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Biomedical subjects

L Corazzi

Publications and source records attributed to L Corazzi.

53 records · Page 3Linked to original sources
PubMed1983

Compartmentation of membrane phosphatidylethanolamine formed by base-exchange reaction in rat brain microsomes.

The compartmentation of membrane phosphatidylethanolamine (PE) formed by base-exchange reaction in rat brain microsomal vesicles has been investigated. After labelling membrane PE by base-exchange in vitro, microsomal vesicles were treated with trinitrobenzenesulfonic acid (TNBS). The amount of membrane PE reacting with TNBS depends on the duration and the temperature of the reaction as well as on the TNBS concentration. It was found that almost all of the labelled PE molecules, but only about 24% of membrane PE, were accessible to TNBS, under very mild reaction conditions. It is concluded that PE labelled by base-exchange is completely localized in the cytoplasmic leaflet of microsomal vesicles.

Animals↗
PubMed1983

Release of endogenous amino acids from superior colliculus of the rabbit: in vitro studies after retinal ablation.

Tissue slices from the superior colliculi (SC) of the rabbit were superfused and investigated 1 week after unilateral eye removal. Amino acid levels were determined both in the tissue slices and in the medium after chemical depolarisation (56 mM K). The amino acid determinations were done fluorimetrically by precolumn derivation and HPLC separation. Colliculi contralateral to the enucleation exhibited a 16% reduction in glutamate compared with the ipsilateral colliculi. The Ca-dependent release of glutamate or other amino acids tested was not appreciably affected by enucleation. However, both the total and the Ca-independent release of glutamate was lower from contralateral SC slices compared with the ipsilateral slices. The results do not favour glutamate as the major optic nerve transmitter in the rabbit, but do not rule out glutamate as a transmitter in a minor population of retinal fibres.

Amino Acids↗
PubMed1981

The action of S-adenosyl-L-methionine on the levels of triglyceride and phospholipid precursors in ethanol-intoxicated rat liver.

Acute ethanol intoxication (7 g/kg body wt) produces modifications of rat liver lipid metabolism. The effect of S-adenosyl-L-methionine (SAM) on hepatic triglyceride accumulation and on some hydrosoluble phospholipid precursors (phosphorylcholine, phosphorylethanolamine, CDP-choline, CDP-ethanolamine) has been examined in this work. The administration of SAM improves the removal of triacylglycerol from ethanol-intoxicated livers and produces modifications of the pools of some hydrosoluble phospholipid precursors.

Alcoholic Intoxication↗
PubMed1981

The effect of some flavolignans on lipid synthesis in ethanol-intoxicated hepatocytes in primary culture.

Rat liver cells in primary culture have been used to investigate the effect of ethanol and of two flavolignans 3,7-dihydroxy-2-(1,4-benzodioxan-6-yl)chroman-4-one (I) and 3,7-dihydroxy-2-[(2,3-diphenyl)-1,4-benzodioxan-6-yl]chroman-4-one (II) on the incorporation of [2-3H]-glycerol into lipids. Ethanol produces a decrease of the incorporation of labelled glycerol into lipids, whereas at the longest times of incubation flavolignans have an opposite effect. Neutral lipid/phospholipid labelling ratio is modified by ethanol in favour of neutral lipids. This action is counteracted by both flavolignans, which are therefore able to hinder, at least partially, the actions of ethyl alcohol on liver lipid metabolism.

Animals↗
PubMed1980

The effect of chronic ethanol administration on membrane-bound enzymes of rat liver.

The chronic treatment with small amounts of ethanol associated with a fat-poor diet produces enzyme modifications in rat liver subcellular fractions. All the enzymic activities tested in this paper increased or remained unaffected after alcohol treatment. Part of the observed effects could be ascribed to the proliferation of the endoplasmic reticulum which follows to ethanol intoxication; the increase of some enzyme activities, in the plasma membranes of treated animals seems to be probably due to modification of the environment of the membrane.

Alcoholism↗
PubMed1979

The effect of acute ethanol administration on phosphorylcholine uptake and metabolism in rat liver slices.

Liver slices obtained from normal and acutely ethanol-intoxicated rats were incubated with labelled choline plus unlabelled orthophosphate or labelled phosphorylcholine (PC). After variable times of incubation hydrosoluble compounds and choline phosphoglycerides (CPG) were extracted from the tissue and analyzed. When compared to controls, the slices obtained from intoxicated livers accumulated more PC and synthesized more CPG when incubated with PC; on the other hand, when incubated with choline, they accumulated less PC. From these results it can be concluded that PC is a better lipid precursor in intoxicated livers, than in normal ones. In any case CPG becomes better labelled after incubation with choline than with PC; base-exchange could be liable for this result.

Alcoholic Intoxication↗
PubMed1977

Biosynthesis of rat brain phosphatidylethanolamines from intracerebrally injected ethanolamine.

[2-3H]Ethanolamine was injected intracerebrally into male rats and the brains of the animals immediately removed by particular procedures at regular intervals over the first 1200 sec. The incorporation of radioactivity into brain phosphorylethanolamine, cytidine-5'-diphosphate (CDP) ethanolamine and phosphatidylethanolamines was examined and quantitated. The nature of phosphatidylethanolamine molecular subspecies, which became labelled, was also investigated after isotope administration. Phosphorylethanolamine, CDP-ethanolamine and phosphatidylethanolamines were all labelled already 5 sec after the administration of labelled ethanolamine. The specific radioactivities of different phosphatidylethanolamine molecular subspecies varied according to the time elapsed from the injection to the sacrifice of the animals. This last result, together with the data on time course of labelling of ethanolamine phosphoglycerides and their precursors, provides indications that this base may be incorporated into lipids not only by net synthesis pathway, but also by base-exchange reaction.

Animals↗
PubMed1977

The effect of acute ethanol administration on phosphorylethanolamine uptake and metabolism in rat liver slices.

Double-labelled phosphorylethanolamine with a [32P]//[14IA1 ratio of 1 was incubated in vitro with rat liver slices prepared from control and ethanol-intoxicated rats, and the radioactivity measured at given time intervals in liver ethanolamine, phosphorylethanolamine, phosphatidylethanolamine and phosphatidylcholine. Evidence is presented that after 10 and 15 minutes phosphorylethanolamine enters the slices as an intact molecule, which is directly converted into lipid forms by the Kennedy's pathways. At longer times a hydrolysis of the ester occurs which lowers considerably the theoretical [32P]/[14C]ratio. Fatty liver slices produced by acute ethanol intoxication uptake from the medium more phosphorylethanolamine than controls, and hydrolyze less efficiently than controls the phosphoric ester to ethanolamine and inorganic phosphate.

Animals↗
PubMedDate not supplied

Omeprazole induces apoptosis in jurkat cells.

We report for the first time a potent apoptotic effect of omeprazole (OM). Apoptosis was induced in Jurkat cells in a time and concentration-dependent mode. Caspase 3 and PARP were rapidly cleaved in response to OM, but apoptosis was only partially inhibited by the caspase 3 inhibitor DEVD-CHO. OM also induced an early lysosomal destabilization which increased progressively and was correlated with a parallel increase in apoptotic cells. The cysteine protease inhibitor E64d gave strong protection against apoptosis thus proving the involvement of lysosomal enzymes in OM-induced apoptosis whereas, it did not impede the caspase 3 cleavage. Instead ZVAD-fmk, a general caspase inhibitor, also able to inhibit cathepsin activity, protected cells completely from OM-induced apoptosis. It therefore seems that both caspases and cysteine cathepsins are involved in the execution stage of OM-induced apoptosis.

Anti-Ulcer Agents↗
PubMedDate not supplied

Microsomal protein mediates a pH-dependent fusion of liposomes to rat brain microsomes.

The fusion between rat brain microsomes and liposomes is investigated by measuring the release of octadecylrhodamine B (R18) fluorescence self-quenching. In the experimental conditions used in this work, the method allows a rapid and quantitative evaluation of the mixing of microsome and liposome lipid phases. The decrease of pH below 7 produces an extensive fusion between microsomes and acidic phospholipid liposomes. Microsomal protein is necessary for fusion, which is inactivated by exposure of microsomes to pronase. Therefore, H(+)-induced fusion differs from Ca(2+)-induced fusion since the latter does not require microsomal protein. The pretreatment of microsomes with trinitrobenzenesulfonic acid (TNBS) in nonpenetrating conditions does not affect the extent of fusion. On the other hand, N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ), a reagent able to react with carboxyl groups, causes an extensive inactivation of fusion. Therefore, the H(+)-induced fusion described here depends on some microsomal protein and may have physiological significance because it occurs at pH values present in the living cell. H(+)-dependent fusion can be also considered as a means to enrich membranes in some selected lipid.

Animals↗
PubMedDate not supplied

Involvement of CDP-choline in phospholipid metabolism of brain tissue in vitro.

The ability of phosphorylcholine and CDP-choline to act as lipid precursors was tested in chick brain microsomes (plus supernatant). CDP-choline was, in every case, a much better precursor of choline glycerophospholipids than phosphorylcholine. The cytidylyltransferase reaction which forms CDP-choline appears, therefore, as the limiting step of the metabolic pathway which introduces phosphorylcholine into lipids. This reaction can be stimulated by the addition of phospholipids to the incubation mixture. Choline lysoglycerophospholipids are the most active in this connection.

Animals↗
PubMedDate not supplied

The effect of ethanol on 5'-nucleotidase of rat liver plasma membranes.

The activity of 5'-nucleotidase of rat liver plasma membranes has been investigated in normal and acutely ethanol-intoxicated rats (7 g ethanol/Kg body wt). Ethanol was also added to the incubation mixture for 5'-nucleotidase assay. The alcohol modified the Km of the enzyme when added to plasma membranes of normal rats; moreover, it increased the activation energy of the reaction. The treatment with the alcohol in vivo lowered the Vmax, but no modifications of Km could be detected in this case, upon further addition of the toxic in vitro. It is concluded that ethanol is able to act by itself on 5'-nucleotidase activity of rat liver plasma membranes; however, ethanol produces other effects in vivo, probably due to its metabolism.

5'-Nucleotidase↗