The neurotoxicity of glutamate, dopamine, iron and reactive oxygen species: Functional interrelationships in health and disease: A review — discussion
@article{Smythies2009TheNO, title={The neurotoxicity of glutamate, dopamine, iron and reactive oxygen species: Functional interrelationships in health and disease: A review — discussion}, author={John Smythies}, journal={Neurotoxicity Research}, year={2009}, volume={1}, pages={27-39} }
The fact that glutamate, dopamine, iron and reactive oxygen species are potentially individually highly neurotoxic molecules is well known. The purpose of this review is to examine the less well known complex ways in which their normal biological, as well as their neurotoxic activity, are interconnected in relation to fundamental neuronal functions. These functions include synaptic plasticity (formation and removal of synapses), endocytosis-based recycling of receptors for neurotransmitters and…
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References
SHOWING 1-10 OF 114 REFERENCES
Inhibition of Glutamate Transport in Synaptosomes by Dopamine Oxidation and Reactive Oxygen Species
- Biology, ChemistryJournal of neurochemistry
- 1997
It is suggested that reactive oxygen species and dopamine oxidation products can modify glutamate transport function, which may have implications for neurodegenerative processes such as ischemia, methamphetamine‐induced toxicity, and Parkinson's disease.
Free radical pathology and antioxidant defense in schizophrenia: a review
- Medicine, BiologySchizophrenia Research
- 1996
Role of iron and iron chelation in dopaminergic‐induced neurodegeneration: Implication for Parkinson's disease
- Biology, ChemistryAnnals of neurology
- 1992
It is demonstrated that intraventricular injection of 130 ng deferoxamine to rats prior to 250 μg of 6‐OHDA partially prevented the decrease in striatal dopamine content caused by 6‐ OHDA, and this protection was sufficient to produce normal dopamine‐related behavioral responses.
The Role of Glutathione in Dopaminergic Neuronal Survival
- BiologyJournal of neurochemistry
- 1997
The data suggest that although a decreased glutathione content is not likely to be the sole cause of dopaminergic neuronal loss in Parkinson's disease, decreased glutATHione content may act in conjunction with other factors such as 1‐methyl‐4‐phenylpyridinium to cause the selective death of dopaminaergic neurons.
Dopamine Neurotoxicity: Inhibition of Mitochondrial Respiration
- Biology, ChemistryJournal of neurochemistry
- 1995
The results suggest that catecholamines can cause toxicity not only by inducing an oxidative stress state but also possibly through direct interaction with the mitochondrial electron transport system.
Free radicals and MPTP-induced selective destruction of substantia nigra compacta neurons.
- Biology, ChemistryAdvances in pharmacology
- 1998
Free radical pathology in schizophrenia: a review.
- Medicine, PsychologyProstaglandins, leukotrienes, and essential fatty acids
- 1996
Dopamine D2‐type agonists protect mesencephalic neurons from glutamate neurotoxicity: Mechanisms of neuroprotective treatment against oxidative stress
- BiologyAnnals of neurology
- 1998
It is demonstrated that preincubation with D2‐type dopamine agonists bromocriptine and quinpirole provides neuroprotection against glutamate‐induced neurotoxicity in cultured rat mesencephalic neurons and indicates that dopamine D2 agonists provide protection mediated not only by the inhibition of dopamine turnover but also via D2-type dopamine receptor stimulation and the subsequent synthesis of proteins that scavenge free radicals.
Monoamine metabolism provides an antioxidant defense in the brain against oxidant- and free radical-induced damage.
- Chemistry, BiologyArchives of biochemistry and biophysics
- 1993
It is shown that norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindole acetic acid(5-HIAA) protect brain homogenate and mitochondria against iron-dependent lipid peroxidation and protect brain microsomes against both iron- dependent and iron-independent lipid per oxidation.
Neural Heme Oxygenase-1 Expression in Idiopathic Parkinson's Disease
- BiologyExperimental Neurology
- 1998
Upregulation ofHO-1 in the substantia nigra of PD subjects supports the view that the affected tissue is experiencing chronic oxidative stress, and excessive cellular levels of heme-derived free iron and carbon monoxide resulting from HO-1 overactivity may contribute to the pathogenesis of PD.