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

100%
Strosznajder R.
Acta Neurobiologiae Experimentalis
|
1996
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vol. 56
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issue 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.
2
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Effect of 3-aminobenzamide on Bcl-2, Bax and AIF localization in hippocampal neurons altered by ischemia-reperfusion injury. The immunocytochemical study

63%
Strosznajder R., Gajkowska B.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 1
15-22
EN
Poly(ADP-ribose) polymerase plays an important role in cell survival and death. Our previous histological and ultrastructural studies showed that PARP inhibitor 3-aminobenzamide (3-AB) protected neurons against death after ischemia. In this study we investigated the effect of 3-AB on the localization and expression of apoptosis inducing factor (AIF) and on two proteins from Bcl-2 family: Bcl-2 and Bax in hippocampal area CA1, on the 4th day after 3 min of forebrain ischemia in gerbils. Our results indicated that after ischemia AIF is preferentially translocated from the mitochondria to the cytoplasm and to the nucleus. Intravenous administration of 3-AB (30 mg/kg b.w.) prevents AIF translocation to the nucleus. AIF was mainly seen in the structurally unchanged mitochondria and Golgi complex. Moreover, after 3-AB administration overexpression of Bcl-2 protein was observed in mitochondrial membranes, rough endoplasmatic reticulum, Golgi complex, nuclear envelopes, and also in cytoplasm and in nucleus. These data suggest that inhibition of PARP activity may have a beneficial effect on hippocampal neurons through overexpression of Bcl-2 protein and suppression of AIF translocation to the nucleus.
3
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Effect of carvedilol on neuronal survival and poly(ADP-ribose) polymerase activity in hippocampus after transient forebrain ischemia

51%
Strosznajder R., Jesko H., Dziewulska J.
Acta Neurobiologiae Experimentalis
|
2005
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vol. 65
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issue 2
137-134
EN
Carvedilol a beta-adrenoreceptor antagonist with potent antioxidant properties raises high expectations in therapy of ischemia. In this study the effect of carvedilol on neuronal survival after transient forebrain ischemia in gerbils was investigated. The role of poly(ADP-ribose) polymerase (PARP-1) in this process was evaluated. Our data indicated that carvedilol administered subcutaneously in a dose of 7 or 70 mg/kg b.w. directly after 5 min of transient forebrain ischemia protects significant population of neurons in hippocampal area CA1, but has no effect after induction of prolonged 10 min ischemia. Carvedilol significantly decreased PARP activity in hippocampus that was markedly increased after both 15 min and 4 days of reperfusion following 5 min of ischemia. Moreover, carvedilol prevented NAD+ depletion after ischemic-reperfusion insult. These results indicated that carvedilol protects neurons against death and suggested that suppression of PARP activity during reperfusion could be involved in this process.
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