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O Barnabei

Publications and source records attributed to O Barnabei.

At least 55 records · Page 3Linked to original sources

Conformational changes of nuclear chromatin related to phospholipid induced modifications of the template availability.

The phospholipid involvement in the regulation of the functional and structural properties of isolated nuclei has been studied by analyzing the composition and the possible function of the nuclear matrix bound phospholipids in rat liver and murine erythroleukemic cells. The digestion of the matrix phospholipids with phospholipases results in the release of essentially all the newly replicated matrix DNA. The exogenous addition of liposomal phosphatidylserine to rat liver nuclei induces chromatin structural changes consisting in a disaggregation of the heterochromatin, probably mediated by the matrix remodeling, and in a transition from the solenoid fiber to the nucleosome filament, due to the removal of the histone H1. These effects occur through a direct interaction of phospholipid molecules with the inner nuclear components, as demonstrated by carboxyfluorescein transfer and electron microscope autoradiography.

Animals↗

Pharmacological manipulation of GABA system does not protect the goldfish optic tectum from the neuroexcitatory and neurotoxic action of kainic acid.

Inhibition of GABA transaminase which led to a several-fold increase of GABA levels in the goldfish optic tectum or diazepam pre-treatment, were unable to protect tectal neurons from kainic acid neurotoxicity, as judged by light and electron microscopic observations and by the drop of marker enzymes for neurotransmitters. In an in vitro preparation of tectal slices GABA, added to the incubation medium, had no effect on a metabolic parameter (CO2 production from exogenous glucose) related to the excitatory action of kainic acid. It is concluded that, in the goldfish optic tectum, pharmacological manipulation cannot enhance the activity of GABAergic circuits to the extent necessary to block the neuroexcitatory and neurotoxic action of kainic acid.

4-Aminobutyrate Transaminase↗

Study of differential effects of kainic acid on metabolic rates, utilizing exogenous or endogenous substrates, in rat brain slices.

CO2 production from exogenous glucose of cortical, whole hippocampal, and CA3 region hippocampal slices, as well as O2 consumption of whole hippocampal slices, were measured in the presence of different concentrations of kainic acid. A moderate, significant increase of CO2 production was seen only in the CA3 region hippocampal preparation at kainic acid concentrations of 10(-4)-10(-2) M. The O2 consumption, at the expense of endogenous energy stores of whole hippocampal slices, was substantially increased by 10(-3) M kainic acid when the slices were incubated without exogenous glucose. The effect was partly paralleled by the use of high (50 mM) K+ concentration. Some of the possible factors involved in the differential metabolic responses of brain slices to the action of kainic acid are discussed briefly.

Animals↗

Role of chromatin phospholipids on template availability and ultrastructure of isolated nuclei.

The influence of phospholipid vesicles has been tested on isolated nuclei by evaluating the endogenous DNA-dependent RNA polymerase and the chromatin ultrastructure. Negatively charged phosphatidylserine liposomes have a stimulating effect on RNA synthesis, while the vesicles obtained with the neutral sphingomyelin, phosphatidylethanolamine and phosphatidylcholine, and the acidic phosphatidylinositol, are inhibitory. The enhancement of transcription by phosphatidylserine seems to be due to both elongation and initiation of RNA transcripts and very likely depends on interactions of the lipid with the template rather than with the enzymes. The morphological analysis indicates deep changes of the chromatin organization, mainly concerning the size and distribution of the fibers, without any variation of the nuclear volume. The rearrangement of the chromatin could account for the variations of the template availability for RNA synthesis induced by the vesicles and might be associated with changes of the nuclear matrix.

Animals↗

Effect of kainic acid, glutamate, and aspartate on CO2 production by goldfish tectal slices.

For a study of the excitatory effect of kainate, glutamate, and aspartate in the goldfish optic tectum, these substances were tested on the production of CO2 from radioactive glucose in tectal slices incubated in Krebs-Ringer medium for fish. Kainate increased the rate of CO2 production for up to 30 min in a dose-related manner, the effect being maximum at 0.1 mM concentration and decreasing at higher doses. The effect was blocked by ouabain (1 mM) as well as by the substitution of choline for Na+ in the incubation medium. Glutamate and aspartate exerted a less pronounced excitatory effect on CO2 production at higher concentration than kainate. This effect was also abolished by ouabain. Glutamate, added to the medium at a concentration at least 100-fold higher than kainate, partially reversed the increase in CO2 production induced by kainic acid. No similar effect was noticed for aspartate. The supposed glutamate antagonists glutamic acid diethylester (1 mM) and proline (5 mM) did not affect the excitatory action of kainic acid or exert an antagonistic effect towards glutamate. At higher concentration (10 mM) glutamic acid diethylester increased CO2 production, an effect that was, however, ouabain insensitive. Methyltetrahydrofolic acid (1 mM), a substance reported to compete for the kainate receptor, did not inhibit the effect of kainic acid or increase CO2 production.

Animals↗

Regulation of cyclic AMP levels in human lymphocytes and lymphoblasts by prostaglandins.

The sensitivity of human lymphocytes to prostaglandins was compared to that of two lines of cultured lymphoblasts. It was found that 25 nM PGE1 increased lymphocyte cyclic AMP levels twofold, but had no effect on lymphoblasts. At 2.8 micrometers PGE1 the increase of cyclic AMP in lymphocytes was 14 fold versus a 1-3 fold increase in lymphoblasts. Lymphoblasts maintained a response to 6-keto-PGE1, isoproterenol and histamine similar to that observed in lymphocytes. Thus, it appears that the rapidly proliferating lymphoblasts excape signals inhibiting proliferation by impairing the function of the PGE receptor.

Alprostadil↗

The effect of 6-keto-prostaglandin E1 on human lymphocyte cAMP levels.

6-keto-PGE1 was capable of increasing cyclic AMP levels of peripheral human blood lymphocytes in a dose and time dependent fashion. The response was maximal after 30 min of incubation at 37 degrees C; 1 microgram per ml of 6-keto-PGE1 elevated cyclic AMP levels 5 fold which compares with a 10 fold increase due to PGE1. Thus 6-keto-PGE1 may play a role as a modulator of lymphocyte function.

Alprostadil↗

Is a slow reacting substance-like compound involved in rat platelet agglutination.

Endoperoxide analogs at doses 100-fold higher than those required to aggregate human platelet-rich plasma (PRP), were ineffective on rat PRP. Indomethacin (20 microM) and imidazole did not affect arachidonate-induced aggregation of rat PRP. On the other hand, prostaglandin (PG) E1 inhibited aggregation at doses similar to those effective on human PRP, while high doses of PGI2 failed to inhibit arachidonate aggregation in the rat. Eicosatetraynoic acid (10 microgram) blocked the second phase of aggregation; the Ca2+-ionophore A 23187 potentiated the arachidonate effect. Thus, it appears that endoperoxides or thromboxane A2 may not be involved in rat platelet aggregation and that the formation of aggregants from arachidonate shares many properties with the biosynthesis of slow reacting substance, a metabolite of arachidonic acid containing a sulphate group. To test this, rat PRP was incubated with labeled sulphate and aggregated with arachidonate. After column and thin layer chromatography a labeled lipid was identified having a mobility higher than phospholipids but lower than PGF2 alpha. Treatment with arylsulphatase decreased radioactivity by at least 70%.

Adenosine Diphosphate↗