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Biomedical subjects

G Arienti

Publications and source records attributed to G Arienti.

At least 73 records · Page 4Linked to original sources

Action of phospholipase A2 of rabbit neuronal and glial cells on 1,2-diacyl-, 2-acyl-1-alk-1'-enyl-, and 2-acyl-1-alkyl-glycerophosphatides.

Pronounced differences in the phospholipase A2 activities were found in neurons and glia, the enzyme activity being two- to threefold higher in neurons than in glial cells. Both phospholipases A2 hydrolyzed the 1,2-diacylglycerophosphatides more rapidly than the acylalkyl and acylalkenyl compounds. Choline plasmalogen and the corresponding alkyl derivative were cleaved at similar rates by the phospholipase A2 from both glia and neurons. There was a tendency by the neuronal phospholipase A2 to release arachidonic acid faster than linolenic acid from both phosphatidylcholine and -ethanolamine, while arachidonic acid was removed less actively from phosphatidylethanolamine by the glial enzyme. The glial phospholipase A2 showed a lag period of 10 or 20 min. Norepinephrine, injection into the lateral ventricle of the rabbit brain, stimulated the hydrolysis of the various 1,2-diacyl-, acylalkyl, and and acylalkenyl-glycerophosphatides by the phospholipase A2 from both glia and neurons.

Animals↗

Glycerophospholipid metabolism in neuronal and glial cell-enriched fractions.

The metabolism of phospholipids in separated glial and neuronal cells has been reviewed in this paper. Lipids are more abundant in glia; on the other hand, in vivo experiments performed with labeled precursors have indicated that lipid turnover is faster in neurons (with the possible exception of oligodendroglia). Biosynthetic and catabolic enzymes of lipid metabolism have been studied in separated cells (mainly in neurons and astroglia) and have been shown to be almost always more active in neurons. Also base exchange is probably more active in these cells. Therefore the results of in vitro and in vivo experiments indicate that neurons are more active than astroglia in metabolizing glycerophospholipids.

Aging↗

Occurrence and properties of phospholipases A1 of plasma membranes prepared from neuronal- and glial-enriched fractions of the rabbit cerebral cortex.

Exogenously added glycerophosphatides, specifically radioactively labelled either in the 1 or in the 2 position, were used to investigate the occurrence and properties of phospholipase A1 in plasma membranes prepared from neuronal- and glial-enriched fractions of rabbit brain. Phospholipase A1 activity was maximal at pH values ranging between 8.0 and 9.0 for the plasma membranes of both cell types. The enzyme activity was most abundant in the microsomal fraction, with a neuronal/glial ratio of about 2. The plasma membranes displayed about half the enzymic activity of the microsomal fraction, whereas only small amounts of phospholipase A1 were present in the neuronal and glial mitochondria. Investigations on the substrate specificity showed a different pattern for the enzyme of neuronal and glial origin. The release of labelled fatty acids from phosphatidylcholine by the neuronal plasma membrane phospholipase A1 decreased with increasing degree of unsaturation of the fatty acids at the 1 position. The presence of plasmalogens and plasmalogen precursors in the incubation mixture appreciably inhibited the hydrolysis of the corresponding diacyl compounds.

Animals↗

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↗

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↗

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↗

Quantitative evaluation of two pathways for ethanolamine phosphoglyceride biosynthesis in rat brain in vivo.

[3H]Ethanolamine and [32P]orthophosphate were injected intraventricularly into adult female rats. At varying time intervals after the injection (1--10 min), the animals were killed by means of a microwave apparatus, and phosphorylethanolamine and ethanolamine phosphoglycerides were extracted from the brains and counted after separation. The kinetic constants for phosphorylethanolamine incorporation into ethanolamine lipids were calculated both from 3H data and from 32P data. From our results, it seems that base exchange reactions for ethanolamine incorporation into ethanolamine lipids are a pathway active in brain in vivo.

Animals↗

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↗

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↗

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↗

The phospholipase activity of sheep pancreatic juice.

Sheep pancreatic juice was found to contain at least two enzymes which hydrolysed biliary lecithin. One enzyme was heat and acid labile and hydrolysed the fatty acid from position 1 (phospholipase A1); the other was heat and acid stable hydrolysing the fatty acid at position 2 (phospholipase A2). Lysophospholipase activity was also present. The phospholipases were active at pH values greater than 4.2, and would therefore function in the acid conditions (pH 3-6) of the sheep small intestine. The activity of the pancreatic phospholipases, and A2 in particular, was dramatically stimulated by the presence of the secretions of Brunner's glands which could be important in accelerating the hydrolysis of biliary lecithin in the lumen of the intestine. Phospholipase A1 was sensitive to acid in the range pH 2.5-3.5 and could therefore be partially inactivated by abomasal digesta; but phospholipase A2 was resistent to acid treatment.

Animals↗