In vitro and in vivo inhibition of plant polyamine oxidase activity by polyamine analogues

2008 ◽  
Vol 69 (14) ◽  
pp. 2552-2558 ◽  
Author(s):  
Santiago J. Maiale ◽  
María Marina ◽  
Diego H. Sánchez ◽  
Fernando L. Pieckenstain ◽  
Oscar A. Ruiz
Keyword(s):  
Oxidase Activity ◽  
Polyamine Oxidase ◽  
Polyamine Analogues

scholarly journals Regulation of polyamine biosynthesis in rat hepatoma (HTC) cells by a bisbenzyl polyamine analogue

1989 ◽  
Vol 257 (3) ◽  
pp. 769-774 ◽  
Author(s):  
A J Bitonti ◽  
T L Bush ◽  
P P McCann
Keyword(s):  
Mammalian Cells ◽  
Oxidase Inhibitor ◽  
Polyamine Oxidase ◽  
Polyamine Biosynthesis ◽  
Polyamine Analogues ◽  
Htc Cells ◽  
Polyamine Analogue ◽  
Rat Hepatoma

A bisbenzyl polyamine analogue, MDL 27695, rapidly repressed ornithine decarboxylase (ODC) and S-adenosyl-L-methionine decarboxylase (AdoMet DC) activity and depleted polyamines in rat hepatoma (HTC) cells. The suppression of ODC and AdoMet DC activity was temporally related to metabolism of MDL 27695 by intracellular polyamine oxidase to a free-amine analogue, MDL 26752, which, when added directly to HTC cells, suppressed ODC activity and polyamine biosynthesis more rapidly and to a greater extent than did the bisbenzyl analogue. The ODC suppression caused by MDL 27695 was completely blocked by the addition of a polyamine oxidase inhibitor to the HTC-cell cultures along with MDL 27695. These data suggested that MDL 27695 acted as a prodrug, with metabolism to an active analogue being necessary for ODC repression to occur. MDL 27695 and MDL 26752 completely abolished division of HTC cells when added to cultures at 1 microM. This established them as being among the most potent antiproliferative polyamine analogues yet described. MDL 27695 has also been shown to possess significant antimalarial effects both in vitro and in vivo, and it is possible that the marked suppression of polyamine biosynthesis described herein may contribute to its anti-malarial effects as well as its antiproliferative effects in mammalian cells.

scholarly journals Cerebral Ischemia Enhances Polyamine Oxidation: Identification of Enzymatically Formed 3-Aminopropanal as an Endogenous Mediator of Neuronal and Glial Cell Death

1998 ◽  
Vol 188 (2) ◽  
pp. 327-340 ◽  
Author(s):  
Svetlana Ivanova ◽  
Galina I. Botchkina ◽  
Yousef Al-Abed ◽  
Malcolm Meistrell ◽  
Franak Batliwalla ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Glial Cell ◽  
Oxidase Activity ◽  
Cell Damage ◽  
Polyamine Oxidase ◽  
Dependent Manner ◽  
Essential Information ◽  
Ischemic Brain

To elucidate endogenous mechanisms underlying cerebral damage during ischemia, brain polyamine oxidase activity was measured in rats subjected to permanent occlusion of the middle cerebral artery. Brain polyamine oxidase activity was increased significantly within 2 h after the onset of ischemia in brain homogenates (15.8 ± 0.9 nmol/h/mg protein) as compared with homogenates prepared from the normally perfused contralateral side (7.4 ± 0.5 nmol/h/mg protein) (P <0.05). The major catabolic products of polyamine oxidase are putrescine and 3-aminopropanal. Although 3-aminopropanal is a potent cytotoxin, essential information was previously lacking on whether 3-aminopropanal is produced during cerebral ischemia. We now report that 3-aminopropanal accumulates in the ischemic brain within 2 h after permanent forebrain ischemia in rats. Cytotoxic levels of 3-aminopropanal are achieved before the onset of significant cerebral cell damage, and increase in a time-dependent manner with spreading neuronal and glial cell death. Glial cell cultures exposed to 3-aminopropanal undergo apoptosis (LD50 = 160 μM), whereas neurons are killed by necrotic mechanisms (LD50 = 90 μM). The tetrapeptide caspase 1 inhibitor (Ac-YVAD-CMK) prevents 3-aminopropanal–mediated apoptosis in glial cells. Finally, treatment of rats with two structurally distinct inhibitors of polyamine oxidase (aminoguanidine and chloroquine) attenuates brain polyamine oxidase activity, prevents the production of 3-aminopropanal, and significantly protects against the development of ischemic brain damage in vivo. Considered together, these results indicate that polyamine oxidase–derived 3-aminopropanal is a mediator of the brain damaging sequelae of cerebral ischemia, which can be therapeutically modulated.

In vitro and in vivo evidence for oxalate oxidase activity of a germin-like protein from azalea

2015 ◽  
Vol 458 (3) ◽  
pp. 536-542 ◽  
Author(s):  
Atsushi Sakamoto ◽  
Takashi Nishimura ◽  
Yoh-ichi Miyaki ◽  
Shunsuke Watanabe ◽  
Hiroshi Takagi ◽  
...  
Keyword(s):  
Oxidase Activity ◽  
Oxalate Oxidase ◽  
Oxalate Oxidase Activity

BEHAVIOUR OF ADREN0CHR0ME PATHWAY IN PATIENTS WITH CEREBROVASCULAR DISEASES

1987 ◽  
Author(s):  
C Alessandri ◽  
F Violi ◽  
M Rasura ◽  
C Caliendo ◽  
P Pelaia
Keyword(s):  
Oxidase Activity ◽  
Brain Infarction ◽  
Preliminary Investigation ◽  
Significant Rise ◽  
Neutrophil Activation ◽  
Radical Mechanism ◽  
Toxic Substances ◽  
Plasma Adrenaline

Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a neutrophil oxidase able to convert,in vitro, adrenaline to adrenochrome.Aim of present study was to evaluate if neutrophil activation can be observed in patients with brain hemor ragie (BH) also.Six patients (females 1,males 5;age 68-79 years) suffering from BH and 15 patients (females 5, Males 10;age 58-86 years) affected by brain infarction (BI) were studied within 20-48 hours from acute episode.Diagnosis of stroke was made by computerized tomography.Neutrophil activation was studied in plasma evaluating the oxidation of adrenaline to adrenochrome according to Matthews and Campbell method.20 matched for age and sex healthy subjects were studied as control.A significant rise of plasma adrenaline oxidase activity was observed in patients with BI.This preliminary investigation suggests that neutrophil activation could be restricted to patients with BI.In fact,patients with BH had plasma oxidase activity similar to controls.Clinical data should be necessary to evaluate if a relation between leucocyte activation and the natural course of cerebral ischemia does exist.

scholarly journals Identification of bioactive compounds from Fraxinus angustifolia extracts with anti-NADH oxidase activity of bovine milk xanthine oxidoreductase

2019 ◽  
pp. 133-147 ◽  
Author(s):  
Nadjia AHMANE ◽  
Dina ATMANI-KILANI ◽  
Nassima CHAHER ◽  
Karima AYOUNI ◽  
Meriem RAHMANI-BERBOUCHA ◽  
...  
Keyword(s):  
Oxidase Activity ◽  
Nadh Oxidase ◽  
Bovine Milk ◽  
Ros Generation ◽  
Xanthine Oxidoreductase ◽  
Fraxinus Angustifolia ◽  
Activity Of Enzymes ◽  
Nadh Oxidase Activity

Fraxinus angustifolia leaves and bark are used in traditional medicine against various inflammatory-related pathologies incumbent to reactive oxygen species (ROS) generation by the NADH oxidase activity of enzymes such as xanthine oxidoreductase (XOR). This study was designed to investigate the in vitro and in vivo inhibitory activities of this enzyme by Fraxinus angustifolia extracts. The leaf organic phase of ethyl acetate (LFA) and its bark aqueous counterpart (BFA) showed the strongest anti-NADH oxidase activity in vitro (IC50 = 38.51 and 42.04 μg mL-1, respectively). They consequently suppressed superoxide generation both enzymatically (53% and 19%, respectively) and nonenzymatically (34% and 19%, respectively). These results were corroborated in vivo, with high anti- NADH oxidase potential of the leaves and bark extracts (75.32% and 51.32%, respectively) concomitant with moderate hypouricemic activities (36.84% and 38.59%, respectively). Bio-guided fractionation led to the identification, by LC-DAD-MS/MS, of esculin and calcelarioside in bark and kaempferol glucoside in leaves as the main compounds responsible for the anti-NADH oxidase activity of XOR. These results plead in favor of the use of F. angustifolia as a source of potentially interesting therapeutic substances.

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