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Biomedical subjects

C Stefanelli

Publications and source records attributed to C Stefanelli.

51 records · Page 3Linked to original sources
PubMed1992

Extraction of lipids and lipophilic antioxidants from fish tissues: a comparison among different methods.

1. Lipids, phospholipids and lipid soluble antioxidants were extracted from Sparus auratus liver and white muscle by three different methods and the yields obtained were compared. 2. None of the three procedures can recover the above components with the same efficiency. 3. For comparison the methods were also applied to rat liver homogenates. 4. The choice of the extraction procedures depends on the tissue investigated and on specific research requirements.

Animals↗
PubMed1992

Polyamine plasma levels and liver regeneration following partial hepatic resection in man.

Polyamines (putrescine, spermidine, and spermine) are widely distributed in animal and vegetal tissues, where their intracellular concentration strictly correlates with normal and pathological cell growth and protein synthesis. By means of a sensitive HPLC technique, the fasting plasma concentrations of polyamines were measured serially in 11 patients who underwent partial hepatic resection because of focal liver lesions. Samples were obtained before surgery and over the next 6 months, during hepatic regeneration. Liver volume was also measured by ultrasound on the basis of the 3 maximum diameters of the liver. From 2 to 4 weeks after surgery, plasma putrescine increased by a maximum of 78%, and spermidine by approximately 50%. No changes were observed in spermine levels. The spermidine/spermine ratio nearly doubled during liver regeneration. The volume of the liver decrease from 1505 [SD 236] ml to 743 [151] ml after resection, and returned to nearly normal values after 6 months (1231 [100] ml, p < 0.05 vs. basal values). The liver regeneration rate was highest 2-4 weeks after resection, and declined thereafter, when prevailing polyamine concentrations returned to normal. These data show that liver regeneration is accompanied by a significant increase in fasting putrescine and spermidine concentrations, which might be biochemical signals of active liver cell regeneration.

Adult↗
PubMed1992

Induction of ornithine decarboxylase by transcriptional inhibitors in quiescent thymocytes.

The transcriptional inhibitors actinomycin D and dichlororibofuranosylbenzimidazole induced ornithine decarboxylase activity in isolated, quiescent thymocytes, which otherwise did not show detectable levels of the enzyme. This paradoxical induction was transient and dependent on the presence of serum and continuous protein synthesis. However, alpha-amanitin, another inhibitor of transcription, did not affect ornithine decarboxylase activity. Dichlororibofuranosylbenzimidazole and actinomycin D were unable to enhance the activity of spermidine acetyltransferase or S-adenosyl-methionine decarboxylase, which are other inducible and short-lived enzymes involved in the metabolism of polyamines.

Animals↗
PubMed1991

Comparison between alpha-adrenergic- and K-opioidergic-mediated inositol (1,4,5)P3/inositol (1,3,4,5) P4 formation in adult cultured rat ventricular cardiomyocytes.

In adult cultured rat ventricular cardiac myocytes, both the alpha-adrenergic agonist phenylephrine and the selective kappa opioid receptor ligand U-50, 488H affected phosphoinositide turnover. Phenylephrine, over a time course of 10 min, caused a transient increase in Ins(1,4,5)P3 which peaked at 1 min and had returned to control at 2 min. In addition, phenylephrine produced a progressive and sustained increase in the formation of Ins (1,3,4,5)P4 which achieved a plateau after 5 min of exposure to the agonist. U-50,488H induced an increase in Ins(1,4,5)P3 which peaked at 1 min at a level significantly higher than that due to phenylephrine and was still elevated after 10 min exposure to the kappa opioid receptor agonist. In addition, U-50,488H caused a sustained increase in Ins(1,3,4,5)P4 which was comparable to that due to phenylephrine. The stimulatory effects produced by phenylephrine and U-50,488H were receptor-mediated events, since they were fully antagonized by their respective antagonists, phentolamine or Mr-1452.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1991

Ubiquinol prevents alpha-tocopherol consumption during liposome peroxidation.

In this study we investigated whether alpha-tocopherol can be spared by ubiquinol-3 during autoxidation of multilamellar liposome. A lipophilic azocompound, 2,2'-azobis-(2,4-dimethyl-valeronitrile), was chosen to initiate liposome autoxidation. The effect of either alpha-tocopherol, ubiquinol-3, or a mixture of them was compared. Rates of conjugated diene formation and concomitant disappearance of the two antioxidants was measured. Since the inhibition rate constant for the scavenging of peroxyl radical for alpha-tocopherol was higher than that for quinol-3, it was concluded that alpha-tocopherol is regenerated by ubiquinol-3.

Free Radicals↗
PubMed1990

Inhibition of autoxidation of egg yolk phosphatidylcholine in homogenous solution and in liposomes by oxidized ubiquinone.

The aim of this study was to obtain a quantification of the antioxidant activity of ubiquinone. To this purpose the oxidation of egg yolk phosphatidylcholine both in solvent and in liposomes initiated by an azocompound has been studied either in the absence or in the presence of ubiquinone-3, using alpha-tocopherol as a reference antioxidant. The two experimental systems gave similar results. In the presence of ubiquinone-3 the oxidation rate was reduced with respect to control experiments but was faster than that in the presence of alpha-tocopherol. The amount of ubiquinone required to decrease the autoxidation rate was so high as to prevent detection of the induction period. The stoichiometric factor was greater than 2 and the rate constant of inhibition was two orders of magnitude lower than that of alpha-tocopherol. It is concluded that high concentrations of ubiquinone are required to exhibit significant antioxidant activity. A possible mechanism compatible with the stoichiometric factor larger than 2 for the inhibiting effect of ubiquinone is also suggested.

Liposomes↗
PubMed1987

Effects of dexamethasone on spermidine N1-acetyltransferase and ornithine activities in rat spleen.

Treatment of rats with the glucocorticoid dexamethasone causes an increase in the activity of cytosolic spermidine N1-acetyltransferase both in the spleen and thymus, but not, however, in liver, kidney or lung. The induced spermidine N1-acetyltransferase activity in the spleen catalyses acetylation of spermidine as well as spermine and sym-norspermidine, but not of diamines and histones. The enzyme induction depends on the dose of dexamethasone, and is suppressed by cycloheximide, which suggests that de novo protein synthesis is required for the action of this glucocorticoid. N1-acetylspermidine accumulates in the spleen after dexamethasone treatment, while spermidine progressively decreases and is partly converted into putrescine, the content of which transiently increases. In accordance with previous reports, dexamethasone was found to cause a rapid and large fall in the activity of spleen ornithine decarboxylase which was effected via the appearance of an inhibitor of the enzyme. Glucocorticoids exert large catabolic effects on lymphoid tissues, and further selectively affect the activities of spermidine N1-acetyltransferase and ornithine decarboxylase in the thymus and spleen. These latter selective responses may represent an important early event in lymphoid tissue response to glucocorticoid hormones.

Acetyltransferases↗
PubMed1987

The effect of treatment with coenzyme Q10 on the mitochondrial function and superoxide radical formation in cardiac muscle hypertrophied by mild aortic stenosis.

A 40% reduction of the diameter of the ascending aorta maintained for 60 days induced the formation of a compensate cardiac hypertrophy in rabbits without changing the value of the azide insensitive Ca2+-ATPase activity in comparison to control hearts. The cardiac mitochondria isolated from constricted animals assayed in presence of glutamate and succinate did not show a change in the R.C.I. and ADP/O values in comparison to the controls, whilst the QO2 value enhanced or decreased respectively when determined with glutamate or succinate. The intramuscular injections of CoQ10 (12 mg/kg body weight/48 h) enhanced the mitochondrial CoQ10 concentrations both in the control and in the constricted animals and further increased the QO2 value determined in both groups of animals when glutamate was used as the substrate. The production of O2.- radicals by the level of the complexes I and III of the respiratory chain, did not change in the constricted animals, nor in the animals administered with CoQ10 in comparison to the control. CoQ10 augmented the rate of oxygen consumption by the submitochondrial particles only in the constricted animals. Moreover, the treatment with the coenzyme or the constriction of the aorta, did not modify the cardiac superoxide dismutase activity, but increased the glutathione peroxidase activity only in the banded animals. In addition, in the CoQ10 treated animals there was a reduction of NADH-diaphorase activity both in the control and constricted animals, while the malondialdehyde, generated during the thiobarbituric acid test, and the cardiac content of lipofuscin were decreased.

Animals↗
PubMed1986

Accumulation of N1-acetylspermidine in heart and spleen of isoprenaline-treated rats.

N1-Acetylspermidine is not detectable in rat heart, but its content greatly increases after a single injection of isoprenaline (10 mg/kg), reaching a concentration of about 10 nmol/g of tissue 4 h after the treatment. Part of the accumulated N1-acetylspermidine was split to putrescine. Isoprenaline also caused an increase of N1-acetylspermidine in the spleen, where its concentration increased 3.5-fold 6 h after the catecholamine. The accumulation of N1-acetylspermidine was dependent on the dose of isoprenaline in both the heart and the spleen, and was strongly inhibited by beta-antagonists and inhibitors of protein synthesis.

Animals↗
PubMed1986

Modulation of ornithine decarboxylase activity and ornithine decarboxylase-antizyme complex in rat heart by hormone and putrescine treatment.

Ornithine decarboxylase was present in a cryptic, complexed form in an amount approximately equivalent to that of free ornithine decarboxylase activity in adult rat heart. Addition of isoproterenol (10 mg/kg) caused a notable rise in ornithine decarboxylase activity and a simultaneous decrease in the amount of the complexed enzyme. During the period of ornithine decarboxylase decay, when cardiac putrescine content had reached high values, the level of the complex increased above that of the control. Administration of putrescine (1.5 mmol/kg, twice) or dexamethasone (4 mg/kg) produced a decrease of heart ornithine decarboxylase activity, while it did not remarkably affect the level of complexed ornithine decarboxylase, therefore raising significantly the ratio of bound to total ornithine decarboxylase. Putrescine also elicited the appearance of free antizyme, concomitantly with the disappearance of free ornithine decarboxylase activity after 3-4 h of treatment. These results indicate that a significant amount of ornithine decarboxylase occurs in an inactive form in the heart under physiological conditions and that its absolute and relative levels may vary following stimuli which affect heart ornithine decarboxylase activity.

Animals↗
PubMed1986

Separation of N1- and N8-acetylspermidine isomers by reversed-phase column liquid chromatography after derivatization with dansyl chloride.

The separation of dansyl derivatives of N1- and N8-acetylspermidine by reversed-phase column liquid chromatography is reported. The influence of organic solvents on the retention of acetylspermidines was studied. Best resolutions were achieved using a C18 column and a ternary mobile phase composed of water, methanol and acetonitrile. The precolumn derivatization method permitted the detection of picomole quantities. A method for the determination of acetylspermidines in rat tissues is described.

Animals↗
PubMed1986

Effect of adrenergic stimulation on ornithine decarboxylase activity in the rat spleen.

The effect of a single administration of catecholamines on ornithine decarboxylase activity and polyamine biosynthesis in the rat spleen was investigated. Isoproterenol elicited a dose-dependent increase in spleen ODC activity which reached a maximum 4 hr after the administration of the drug. Putrescine content was also found to increase within a few hours, whereas S-adenosylmethionine decarboxylase activity and spermidine and spermine levels did not change significantly. Adrenaline and noradrenaline proved to be even more effective in increasing splenic ODC activity than isoproterenol. alpha- and beta-adrenergic antagonists prevented the ODC increase by catecholamines to a different extent.

Adenosylmethionine Decarboxylase↗