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Biomedical subjects

L Galzigna

Publications and source records attributed to L Galzigna.

At least 37 records · Page 2Linked to original sources
PubMed1996

Horseradish peroxidase-catalyzed sulfoxidation of promethazine and properties of promethazine sulfoxide.

Promethazine sulfoxide was obtained with a quantitative yield in a horse radish peroxidase-catalyzed reaction of promethazine and hydrogen peroxide and was also prepared by direct chemical synthesis. The enzymatic sulfoxidation of promethazine was studied in vitro as a function of pH, promethazine, and hydrogen peroxide concentration. Promethazine sulfoxide inhibits with an apparent K(i) of 59.7 microM at pH 5.5 the enzymatic reaction, followed spectrophotometrically, polarographically, potentiometrically, and luminometrically. The reaction was also inhibited by ascorbic acid (K(i) 26.8 microM) and glutathione (K(i) 41.8 microM). The spectrophotometric techniques employed, together with ESR spectrometry, allowed the identification of at least three radical species formed in the course of the reaction. Promethazine sulfoxide is devoid of the antioxidant effect exhibited by promethazine on rat brain synaptosomes. The sulfoxide also lacks photosensitizing action, while retaining the neuroleptic effect of the parent compound.

Animals↗
PubMed1994

Fructose 1,6-bisphosphate prevents oxidative stress in the isolated and perfused rat heart.

Rat hearts were perfused with the Langendorff technique at constant flux in the presence of the oxidizing agents hydrogen peroxide and diamide. Fructose 1,6-bisphosphate strongly prevented the decline of heart contractility due to the infusion of these oxidizing agents. On the other hand, fructose 1,6-bisphosphate had no effect on the release of total glutathione into the perfusate but prevented the loss of lactate dehydrogenase indicating a protective effect on cell membranes. Comparing the cytosolic and mitochondrial loss of glutathione, fructose 1,6-bisphosphate exerted a beneficial action only on the mitochondrial fraction. Several mechanisms of action have been considered to explain the protective action of fructose 1,6-bisphosphate. In our experimental conditions fructose 1,6-bisphosphate might stimulate its own production giving rise to dihydroxyacetone phosphate, that, after reduction to glycerol 3-phosphate, can permeate the mitochondrial membrane with the final production of energy.

Animals↗
PubMed1993

Substrate-stimulated oxygen consumption by isolated rat brain microvessels in the presence and absence of ATP.

We report here properties of isolated brain microvessels such as the rate of oxygen consumption with different substrates; the permeabilizing effect of added ATP is studied. With the isolation procedure presented the cerebral endothelium has a metabolic activity comparable to that reported in the literature. The respiratory rate of the microvessels is not affected by the addition of ATP, whereas it is significantly increased by addition of succinate and alpha-chetoglutarate. The exposure of the isolated brain capillaries to ATP, in a Ca(2+)-free medium, increases the uptake of 6-carboxyfluorescein. This may be due to pores opened by ATP in the endothelial cell membrane in the absence of divalent cations.

Adenosine Triphosphate↗
PubMed1993

Synthesis and some properties of two salsalate derivatives.

The synthesis of esters of 2-hydroxy benzoic acid-2-carboxyphenyl ester (salsalate) with guaiacol for the treatment of inflammatory bronchopneumopathies is reported. The antiinflammatory, analgesic and antipyretic activities of these derivatives were evaluated, together with their antioxidant, mucolytic and broncho-bacteriostatic properties in comparison to acetylsalicylic acid.

Animals↗
PubMed1992

ATP-stimulated glutamate-dependent calcium uptake by rat synaptosomes.

The entry of Ca2+ in rat synaptosomes was followed with a Ca(2+)-selective electrode. Extracellular ATP is necessary for the entry which is a function of synaptosomal protein, free Ca2+ and glutamate concentrations. Ketamine, glycine and kainate have negligible effect while quisqualate slightly inhibits the uptake of Ca2+ in the presence of glutamate. The added ATP is hydrolyzed by the synaptosomes through an ouabain-insensitive ecto-ATPase affected by the presence of Ca2+, glutamate and, to a slight extent, NMDA.

Adenosine Triphosphate↗
PubMed1992

Added ATP influences some responses of rat synaptosomes to glutamate.

ATP added externally to rat synaptosomes activated uptake of both Ca2+ and glutamate which was partially accounted for by the uptake phenomena of synaptic vesicles and mitochondria, as shown by using specific inhibitors of the latter. Increasing concentrations of glutamate stimulated Ca2+ entry linearly, as shown by using 45Ca or a Ca-specific electrode. The processes of glutamate and Ca2+ uptake shared some common features and their ATP-dependence may be correlated with an ouabain-insensitive synaptosomal ectonucleotidase activity measured by a 31P-NMR or a luminometric technique. The ATP hydrolysis catalysed by the synaptosomes was activated by both Ca2+ and glutamate. The present synaptosomal activities may represent a model for studying the modulatory effects of ATP on the glutamatergic neurotransmission.

Adenosine Triphosphate↗
PubMed1992

Interaction between thiopentone and subhypnotic doses of ketamine.

The hypnotic effects of thiopentone and ketamine were studied in ASA Grade I female patients aged 20-30 without premedication. The dose-response curves of ketamine 0.4 mg kg-1 and thiopentone following ketamine 0.4 mg kg-1 were determined by probit analysis. The interaction between ketamine and thiopentone was found to be an antagonistic one. This effect can be interpreted as a consequence of the different neurophysiological spectra of action of the two drugs.

Adult↗
PubMed1991

2,6-diisopropylphenol, a general anesthetic, inhibits glutamate action on rat synaptosomes.

2,6-diisopropylphenol (propofol), a general intravenous anesthetic, inhibits the glutamate-dependent Ca2+ entry in rat synaptosomes with an approximate IC50 of 3.0 x 10(-5) M. Propofol, at concentrations above 10(-6) M, also inhibits the ATP-dependent uptake of glutamate in the presence of Ca2+, with an approximate IC50 of 3.5 x 10(-5) M, while it only has a slight inhibitory effect on the release of glutamate. The ouabain-insensitive synaptosomal ATPase is strongly inhibited by propofol, with an IC50 of about 2.5 x 10(-6) M, at concentrations which do not affect the luciferase system.

Adenosine Triphosphatases↗
PubMed1991

Protective action of a new benzofuran derivative on lipid peroxidation and sulphydryl groups oxidation.

The antioxidant properties of a novel water-soluble antioxidant of the benzofuran family (5-hydroxy-4,6,7-trimethyl-2,3-dihydrobenzofuran-2-acetic acid, BFA) were studied. In rat liver mitochondria BFA increases the lag-time and decreases the extent of lipid peroxidation induced by ascorbate/Fe2+; an IC50 value of about 12 microM was observed. In rat liver microsomes it inhibits the lipid peroxidation induced both by NADPH/Fe2+/ADP (iron-dependent) and by cumene hydroperoxide (iron-independent), showing IC50 values of 25 and 30 microM respectively. The antioxidant efficiency of BFA is slightly higher than that of the congener compound Trolox C. BFA is also able to inhibit the oxidation of protein sulphydryl groups consequent to microsomal lipid peroxidation induced by NADPH/Fe2+/ADP. The antioxidant properties of BFA are discussed considering its hydrophilic character and pharmacological features.

Adenosine Diphosphate↗
PubMed1990

Fructose-1,6-diphosphate counteracts ethanol-stimulated calcium uptake in isolated BHK cells.

Ethanol increases the uptake of 45Ca by isolated baby hamster kidney (BHK) cells in vitro. The effect is dependent on ethanol and 45Ca++ concentration and on the incubation time. Fructose-1,6-diphosphate (FDP) added at different concentration during the pre-incubation exerts a protective effect through a membrane-stabilizing action which is consistent with its in vivo anti-alcohol activity documented in previous studies.

Animals↗
PubMed1990

Direct and respiratory chain-mediated redox cycling of adrenochrome.

Adrenochrome is reduced by ascorbate in a reaction accompanied by a large and rapid oxygen uptake. The rates of adrenochrome reduction and the concomitant oxygen uptake are decreased in the presence of superoxide dismutase or catalase. The species formed on the one-electron reduction of adrenochrome (i.e., the semiquinone) was shown by pulse radiolysis to rapidly react with oxygen (9.10(8) M-1.s-1), indicating the occurrence of a redox cycling in a system formed by adrenochrome, a reducing agent, and oxygen. Adrenochrome is also reduced to the corresponding semiquinone by complex I of beef heart submitochondrial particles supplemented with NADH, while succinate is unable to support this reduction. The o-semiquinone is the intermediate species in the superoxide-generating cycle resulting from both non-enzymatic and enzymatic reduction. The toxic effects of adrenochrome and its pathophysiological role can be explained, at least in part, on the basis of the demonstrated cycle.

Adrenochrome↗
PubMed1990

Fructose-1,6-diphosphate as an in vitro and in vivo anti-alcohol agent in the rat.

Fructose-1, 6-diphosphate (FDP) decreases the effect of ethanol on Ca++ entry and inhibits the ethanol-stimulated phosphate efflux in rat heart slices. FDP also inhibits the ethanol-stimulated [36Cl-]-uptake by rat brain microvesicles and affects the isolated GABA-receptor in a way opposite to that of ethanol. The in vivo effects of FDP include a dose-dependent decrease in ethanol-induced gastric ulcers and a decrease in the serum transaminase levels raised by chronic ethanol administration. Other central actions of ethanol such as diuresis, narcosis, dependence and withdrawal symptoms are also counteracted by FDP.

Animals↗
PubMed1990

Reduction of adrenochrome by rat liver and brain DT-diaphorase.

Liver and brain exhibit DT-diaphorase activity with adrenochrome as a substrate; the latter is an o-quinone derived from the autoxidation of adrenaline exhibiting neurotoxic and cardiotoxic properties. The reaction is strongly inhibited by dicoumarol, a classical inhibitor of DT-diaphorase. DT-diaphorase-reduced adrenochrome undergoes autoxidation as shown by the oxygen uptake occurring during the reaction. It is proposed that, physiologically, DT-diaphorase might exert a protective role by maintaining adrenochrome in its reduced, non-toxic form.

Adrenochrome↗
PubMed1990

Absorption, distribution, metabolism and excretion of 2-[2-thiophenecarboxythio]-N-[dihydro-2-(3H)-thiophenone-3-yl]-propiona mide in the rat.

2-[2-Thiophenecarboxythio]-N-[dihydro-2-(3H)-thiophenone-3-y l]- propionamide (MR 889) was administered orally to rats in order to investigate its pharmacokinetics. 1-2 h after the administration, MR 889 was detected as unchanged compound in plasma only in traces whereas some catabolites, i.e. 2-thiophene carboxylic acid and its glycinate were detected with a tmax of 2 h. The thiolic component of MR 889 induced an evident and sustained increase of total sulfhydryl groups in plasma (tmax 2 h), tissues and urine. Relevant concentrations of 2-thiophene carboxylic acid were found in small intestine and gastric wall followed by liver, lungs and kidneys. The thiolic component also increased, mainly in liver and lungs followed by small intestine and gastric wall. Homocysteine thiolactone S-methyl thiolactamide was identified as a minor metabolite of MR 889.

Administration, Oral↗