spermidine/enfarktüs

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Spermidine: A predictor for neurological outcome and infarct size in focal cerebral ischemia?

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OBJECTIVE Polyamines are mainly restricted to the intracellular space. During focal cerebral ischemia, polyamines are released from the intracellular compartment. Experimental studies have implicated a marked elevation in brain tissue and blood. The aim of our study was to investigate whether the

Spermidine-enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway.

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Spermidine, a natural polyamine, is abundant in mammalian cells and is involved in cell growth, proliferation, and regeneration. Recently, oral spermidine supplements were cardioprotective in age-related cardiac dysfunction, through enhancing autophagic flux. However, the effect of

Spermidine/spermine-N¹-acetyltransferase in kidney ischemia reperfusion injury.

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Ischemic reperfusion injuries such as acute renal failure, acute liver failure, stroke, and myocardial infarction are prevalent causes of morbidity and mortality. Kidney ischemic reperfusion injury is the leading cause of acute renal failure and dysfunction of transplanted kidneys. Although

Differing effects of alpha-difluoromethylornithine and CGP 40116 on polyamine levels and infarct volume in a rat model of focal cerebral ischaemia.

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Focal cerebral ischaemia was induced in rats by occlusion of the left middle cerebral artery. Two days later, infarct volume was determined by magnetic resonance imaging and the concentrations of the polyamines putrescine (PU), spermine and spermidine by HPLC. In control (occluded) animals, PU

Intense correlation between brain infarction and protein-conjugated acrolein.

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OBJECTIVE We recently found that increases in plasma levels of protein-conjugated acrolein and polyamine oxidases, enzymes that produce acrolein, are good markers for stroke. The aim of this study was to determine whether the level of protein-conjugated acrolein is increased and levels of spermine

Brain infarction correlates more closely with acrolein than with reactive oxygen species.

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Although it is thought that the major factor responsible for cell damage is reactive oxygen species (ROS), our recent studies have shown that acrolein is more toxic than ROS. Thus, the relative importance of acrolein and ROS in cell damage during brain infarction was compared using photochemically

[Changes in the specific activity and content of free nucleotides and polyamines of the infarct and pre-infarct area of the revascularized dog heart].

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Changes on specific radioactivity and levels of free nucleotides and polyamines in infarcted and borderline tissue of reperfused dog heart. The changes on specific radioactivity and levels of free nucleotides and polyamines, spermine and spermidine, of reperfused heart show a different behaviour of

Akt and Erk1/2 activate the ornithine decarboxylase/polyamine system in cardioprotective ischemic preconditioning in rats: the role of mitochondrial permeability transition pores.

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Ornithine decarboxylase (ODC) is the first rate-limiting enzyme in polyamine biosynthesis, which is essential for cell survival. We hypothesized that the ODC/polyamine system is involved in ischemic preconditioning (IPC)-mediated cardioprotection through the activation of Erk1/2 and Akt and through

Involvement of the ornithine decarboxylase/polyamine system in precondition-induced cardioprotection through an interaction with PKC in rat hearts.

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Polyamines (putrescine, spermidine, and spermine) play an essential role in cell growth, differentiation, and apoptosis. Protein kinase C (PKC) stimulates polyamine biosynthesis through the induction of ornithine decarboxylase (ODC), a rate-limiting enzyme in polyamine biosynthesis. Activation of

Dual role of polyamines in heart ischemia/reperfusion injury through regulation of mitochondrial permeability transition pore.

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Polyamines (putrescine, spermidine, and spermine) are essential polycations that play important roles in various physiological and pathophysiological processes in mammalian cells. The study was to investigate their role in cardioprotection against ischemia/reperfusion (I/R) injury and the underlying

Elevated N1-acetylspermidine levels in gerbil and rat brains after CNS injury.

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The polyamine system is very sensitive to different pathological states of the brain and is perturbed after CNS injury. The main modifications are significant increases in ornithine decarboxylase activity and an increase in tissue putrescine levels. Previously we have shown that the specific

Use of polyamine metabolites as markers for stroke and renal failure.

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Acrolein and H(2)O(2) are among the metabolic products of spermine and spermidine, and it was found that acrolein was more toxic than H(2)O(2). It was determined whether acrolein can serve as a biochemical marker for stroke (brain infarction) and chronic renal failure. Since acrolein rapidly reacts

Neuroprotective effects of spermine following hypoxic-ischemic-induced brain damage: a mechanistic study.

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The polyamines (spermine, putrescine, and spermidine) can have neurotoxic or neuroprotective properties in models of neurodegeneration. However, assessment in a model of hypoxia-ischemia (HI) has not been defined. Furthermore, the putative mechanisms of neuroprotection have not been elucidated.

Inhibition of eIF5A hypusination pathway as a new pharmacological target for stroke therapy

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In eukaryotes, the polyamine pathway generates spermidine that activates the hypusination of the translation factor eukaryotic initiation factor 5A (eIF5A). Hypusinated-eIF5A modulates translation, elongation, termination and mitochondrial function. Evidence in model organisms like drosophila

The role of polyamines in protein-dependent hypoxic tolerance of Drosophila.

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BACKGROUND Chronic hypoxia is a major component of ischemic diseases such as stroke or myocardial infarction. Drosophila is more tolerant to hypoxia than most mammalian species. It is considered as a useful model organism to identify new mechanisms of hypoxic tolerance. The hypoxic tolerance of

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