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salsolinol/atrofia
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 20 risultati
Elevated interleukin-1β serum level after chronic peripheral salsolinol administration.
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The catechol isoquinoline derivatives are endogenous compounds present in the mammalian brain and the representative one is referred to as salsolinol. It may be formed from aromatic amines leading to neurotoxic N-methyltetrahydroquinolinium ions that may play a role in the etiology of Parkinson's
Neuroprotective effects of nicotine against salsolinol-induced cytotoxicity: implications for Parkinson's disease.
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Parkinson's disease is associated with degeneration of dopaminergic cell bodies in the substantia nigra. It has been suggested that salsolinol, an endogenous metabolite of dopamine, may be involved in this process. An inverse relationship between Parkinson's disease and smoking (nicotine intake) has
Effect of (R)-salsolinol and N-methyl-(R)-salsolinol on the balance impairment between dopamine and acetylcholine in rat brain: involvement in pathogenesis of Parkinson disease.
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BACKGROUND
Parkinson disease (PD), a progressive neurodegenerative disease, affects at least 1% of population above the age of 65. Although the specific etiology of PD remains unclear, recently the endogenous neurotoxins such as (R)-salsolinol [(R)-Sal] and N-methyl-(R)-salsolinol [(R)-NMSal] have
An endogenous MPTP-like dopaminergic neurotoxin, N-methyl(R)salsolinol, in the cerebrospinal fluid decreases with progression of Parkinson's disease.
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There have been an increasing number of evidences indicating that dopamine-derived N-methyl(R)salsolinol is an endogenous MPTP-like neurotoxin to cause Parkinson's disease. In the cerebrospinal fluid from newly diagnosed untreated patients with Parkinson's disease, the level of this toxin was found
Type A monoamine oxidase is the target of an endogenous dopaminergic neurotoxin, N-methyl(R)salsolinol, leading to apoptosis in SH-SY5Y cells.
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Mitochondrial monoamine oxidase (MAO) has been considered to be involved in neuronal degeneration either by increased oxidative stress or protection with the inhibitors of type B MAO (MAO-B). In this paper, the role of type A MAO (MAO-A) in apoptosis was studied using human neuroblastoma SH-SY5Y
Oxidative modification of human ceruloplasmin induced by a catechol neurotoxin, salsolinol.
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Salsolinol (SAL), a compound derived from dopamine metabolism, is the most probable neurotoxin involved in the pathogenesis of Parkinson's disease (PD). In this study, we investigated the modification and inactivation of human ceruloplasmin (hCP) induced by SAL. Incubation of hCP with SAL increased
Salsolinol, an endogenous compound triggers a two-phase opposing action in the central nervous system.
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Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline), an endogenous compound present in the brain, was suspected of participation in the etiopathogenesis of Parkinson's disease, the most common serious movement disorder worldwide. In this study, we evaluated the effect of different
Isolation and Sequencing of Salsolinol Synthase, an Enzyme Catalyzing Salsolinol Biosynthesis.
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Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline), a derivate of dopamine, is suspected to be the most probable neurotoxin in the degeneration of dopaminergic neurons. Numerous hypotheses regarding its pathophysiological roles have been raised, especially related to Parkinson's
Synergistic Neuroprotective Effect of Endogenously-Produced Hydroxytyrosol and Synaptic Vesicle Proteins on Pheochromocytoma Cell Line Against Salsolinol.
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Oxidative stress triggers a lethal cascade, leading to Parkinson's disease by causing degeneration of dopaminergic neurons. In this study, eight antioxidants were screened for their neuroprotective effect on PC12 cells (pheochromocytoma cell line) under oxidative stress induced by salsolinol
Salsolinol, a catechol neurotoxin, induces oxidative modification of cytochrome c.
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Methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol), an endogenous neurotoxin, is known to perform a role in the pathogenesis of Parkinson's disease (PD). In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with salsolinol. When cytochrome c was
Differential effects of dopaminergic neurotoxins on DNA cleavage.
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OBJECTIVE
Environmental and endogenous toxins are considered to increase the risk of dopaminergic neurodegeneration. Parkinson's disease is a neurological disorder occurring due to the death of dopaminergic neurons in substantia nigra. The present study investigated the effect of parkinsonian
Functional alterations in cerebral GABAA receptor complex associated with formation of alcohol dependence: analysis using GABA-dependent 36Cl- influx into neuronal membrane vesicles.
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The effect of alcohol dependence induced by ethanol inhalation on GABA-dependent 36Cl- influx into membrane vesicles prepared from the mouse brain has been examined. Ethanol, flunitrazepam and salsolinol induced a significant facilitation of the GABA-dependent 36Cl- influx into membrane vesicles
Ethanol-induced alterations in the function of cerebral GABAA receptor complex: effect on GABA-dependent 36Cl- influx into cerebral membrane vesicles.
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Effect of addition in vitro of ethanol on the functions of the GABAA receptor complex was investigated using synaptic membrane preparation obtained from mouse brain. Ethanol (50-200 mM) had no significant effect on the specific bindings of [3H]muscimol to GABAA receptor and [3H]flunitrazepam to
The formation of catechol isoquinolines in PC12 cells exposed to manganese.
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Chronic exposure to manganese causes parkinsonian symptoms and has been implicated as an environmental factor in the pathogenesis of Parkinson's disease (PD). Here we show that manganese inhibits the proliferation of PC12 cells and induces apoptosis through the formation of catechol isoquinolines.
The influence of acute and chronic administration of 1,2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline on the function of the nigrostriatal dopaminergic system in rats.
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The contribution of (R)-enantiomer of N-methyl-salsolinol (1,2-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline; NMSal) to the degeneration of dopaminergic neurons in the course of Parkinson's disease (PD) has been predominantly suggested by in vitro experiments in cell culture and by an in
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