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putrescine/sembap
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Putrescine as a marker of the effects of 2-chloropropionic acid in the rat brain.
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The neurotoxin 2-chloropropionic acid (2CPA, 750 mg/kg, per os) induces ataxia in rats causing neuropathological changes (necrosis and edema) localized mainly in the cerebellum (CB). It has been described that putrescine (PUT) is a good marker of severe brain damage. We measured the concentration of
Toxic effects of putrescine in rat brain: Polyamines can be involved in the action of excitotoxins.
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After treatment with putrescine (PUT) 200 mg/kg, i.p., male rats displayed a behavioural pattern that included wet dog shakes and motor inco-ordination. The concentration of PUT in the brain paralleled the severity of clinical signs. Histological examination showed the presence of perivascular edema
Effects of MDL 72527, a specific inhibitor of polyamine oxidase, on brain edema, ischemic injury volume, and tissue polyamine levels in rats after temporary middle cerebral artery occlusion.
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The possible effects of the polyamine interconversion pathway on tissue polyamine levels, brain edema formation, and ischemic injury volume were studied by using a selective irreversible inhibitor, MDL 72527, of the interconversion pathway enzyme, polyamine oxidase. In an intraluminal suture
Suppression of polyamine biosynthesis prevents monocrotaline-induced pulmonary edema and arterial medial thickening.
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Previous work in our laboratory has shown that the continuous administration of alpha-difluoromethylornithine (DFMO), a highly specific irreversible inhibitor of ornithine decarboxylase (ODC), which is the rate-limiting enzyme in polyamine biosynthesis, prevented the development of pulmonary
Blood brain barrier breakdown in brain edema following cold injury is mediated by microvascular polyamines.
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A focal freeze injury to rat cerebral cortex induces an early (less than 5 min) increase in brain ornithine decarboxylase activity and an accumulation of polyamines involving cerebral microvessels. This polyamine synthesis correlates with the abnormal increase in microvascular permeability,
[Protective effect of putrescine on oleic acid-induced respiratory distress syndrome (RDS)].
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The effect of putrescine on oleic acid-induced RDS were studied in rat, it was found that preadministration of putrescine to rat with RDS significantly improved its hypoxemia, pulmonary edema and histologic injury; inhibited the leakage of protein from plasma; lowered increase of pulmonary lipid
[Exogenous putrescine causes renal function impairment and cell apoptosis in rats].
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OBJECTIVE
To explore the effect of exogenous putrescine on renal function and cell apoptosis in rats.
METHODS
Ninety SD rats were randomized into control group (n=10), high-dose putrescine group (P1 group, n=40), and low-dose putrescine group (P2 group, n=40) with intraperitoneal injections of 2 ml
[Influence of exogenous putrescine on the function of liver and apoptosis of liver cells in rats].
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OBJECTIVE
To explore the influence of exogenous putrescine on the function of liver and apoptosis of liver cells in rats.
METHODS
Ninety healthy clean SD rats were divided into control group (C, n = 10, intraperitoneally injected with 2 mL normal saline), low dosage putrescine group (LP, n = 40),
Difluoromethylornithine decreases postischemic brain edema and blood-brain barrier breakdown.
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Brain polyamines have been associated with posttraumatic vasogenic edema and blood-brain barrier (BBB) breakdown seen in some models of brain injury. We hypothesized that the inhibition of the enzyme responsible for polyamine production with the decarboxylase difluoromethylornithine (DFMO) may
Polyamines induce blood-brain barrier disruption and edema formation in the rat.
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Polyamines (PA) are derived from ornithine by the enzyme ornithine decarboxylase (ODC), which is activated very rapidly as acute and delayed responses to brain ischemia and trauma. Polyamines play a role in the disruption of the blood-brain barrier (BBB) in different pathological states. This study
Melatonin attenuates the changes in polyamine levels induced by systemic kainate administration in rat brains.
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Systemically administered kainate has been demonstrated to induce neuronal damage and changes of the levels of biochemical substances related to neurotoxicity. Polyamines are thought to be important in the generation of edema and neuronal cell loss associated with various type of excitotoxicity.
Radiation brain injury is reduced by the polyamine inhibitor alpha-difluoromethylornithine.
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Alpha-difluoromethylornithine (DFMO) was used to reduce 125I-induced brain injury in normal beagle dogs. Different DFMO doses and administration schedules were used to determine if the reduction in brain injury was dependent on dose and/or dependent upon when the drug was administered relative to
Polyamine synthesis blockade in monocrotaline-induced pneumotoxicity.
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Based on the documented regulatory role of polyamines in cell growth and differentiation, we have proposed that these organic cations are involved with the development of monocrotaline (MCT)-induced hypertensive pulmonary vascular disease. Two lines of evidence support this hypothesis: (1) MCT
Blockade of ornithine decarboxylase enzyme protects against ischemic brain damage.
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Polyamines are derived from ornithine by the actions of ornithine decarboxylase (ODC), which is the rate-limiting step in this pathway. Polyamines play a role in cell growth, neoplasia, differentiation, and response to injury. We have shown that transient cerebral ischemia gives rise to increased
Simultaneous assay of ornithine decarboxylase and polyamines after central nervous system injury in gerbil and rat.
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Ornithine decarboxylase (ODC) is considered the rate-limiting enzyme in polyamine biosynthesis. An increase in putrescine (a natural polyamine) synthesis after central nervous system (CNS) injury appears to be involved in blood-brain barrier dysfunction, development of vasogenic edema and neuronal
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