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Biomedical subjects

A Leon

Publications and source records attributed to A Leon.

At least 199 records · Page 11Linked to original sources
PubMed1981

Activation of (Na+, K+)-ATPase by nanomolar concentrations of GM1 ganglioside.

GM1 ganglioside binding to the crude mitochondrial fraction of rat brain and its effect on (Na+, K+)-ATPase were studied, the following results being obtained: (a) the binding process followed a biphasic kinetics with a break at 50 nM-GM1; GM1 at concentrations below the break was stably associated, while over the break it was loosely associated; (b) stably bound GM1 activated (Na+, K+)-ATPase up to a maximum of 43%; (c) the activation was dependent upon the amount of bound GM1 and was highest at the critical concentration of 20 pmol bound GM1 X mg protein-1; (d) loosely bound GM1 suppressed the activating effect on (Na+, K+)-ATPase elicited by firmly bound GM1; (e) GM1-activated (Na+, K+)-ATPase had the same pH optimum and apparent Km (for ATP) as normal (Na+, K+)-ATPase but a greater apparent Vmax; (f) under identical binding conditions (2 h, 37 degrees C, with 40 nM substance) all tested gangliosides (GM1, GD1a, GD1b, GT1b) activated (Na+, K+)-ATPase (from 26-43%); NeuNAc, sodium dodecylsulphate, sulphatide and cerebroside had only a very slight effect. It is suggested that the ganglioside activation of (Na+-K+)-ATPase is a specific phenomenon not related to the amphiphilic and ionic properties of gangliosides, but due to modifications of the membrane lipid environment surrounding the enzyme.

Animals↗
PubMed1981

Ontogeny of 3H-diazepam binding sites in different rat brain area. Effect of GABA.

The ontogenesis of the 3H-diazepam binding sites and their modulation by gamma-aminobutyric acid have been studied in different brain areas of rat at various ages, using frozen and two Triton X-100 treated crude synaptic membrane preparations. Benzodiazepine recognition sites are present at birth in all the brain regions investigated and reach adult levels about 3 weeks later. The changes of 3H-diazepam binding with age are due to an increase in the total number of binding sites. In vitro addition of GABA produces, in newborn and adult cerebral cortex, an increase in affinity, but not in number of binding sites for 3H-diazepam. The effect is age dependent.

Aging↗
PubMed1980

Interactions of GM1 ganglioside with crude rat brain neuronal membranes.

The binding of GM1 ganglioside to crude preparations of rat brain neuronal membranes was studied, the following results being obtained: (a) the binding process followed a biphasic kinetics, which displayed a break at 0.07-0.08 x 10(-6) M GM1 concentration; (b) the features of the binding process at GM1 concentrations below the break and, over the break, above 10(-6) M appeared to be different. Below the break the process proceeded slowly and brought a stable and irreversible association of GM1 molecules to the membranes. Over 10(-6) M the process was much more rapid and caused GM1 molecules to interact in such a way that they were releasable by washing and could exchange with newly added free ganglioside; (c) the two binding processes displayed the characteristics of a saturation phenomenon; (d) in both cases, GM1 taken up was freely available to galactose oxidase, indicating that the oligosaccharide chains protrude from the membrane surface. We postulate that GM1 occurs, below and above the break, in different physical forms, each of them having a different mechanism of interaction with the membrane. Above 10(-6) M GM1 interacts as micelles, and the basis of the micelle-membrane interaction is a fusion process. Below the break, in the 10(-8)--10(-7) M range, the binding is the result of hydrophobic interactions between sites on the membrane and the hydrophobic portion of individual ganglioside molecules, most likely in the monomeric form.

Animals↗
PubMed1979

Pharmacological effects of phosphatidylserine liposomes: the role of lysophosphatidylserine.

1. Unique among the phospholipids, phosphatidylserine depresses brain energy metabolism when injected intravenously into mice in the form of sonicated liposomes. The possibility that this effect results from a metabolic transformation of phosphatidylserine is examined in this paper. 2. A strong enhancement of the phosphatidylserine effect is induced by the incubation of liposomes with rat serum. Similar phosphatidylserine activation is observed after the incubation of the phospholipid with purified phospholipase A2 from pancreas. In both cases phosphatidylserine is split into the deacylated derivative, lysophosphatidylserine. 3. Lysophosphatidylserine reproduces with greater efficacy the effect of phosphatidylserine on brain energy metabolism. Other lysophospholipids are not effective. 4. It is concluded that the pharmacological effects of phosphatidylserine liposomes is due to the generation of lysophosphatidylserine.

Animals↗
PubMed1979

Pharmacological effects of phosphatidylserine liposomes: regulation of gylcolysis and energy level in brain.

1 The accumulation of glucose in the brain produced by the administration of phosphatidylserine liposomes into mice has been studied by measurement of the cerebral contents of glycolytic intermediates and high-energy compounds. 2 With a normal supply of oxygen to the brain, inhibition of glycolysis is indicated mainly at the phosphofructokinase step. The ratio of glucose-6-phosphate to fructose-1,6-diphosphate increased, whereas the levels of pyruvate and especially lactate decreased. 3 Under conditions of cerebral ischaemia, the administration of phosphatidylserine delays glycogen mobilization and ATP use. As a consequence of decreased energy utilization, the brain adenylate energy charge remains at a high level. 4 It is concluded that the phosphatidylserine-induced glucose accumulation in the brain is due to reduced energy expenditure and therefore to a decrease in carbohydrate consumption. The inhibition of glycolysis by the high level of adenylate energy charge is probably the control mechanism explaining the decreased carbohydrate utilization.

Adenine Nucleotides↗
PubMed1978

Synthesis and antiinflammatory activity of 6,11-dihydro-11-oxodibenzo[b,e]thiepinalkanoic acids and related compounds.

Acetic acid derivatives of tricyclic systems, such as 6,11-dihydro-11-oxodibenzo[b,e]thiepin, 4,10-dihydro-4-oxo-thieno[2,3-c][1]benzothiepin, dibenzo[b,f]thiepin, dibenz[b,f]oxepin, etc., were synthesized and assayed for antiinflammatory activity. One of the compounds, 6,11-dihydro-11-oxodibenzo[b,e]thiepin-3-acetic acid (52), was chosen for evaluation in man on the basis of high antiinflammatory activity in both short- and long-term animal assays and a low gastric irritation liability in rats and dogs.

Acetates↗
PubMed1977

Effect of phospholipids on cholesterol-induced modifications in mouse brain.

Mice on an atherogenic diet for 40 days show a decrease in brain content of catecholamines, cyclic AMP and in dopamine degradation, and modification of the glycolytic pathway. The metabolic changes are paralleled by changes in behaviour, i.e. decrease in spontaneous motor activity and in conditioning avoidance response. The decrease in dopamine degradation and in behaviour parameters is partly due to the propylthiouracil present in the diet. Endovenous treatment with sonicated dispersions of bovine brain phospholipids induces a modification in the parameters of behaviour and metabolism. The possibility is discussed that some of the defects arising during the atherogenic diet are related with the establishment of a hypoxic state.

Animals↗