosclerotic lesions.

Amines↗
PubMed1988

Binding of spin-labeled clofibrate to lipoproteins.

The binding of spin-labeled clofibrate to native and partially delipidated lipoproteins is a rapid, linear and non-saturable process observed up to the critical micellar concentration of the drug. Low-density lipoproteins (LDL) display a lower affinity for the drug than very-low-density lipoproteins (VLDL) and high-density lipoproteins (HDL) relative to their respective specific volume. Unlike various lipophilic drugs, uptake of spin-labeled clofibrate does not correlate with lipoprotein lipid volume. Spin-labeled clofibrate binding to LDL is enhanced when the temperature increases above 25 degrees C. The binding to HDL and VLDL is less temperature-sensitive. The simulation of the ESR spectra has shown that two types of motion should be superimposed for the spin-labeled clofibrate in HDL, in LDL or in partially delipidated LDL. From 40 down to 25 degrees C for HDL and LDL, a fast anisotropic motion is observed. From 25 degrees C down to 5 degrees C, a two-component motion takes place, including a slow isotropic motion of the probe tumbling in a highly hydrophobic environment. Interactions of spin-labeled clofibrate with the apolipoproteins in HDL and LDL are assumed from the emergence of this strongly immobilized component observed when the temperature decreases. In contrast, for spin-labeled clofibrate inserted in the apolar core of VLDL, ESR shows only one component in the whole temperature range (5-40 degrees C). The location of the spin-labeled drug inside the various lipoprotein particles is discussed as a function of temperature.

Clofibrate↗
PubMed1988

Cyclic AMP decreases LDL catabolism and cholesterol synthesis in the human hepatoma cell line HepG2.

A 24h pretreatment of the human hepatoma cell line HepG2 with dibutyryl cyclic AMP in the presence of theophylline induced a dose dependent decrease in low density lipoprotein binding, uptake and degradation. This effect is most likely due to a reduction of the LDL receptor number. Sterol synthesis from sodium acetate is markedly inhibited, either in the presence or absence of LDL, whereas synthesis from mevalonic acid is unchanged. Cyclic AMP also induced a decrease in hydroxy methyl glutaryl coenzyme A reductase activity. These effects of cyclic AMP might be involved in some hormonal regulation of the LDL pathway and cholesterol metabolism in the liver.

Acetates↗
PubMed1988

The antidiabetic drug metformin decreases cholesterol metabolism in cultured human fibroblasts.

The effect of the hypoglycemic biguanide drug Metformin was investigated after a 72 h pretreatment of human cultured fibroblasts. Metformin induced a moderate increase in low density lipoprotein binding, uptake and internalization (25% increase after treatment with 5 X 10(-4) M of drug). A decrease in sterol, fatty acid and triacyglycerol synthesis from sodium acetate was observed after pretreatment with the drug, with a dose-dependent effect in the range of 5 X 10(-5) to 5 X 10(-4) M (50% reduction of sterol synthesis after treatment with Metformin 5 X 10(-4) M). This effect was also observed in fibroblasts from a patient with homozygous familial hypercholesterolemia. Cholesterol esterification studied by incorporation of radiolabeled oleic acid was reduced by Metformin (40% of control after treatment with Metformin 5 X 10(-4) M) whereas incorporation into triacylglycerols was less impaired. These effects of Metformin on cholesterol metabolism were observed either in the presence or in the absence of low density lipoproteins. Moreover, Metformin also reduced cholesterol esterification in J774 monocyte-macrophage cells. Metformin also induced a decrease of hydroxymethylglutaryl coenzyme A reductase activity in cultured fibroblasts and a reduction of acyl-coenzyme A: cholesterol-O-acyltransferase activity in cultured fibroblasts and J774 cells.

Cells, Cultured↗
PubMed1988

[Oxidation of the indole ring induced by the auto-oxidation of unsaturated lipids. Application to tryptophan residues of high and low density lipoproteins of human serum].

Tryptophan residues are rapidly destroyed during Cu2+-catalyzed autoperoxidation of human serum lipoproteins. The same phenomenon occurs in the peroxidation of arachidonic acid incorporated into phosphatidylcholine liposomes using tryptophan, tryptamine and serotonin as oxidizable substrates. Replacing arachidonic acid by cholesterol inhibits the indole ring degradation.

Arachidonic Acids↗
PubMed1987

Immunological detection of low-density lipoproteins modified by malondialdehyde in vitro or in vivo.

We describe an ELISA technique able to recognize malondialdehyde-modified low-density lipoproteins (LDL). For this purpose we produced antibodies to malondialdehyde-LDL, specific for the malondialdehyde modification of LDL; these antibodies recognized essentially malondialdehyde-LDL. Coating ELISA plates with the antibodies to malondialdehyde-LDL and using peroxidase-labelled antibodies to LDL, which reveal only apolipoprotein B, we obtained an accurate method of detecting malondialdehyde-modified apolipoprotein B. Preliminary studies demonstrated that this method allows the detection of lipoproteins containing malondialdehyde-modified apolipoprotein B in the serum of patients with cardiovascular diseases.

Animals↗
PubMed1986

Effect of manipulation of phospholipid polar head group on low density lipoprotein metabolism in human cultured fibroblasts.

Modification of phospholipid polar head group was achieved by growing human cultured fibroblasts in medium devoid of serum and supplemented with N-methyl ethanolamine or N,N-dimethylethanolamine during 48 h. The corresponding phospholipids accounted for approximately 45% of total phospholipids. Whereas low density lipoprotein (LDL) binding was unaffected, LDL internalization and degradation appeared to be markedly reduced in the presence of N-methylethanolamine. N,N-dimethylethanolamine had no effect on the three studied parameters. These results emphasize the importance of phospholipid polar head group in LDL processing by receptor-mediated endocytosis.

Cells, Cultured↗
PubMed1986

Hypernociceptive syndromes and pharmacological inhibition of endogenous opioid degradation.

Endogenous opioid peptides, by modulating the release of sympathetic transmitters, may play a role in the pathogenesis of migraine and related headaches which are considered hypernociceptive syndromes. Hypoendorphinaemia has been demonstrated in migraine attack. Captopril, a drug able to potentiate morphine analgesia in rats and inhibit enkephalinase in animals and in man, improves the clinical course of migraine. In the present research the cerebrospinal fluid and plasma beta-endorphin (beta-EP) levels have been evaluated following a single oral dose of captopril. The drug increased plasma beta-EP levels in migraine sufferers, and these data may be relevant in the mechanism of action of this drug in migraine and related headaches.

Captopril↗
PubMed1986

[Structure and metabolism of lipoproteins].

Lipoproteins constitute in plasma a dynamic system allowing lipid transport. For this purpose, apolipoproteins play a very important part. They control and regulate lipid transfer between lipoproteins themselves and among cells, from their hepatic as intestinal synthesis sites to their hepatic as peripheral degradation sites. Enzymatic systems and specific receptors are involved to operate this metabolic pathway.

Chemical Phenomena↗
PubMed1984

Monoclonal antibodies to low density lipoprotein used for the study of low- and very-low-density lipoproteins, in "ELISA" and immunoprecipitation technics.

Seven monoclonal antibodies to low-density lipoprotein were studied by the ELISA for their reactivity with LDL or VLDL. Cotitration experiments showed that five of them are addressed to different antigenic epitopes. Two of the monoclonal antibodies were temperature independent whereas the others had a decreased binding activity at 37 degrees C compared to that obtained at 25 degrees C or 4 degrees C, suggesting the presence of antibodies directed to sequence or conformation epitopes, respectively. All antibodies reacted with both LDL and VLDL; four of them had a higher affinity for LDL and two others for VLDL. Immunoprecipitation of LDL and/or VLDL was observed upon immunodiffusion with certain pairs of antibodies. This may allow the use of pairs of monoclonal antibodies to LDL for the quantitative determination of apolipoprotein B in serum LDL and VLDL.

Antibodies, Monoclonal↗
PubMed1984

Acquisition of host cell genetic information by avian sarcoma virus rescued from rat cells transformed by B77 virus.

The properties of avian sarcoma virus B77 grown in chick cells were compared with those of virus obtained by fusion of rat cells transformed by B77 virus ( RB77 cells) with chick cells ( FB77 virus). Differences in the B77 and FB77 viral genomes were demonstrated by the fingerprint technique. The rescued FB77 virus contained sequences homologous to the normal cell genome. These results suggest that the rescued FB77 virus is a recombinant between B77 virus and rat genomic elements. The RNAs from B77 and FB77 viruses were found to have similar molecular weights. The migration rates of the structural proteins and the large glycoprotein (gp 85) in polyacrylamide gels were the same for the B77 and FB77 viruses, but the small glycoprotein (gp) of the FB77 virus was found to be slightly larger than the gp37 of the B77 virus.

Animals↗
PubMed1984

[Dissociation of human serum low density lipoproteins in several immunologically distinct subunits. Isolation and characterization of a B-III subunit].

Low density lipoproteins (d = 1.030-1.055) were partially delipidated with ethyl-ether (LDLe). These LDLe exhibit a spontaneous dissociation several days after delipidation. Four different immunoprecipitation complexes (B-I to B-IV) are observed when using two dimensional immunoelectrophoresis against anti LDLe immunserum. The various subunits of LDLe have different behaviour upon electrophoresis. On disc gel electrophoresis containing urea three bands can be seen; all are phospholipoproteins. The apolipoprotein moiety of LDL and LDLe have the same apparent molecular weight around 550 000. With time several subunits appear in LDLe, the majority of them have a molecular weight around 370 000, 260 000 and 125 000. One of the components from dissociated LDLe containing the immunodeterminant B-III, has been separated by chromatography on heparin-agarose. This LDLe-B-III has the same phospholipid/protein ratio as total LDLe and a protein moiety with an apparent molecular weight of 110 000. This part of apolipoprotein B has no affinity for heparin. Immunocompetition studies by the ELISA technique indicated that sialic acid, one of terminal residues of LDL glycoprotein, is involved in the immunological recognition of LDL and of its derivatives by anti LDL and anti LDLe antisera.

Amino Acids↗
PubMed1982

[Lipoproteins associated with lipoprotein B in human serum low density lipoproteins].

Small amounts of lipoprotein C and lipoprotein D could be observed in low density lipoproteins (1.030-1.055 g/ml), using electroimmunomigration and polyacrylamide gel electrophoresis. Lipoprotein structures containing several apolipoproteins such as lipoprotein (B+C) or (B+D) were not detected in these low density lipoproteins. Lipoproteins C and D could not be separated from lipoprotein B by using gel filtration and affinity chromatography on heparin-Sepharose. Apolipoproteins C-III and D measured by electroimmunoassay are 3.2 +/- 1.2% and 1.15 +/- 0.6%, respectively, of the proteins found in the density range 1.030-1.055 g/ml, so there is, therefore, about 1 mol of apolipoprotein C-III and 0.1 mol of apolipoprotein D per mol of apolipoprotein B.

Apolipoproteins↗
PubMed1982

Intermittent hypoendorphinaemia in migraine attack.

Beta-endorphin (RIA method, previous chromatographic extraction) was evaluated in plasma of migraine sufferers in free periods and during attacks. Decreased levels of the endogenous opioid peptide were found in plasma sampled during the attacks but not in free periods. Even chronic headache sufferers exhibited significantly lowered levels of beta-endorphin, when compared with control subjects with a negative personal and family history of head pains. The mechanism of the hypoendorphinaemia is unknown: lowered levels of the neuropeptide, which controls nociception, vegetative functions and hedonia, could be important in a syndrome such as migraine, characterized by pain, dysautonomia and anhedonia. The impairment of monoaminergic synapses ("empty neuron" condition) constantly present in sufferers from serious headaches, could be due to the fact that opioid neuropeptides, because of a receptoral or metabolic impairment, poorly modulate the respective monoaminergic neurons, resulting in imbalance of synaptic neurotransmission.

Adult↗