Search PubMed⌕ Search

Biomedical subjects

L Galzigna

Publications and source records attributed to L Galzigna.

At least 55 records · Page 3Linked to original sources
PubMed1989

Some effects of fructose-1,6-diphosphate on rat myocardial tissue related to a membrane-stabilizing action.

This study aims at elucidating the mechanism of action of extracellular fructose-1,6-diphosphate (FDP). FDP is able to inhibit Ca++ entry into the myocardial tissue with an IC50 value of 11.5 mM and in addition, it is bound by rat heart slices, the binding being activated by Zn and conditions of chemical hypoxia induced by KCN and iodoacetate. The overall effect of extracellular FDP includes an increase of frequency and amplitude of contraction of perfused heart at concentration below 1 mM, and, in general, a stimulation of the oxygen consumption of the tissue. The antihaemolytic effect of FDP suggests its action as a membrane stabilizer. The effects of extracellular FDP on the myocardial cell can be interpreted both on the basis of a limited permeability of the cell membrane to it and as a purely extracellular effect transduced through the cell membrane with a final response consisting of an increase in the intracellular FDP.

Animals↗
PubMed1989

Synthesis and some properties of a homologous series of beta-carboline-3-carboxylic esters.

A homologous series of esters of beta-carboline-3-carboxylic acid was prepared by a new synthetic procedure. The first members of the series are convulsant or pro-convulsant agents while those with acyl residues longer than C4 show anticonvulsant activity. The affinity of the members of the series for the benzodiazepine receptor from rat brain decreases with the increasing chain length of the esters. The pentyl ester was studied in particular for its anti-convulsant effect on rats and mice treated with cardiazol. The compound also acts as a membrane stabilizer by inhibiting red cell hypotonic hemolysis and rat brain Na/K ATPase; its LD50 value is 12.5 mg/Kg and of particular interest is its lack of inhibitory effect on memory retention in mice at doses at which diazepam has inhibitory effects.

Animals↗
PubMed1989

Toxicity of aminochromes.

The first part of the present review deals with the chemical and enzymatic synthesis of adrenochrome and other aminochromes from the corresponding catecholamines. A description of the most significant pathways of formation and the reactivity of the aminochromes is presented. In the second part of the toxicity of aminochromes, mainly at the cardiac and CNS level, is described and some of the molecular mechanisms of the toxic action are outlined. The toxicity of the aminochromes appears to depend mainly on the production of reduced oxygen species through redox cycling. The interaction of aminochromes with sulfhydryl groups and the induced depletion of oxygen, ascorbate and glutathione are additional mechanisms resulting in noxious effects at a cellular level.

Adrenochrome↗
PubMed1989

A new synthetic peptide with elastase inhibiting effect.

A new peptide, obtained by chemical synthesis, inhibits porcine pancreatic elastase activity "in vitro" with an IC50 of 24 mmol/l. The effect of the peptide was also tested on human plasma elastase by using plasmas with different levels of alpha-1-antitrypsin. The synthetic peptide apparently decreased the amount of normal plasma elastase, assayed by an immunoenzymatic method, with a dose-dependent effect and an IC50 of 13 mmol/l. In plasma with higher amounts of alpha-1-antitrypsin the IC50 value was 18 mmol/l.

Animals↗
PubMed1988

Antioxidant action and photosensitizing effects of three different chlorpromazines.

Chlorpromazine inhibits by about 60% the lipid peroxidation stimulated by Fe2+/ascorbate in liposomes and the lipid peroxidation stimulated by cumene hydroperoxide in microsomes. Under the same conditions, two new synthetic derivatives of chlorpromazine, i.e., a N-benzoyloxymethylchlorpromazine and a N-pivaloyloxymethylchlorpromazine, induce no more than a 20% inhibition. On the other hand, when the different chlorpromazines are entrapped in liposomes and subsequently irradiated with near-UV light, they act as photosensitizing agents giving rise to lipid peroxidation. The latter is quite extensive in the presence of chlorpromazine or N-pivaloyloxymethylchlorpromazine, whereas it is drastically lower in the presence of N-benzoyloxymethylchlopromazine. The N-benzoyloxymethylchlorpromazine molecule, despite its low photodynamic effect, retains its neuroleptic properties. The possible mechanisms of the antioxidant and prooxidant actions of these compounds are discussed.

Animals↗
PubMed1988

Dopamine-depleting activity of L-3,4-(dioxyphenylacetyl)-phenylalanine.

Dioxyphenylacetyl-L-DOPA was synthesized and shown to be resistant toward oxidative cyclization in the presence of plasma and brain extracts. This new DOPA derivative is slightly inhibitory towards monoamine oxidase (IC50 2.5 mM) and the synaptosomal uptake of dopamine (IC50 0.35 mM) and acts as an antagonist of haloperidol (IC50 0.6 microM) in displacing 3H-spiroperidol from isolated dopamine receptors. The substance, although more hydrophobic than DOPA, overcomes the blood-brain barrier to a lower extent than DOPA and lowers the levels of dopamine and norepinephrine in the left and right hemisphere of mice treated with it for 10 days at a dose of 10 mg/kg/day. Dioxyphenylacetyl-L-DOPA inhibits red cell hypotonic hemolysis and brain Na/K+-ATPase activity in vitro and potentiates the barbiturate-induced sleep.

Animals↗
PubMed1988

Effect of 2-pyrrolidone on the concentration of GABA in rat tissues.

The effects of 2-pyrrolidone, a cyclic lactam of GABA, were studied on blood and organ levels of 2-pyrrolidone, GABA, glutamic acid, glutamate decarboxylase (GAD) and GABA-transaminase (GABA-T). When administered i.p., the only significant effects observed were increases of brain and liver 2-pyrrolidone. In contrast, regular oral administration for 7 months produced significant increases of GABA and glutamic acid in brain and of glutamic acid alone in liver while GAD decreased in brain and increased in liver; GABA-T was unchanged. A new method for the synthesis of radioactive 2-pyrrolidone was set up and the enzymatic conversion of 2-pyrrolidone to GABA was measured by an original procedure. The results obtained in vitro by this method on the conversion of 2-pyrrolidone to GABA catalyzed by tissue slices, together with the observed inhibition of the GABA-dependent oxygen consumption by 2-pyrrolidone, partially explain the effects of the oral administration.

4-Aminobutyrate Transaminase↗
PubMed1987

Decrease of serum malondialdehyde in patients treated with chlorpromazine.

Malondialdehyde determination in serum from schizophrenic patients before and after treatment with chlorpromazine showed that, after treatment, patients had significantly lower values than before. The antioxidant properties of chlorpromazine can be related to its effect on the level of serum lipid peroxides and possibly to its neuroleptic action.

Adult↗
PubMed1987

Effect of 3-hydroxy-3-methylglutarate treatment on plasma ketone bodies, triglycerides, and HDL-cholesterol in streptozotocin-diabetic rats.

3-Hydroxy-3-methylglutaric acid administration to streptozotocin-diabetic rats produced a net decrease of plasma ketone bodies and triglycerides together with a slight decrease of total cholesterol. A nonsignificant enhancement of HDL-cholesterol and a negligible change in HDL-phospholipid was also observed. The effect of 3-hydroxy-3-methylglutarate was dose dependent and was more evident with the compound intraperitoneally injected than orally administered with drinking water. [14C]-3-hydroxy-3-methylglutarate was administered either orally or intraperitoneally both to diabetic and control groups of animals, and a higher radioactivity accumulated in liver and kidneys of diabetic rats compared to the controls. The possible mechanism of action of 3-hydroxy-3-methylglutarate is briefly discussed.

Animals↗
PubMed1985

Inhibition of rat liver hydroxymethylglutaryl-CoA reductase by sulfhydryl reagents, coenzyme A esters and synthetic compounds.

The activity of the microsomal 3-hydroxy-3-methylglutaryl-coenzyme A reductase was assayed with a procedure based on the extraction of the product mevalonolactone in a benzene phase. Diamide is an uncompetitive inhibitor of the reaction, while coenzyme A disulfide and tetraethylthiouram disulfide act as non-competitive inhibitors. Diamide inhibition cooperatively increases with the inhibitor concentration. HMG produces a decrease in enzyme activity that combines with that of coenzyme A disulfide. Both CoASH and coenzyme A esters strongly inhibit the reductase activity. Three new synthetic compounds with either thio-ether or thio-ester groups also show inhibitory effect on the enzyme activity.

Acyl Coenzyme A↗
PubMed1985

Interaction of low doses of ionizing radiation and carbon tetrachloride on liver superoxide dismutase and glutathione peroxidase in mice.

Male BALB/c mice were treated with intraperitoneal injections of carbon tetrachloride (CCl4) (0.2 g/kg body weight) and/or 50 R of whole-body gamma irradiation, three times per week, for 4 weeks. The effects of the treatments on superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in liver extracts and homogenates, and on alkaline phosphatase (ALP) in serum were investigated. A significant decrease in the SOD and GSH-Px activities in liver extracts and an increase of serum ALP of hepatic origin were found in CCl4-treated animals. In contrast, only an increase in SOD activity was observed in liver homogenates after the combined treatment.

Alkaline Phosphatase↗
PubMed1984

Properties of a new calcium ion antagonist on cellular uptake and mitochondrial efflux of calcium ions.

Compound YS 035 [NN-bis-(3,4-dimethoxyphenethyl)-N-methylamine] is a new synthetic compound capable of inhibiting Ca2+ uptake by different cells. The inhibition of Ca2+ uptake by muscle cells isolated from chicken embryo is dose-dependent in the compound YS 035 concentration range 10-30 microM. The new compound also inhibits Ca2+ entry into rat brain synaptosomes and less effectively into baby-hamster kidney cells. Compound YS 035 partially inhibits the slow Ca2+ release induced by Ruthenium Red and the rapid Na+-dependent efflux from heart mitochondria. The inhibition of the Na+/Ca2+ exchange appears to be of a non-competitive type with an apparent Ki of 28 microM. The new Ca2+ antagonist totally inhibits the Ca2+ efflux from liver mitochondria induced by Ruthenium Red, but it does not affect the release induced by uncoupler, respiratory inhibitor or chelator, nor the mitochondrial ATP synthesis and membrane potential. The properties shown by the new compound indicate it to be a Ca2+ antagonist and a useful tool for studies on the mitochondrial Ca2+ transport.

Animals↗
PubMed1984

Increase of intraerythrocytic fructose-1,6-diphosphate after incubation of whole human blood with fructose-1,6-diphosphate.

The incubation of whole blood with fructose-1,6-diphosphate (FDP) entails a statistically significant increase of intraerythrocytic FDP together with a decrease of blood glucose. The increase is not significant when equimolar amounts of fructose plus twice molar phosphate are used. The effect of FDP is decreased in the presence of an excess of oxygen. FDP added to the whole blood is removed from plasma by the activity of plasma enzymes and by the presence of blood cells as well. No specific interaction of FDP with plasma proteins seems to occur and the effects of FDP addition last longer than is compatible with the presence of FDP in the plasma.

Adolescent↗
PubMed1984

Fructose-1,6-diphosphate counteracts potassium effects on cardiac muscle.

Fructose-1,6-diphosphate (FDP) counteracts the inhibition of contractile strength of rabbit cardiac muscle induced by KCl "in vitro" and the valinomycin induced depolarization. FDP also protects in a dose-dependent fashion, up to 100 mg/kg, different strains of mice from the lethal effect of KCl that is due to a complete atrio-ventricular block and related to a high value of plasma potassium level. A protective effect of FDP is observed when increasing doses of (+/-) propranolol are injected before maximum non lethal dose of KCl.

Animals↗
PubMed1984

An N-protected gamma-aminobutyric acid dipeptide with anticonvulsant action.

N-Pivaloyl-leucyl-gamma-aminobutyric acid (PLG) is a synthetic dipeptide with a partition coefficient of 1.67 in an ethyl acetate/water system that partially inhibits the synaptosomal uptake and activates the release of [U-14C]gamma-aminobutyric acid [( U-14C]GABA). The displacement of GABA from crude synaptic membranes by PLG occurs with an IC50 of 10(-5) M. The compound has the capacity to cross the blood-brain barrier and increase central GABA levels. Its ED50 on cardiazol -induced convulsions is 60-65 mg/kg. PLG is resistant to hydrolysis by chymotrypsin and partially inhibits the proteolytic activity of trypsin.

Animals↗