Wyniki wyszukiwania - Biblioteka Nauki

1

Effect of arachidonic acid on specific binding of [3H]naloxone to opioid receptors

100%

Apaydin S. , Oktem H. A.

Acta Neurobiologiae Experimentalis

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2000

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tom 60

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nr 3

361-363

EN

The effects of arachidonic acid (AA) on binding of [3H]naloxone to the agonist and antagonist configurations of opioid receptors were investigated in rat brain. Equilibrium binding parameters of the agonist and antagonist configurations of the receptors were evaluated from homologue displacement data in the presence or absence of AA. Addition of AA at a concentration of 0.6 mM (1.5 m mole/mg of protein) reduced by 22% and 53% the maximal number of binding sites (Bmax) respectively in the absence or presence of 100 mM NaCl. Binding affinity (KD) was not altered significantly (P<0.05) either in the presence or absence of 100 mM NaCl and AA. We conclude that AA mediated reduction in [3H]naloxone specific binding was chiefly due to a decrease in the number of binding sites.

2

Acute hypoxia modulates arachidonic acid metabolism in cat carotid bodies.Role of dopamine

80%

Strosznajder R.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 2

535-543

EN

The hypoxic stimulus of arterial blood is transformed at the carotid body (CB) chemoreceptors into neuronal signals regulating respiration.The mechanism of chemotransduction is until now not well understood.In this study the regulation of arachidonic acid (AA) release and its incorporation into membrane glycerolipids were investigated.Moreover, the effect of hypoxia and dopamine (DA) on these processes was calculated.The CB were excised from cats exposed in situ to normoxia or hypoxia.Then CB were homogeni and used as a source of enzyme (s).It was observed thar Ca2+ enhanced the release of AA by 40-50% through the action of phospholipase C together with diacyl-glycerol lipase and phospholipase A2.Acute hypoxia significantly decreased AA incorporation into phosphatidylinositol (PtdIns) and enhanced the level of AA radioactivity in diacylglycerol and AA-CoA.These results suggest that hypoxia induces inhibition of AA on the level of acyl-CoA-lysophospholipid:acylotransferases.DA decreased AA incorporation into PtdIns and exerted an additive inhibitory effect in hypoxic samples.These results demonstrated that AA metabolism in CB is significantly affected by hypoxia and that DA is not responsible for the hypoxia-induced alteration of lipid metabolism in CB.

3

The effect of packed red blood cell storage on arachidonic acid and advanced glycation end-product formation

80%

Lysenko L. , Mierzchala M. , Gamian A. , Durek G. , Kubler A. , Kozlowski R. , Sliwinski M.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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tom 54

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nr 5

357-362

EN

Introduction: The transfusion of packed red blood cells (PRBCs) is a significant risk to blood recipients. Blood banking procedures permit the storage of PRBCs for up to 42 days. Storage of PRBCs can cause polymorphonuclear granulocytes (PMN) activation and the development of neutrophil-mediated transfusion-related acute lung injury. The aim of our study was to determine if PRBC storage has an influence on the formation of arachidonic acid (AA) and advanced glycation end products (AGEs). Materials and Methods: Twenty units of PRBCs were used to measure AA and AGE levels. The samples were taken on the 0th, 14th, 28th, and 42nd days of PRBC storage. The AA level was analyzed by gas-liquid chromatography-mass spectrometry and AGE level by an immunoenzymatic test. Results: During the first 14 days of PRBC storage, the AA level significantly increased and then slowly decreased. The AGE level increased continuously during the whole time of the study. In a model experiment, the AA glycoxidation product trans-2-nonenal (T2N) formed adducts in reaction with hemoglobin which were detectable with the test for AGE. Conclusions: It is highly probable that the observed increase in AGE level is related to the decrease in AA in PRBCs, which can be associated with the formation of toxic aldehydes, especially T2N and 4-hydroxynonenal (HNE), from AA. Glucose in the PRBCs (preservative solution) can contribute to AGE formation as well. The formation of AGEs, HNE, and T2N in PRBCs, their influence on PMNs in vitro, and confirmation of our assumption need further studies.

4

Regulation of the NADPH oxidase activity and anti-microbial function of neutrophils by arachidonic acid

80%

Hii C. S. , Ferrante A.

Archivum Immunologiae et Therapiae Experimentalis

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2007

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tom 55

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nr 2

99-110

EN

Arachidonic acid (AA), a second-messenger molecule released from membrane phospholipids by phospholipase A2 in activated cells, is a stimulator of neutrophil responses, including the oxygen-dependent respiratory burst. The polyunsaturated fatty acid is also the precursor of biologically active eicosanoids. There are several mechanisms by which AA stimulates the respiratory burst. These include the direct binding of AA to S100 proteins which regulate the assembly of the NADPH oxidase as well as the activation of key signaling molecules which control the respiratory burst. Arachidonic acid also stimulates it own release from membrane phospholipids and this contributes to optimal respiratory burst activity. Thus, increased levels of AA at sites of inflammation will influence the magnitude and course of the inflammatory response, not only by directly affecting the function of infiltrating neutrophils and other leukocytes, but also through its metabolites generated by lipoxygenases and cyclooxygenases.

5

Modulation of NMDA receptor - mediated release of [3h}arachidonate in hippocampal slices of immature rats

70%

Salinska E. , Lazarewicz J. W.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

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nr 1

11-21

EN

Using superfusion with albumin-containing medium of hippocampal and striatal slices of adult and developingrats at postnatal days(PND) 7-10, prelabelled with [3H]arachidonic acid ([3H]AA) we detected N-methyl-D-aspartate (NMDA) evoked release to the superfusion medium of radiolabelld material, 70% of which was associated with arachidonic acid (AA) and its metabolite.[3H[AA release was much more pronounced in PND 7-10 rats than in adults, and the response to NMDA in the hippocampal slices exceed the reactions in the striatal slices.The subsequent experiments, emplyoing only hippocampal slices of PND 7-10 rats, demonstrated that NMDA-stimulated [3H]AA release was dose-depended in the micromolar range,was sensitive to NMDA receptor antagonists, and wasinhibited in calcium-free medium and the presence of quinacrine.[3H]AA release induced by 100 ?M NMDA was not significantly inhibited by magnesium but was completly blocked by 7 Cl-kynurenic acid and ifenprodil (both antagonists 100 ?M).The sulfhydryl reducing reagent dithiothreitol induced [3H]AA release; this response was sensitive to NMDA receptor antagonists.These data indicate that the NMDA induced, calcium triggered, and phospholipides A2 depended AA release is highly pronounced in the developing rat hippocampus.NMDA receptors mediating AA release in the hippocampus of PND 7-10 rats are subject to glycine, polyamine and redox modulationn, but they show low sensitivity to Mg2+ inhibition.

6

Prostaglandins and the kidney

60%

Senatorski G. , Paczek L. , Lac M.

Postępy Higieny i Medycyny Doświadczalnej

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1993

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tom 47

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nr 5

305-324

7

GP IIb/IIIa receptor antagonists ? molecular and clinical aspects

60%

Francuz T.

Postępy Higieny i Medycyny Doświadczalnej

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2001

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tom 55

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nr 3

419-432

EN

Recently many investigators have found that platelet glycoprotein GP IIb/IIIa is responsible for platelet aggregation and plays a pivotal role in acute coronary thrombosis. Thus, GP IIb/IIIa antagonists may play an important role by inhibiting platelet aggregation and their binding to fibrinogen. Drugs that antagonize this binding have been developed for the treatment of thrombotic diseases and acute coronary syndrome. Now, there are three group of platelet receptor antagonists: monoclonal antibodies, synthetic peptides and non-peptide antagonists. As a result of large clinical trials the potency of those compounds in preventing of coronary thrombosis have been demonstrated. In this article molecular aspects of GP antagonists action and selected clinical trials have been presented.