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2 4 dihydroxybenzoic acid/atrofia
Odkaz sa uloží do schránky
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In vivo evidence against clomethiazole being neuroprotective against MDMA ('ecstasy')-induced degeneration of rat brain 5-HT nerve terminals by a free radical scavenging mechanism.
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Clomethiazole is an effective neuroprotective agent against the degeneration of 5-HT neurones that follows administration of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy'). Since there is good evidence that free radical formation resulting from auto-oxidation of MDMA metabolites is
In vivo evidence for free radical involvement in the degeneration of rat brain 5-HT following administration of MDMA ('ecstasy') and p-chloroamphetamine but not the degeneration following fenfluramine.
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1. Administration of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') to several species results in a long lasting neurotoxic degeneration of 5-hydroxytryptaminergic neurones in several regions of the brain. We have now investigated whether this degeneration is likely to be the result of free
Regulation of the cholesterol efflux transporters ABCA1 and ABCG1 in retina in hemochromatosis and by the endogenous siderophore 2,5-dihydroxybenzoic acid.
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Hypercholesterolemia and polymorphisms in the cholesterol exporter ABCA1 are linked to age-related macular degeneration (AMD). Excessive iron in retina also has a link to AMD pathogenesis. Whether these findings mean a biological/molecular connection between iron and cholesterol is not known. Here
Studies on the role of dopamine in the degeneration of 5-HT nerve endings in the brain of Dark Agouti rats following 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration.
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1. We investigated whether dopamine plays a role in the neurodegeneration of 5-hydroxytryptamine (5-HT) nerve endings occurring in Dark Agouti rat brain after 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') administration. 2. Haloperidol (2 mg kg(-1) i.p.) injected 5 min prior and 55 min post
Aspirin protects striatal dopaminergic neurons from neurotoxin-induced degeneration: an in vivo microdialysis study.
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The effect of aspirin on dopaminergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) and 6-hydroxydopamine (6-OHDA) was studied in rats, using microdialysis. Rat striata were perfused with 1 mM MPP(+) or 6-OHDA for 10 min, causing peak levels of dopamine
Hydroxyl radical formation in skeletal muscle of rats with glucocorticoid-induced myopathy.
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Steroid myopathy is a well-known adverse effect of glucocorticoids that causes muscle weakness and atrophy; however, its pathogenic mechanism is still unclear. Recently, oxidative stress was reported to contribute to steroid myopathy, but there is no report that actually attempts to measure hydroxyl
Iodoacetate produces striatal excitotoxic lesions.
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Impairment of energy production may play a role in the pathogenesis of Huntington's disease (HD). It was recently shown that huntingtin can bind to and possibly inhibit the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). We found that intrastriatal administration of the GAPDH
Paradoxical effects of adenosine receptor ligands on hydroxyl radical generation by L-DOPA in the rat striatum.
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Parkinson's disease (PD) is a progressive neurodegenerative disorder associated with selective loss of dopaminergic neurons in substantia nigra pars compacta. Among the proposed mechanisms of dopaminergic degeneration, oxidative stress is believed to play an important role. On the other hand, L-DOPA
Hydroxyl radical production in the substantia nigra after 6-hydroxydopamine and hypoxia-reoxygenation.
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To study the involvement of oxidative stress in 6-OHDA neurotoxicity, we investigated the production of the hydroxyl free radical (OH.) in the substantia nigra (SN) and the striatum (CS) several moments after intranigral injection of the neurotoxin, with or without an added episode of hypoxia (30
The effect of tamoxifen on opening ATP-sensitive K+ channels enhances hydroxyl radical generation in rat striatum.
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The present study was examined the antioxidant effect of tamoxifen, a synthetic non-steroidal antiestrogen, on cromakalim or nicorandil (ATP-sensitive K+ (KATP) channels opener)-enhanced hydroxyl radical (OH) generation induced by 1-methyl-4-phenylpyridinium ion
Systemic administration of d-amphetamine induces long-lasting oxidative stress in the rat striatum.
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The long-term effect of d-amphetamine (AMPH) on the induction of oxidative stress was examined in vivo in the rat brain. In this study, 2,3-dihydroxybenzoic acid (2,3-DHBA) and malonaldehyde (MDA) were used as the index of the hydroxyl radical and lipid peroxidation, respectively. The levels of
Oxidation chemistry of norepinephrine: partitioning of the O-quinone between competing cyclization and chain breakdown pathways and their roles in melanin formation.
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Aberrant oxidation of norepinephrine (1) via the transient o-quinone has been implicated as a critical pathogenetic mechanism underlying the degeneration of noradrenergic cell bodies in the locus coeruleus in Parkinson's disease, the degeneration of noradrenergic nerve terminals in Alzheimer's
The Effect of Buckwheat Hull Extract on Lipid Oxidation in Frozen-Stored Meat Products.
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This study investigated the effect of antioxidants on lipid stability of frozen-stored meat products. Buckwheat hull extract was used to enrich fried meatballs made from ground pork. During 180-d storage of meat products, lipid oxidation (peroxide and 2-thiobarbituric acid reactive substances
[Dimethyl sulphoxide suppresses hydroxyl radical formation of muscle fiber necrosis induced by bupivacaine hydrochloride].
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We induced acute skeletal muscle necrosis by using bupivacaine hydrochloride in Wistar rats and found that both 2,5- and 2, 3-dihydroxybenzoic acid significantly increased in the skeletal muscle. Dimethyl sulphoxide, a free radical scavenger, was administrated for 5 days, and resulted in significant
Defibrillatory action of glibenclamide is independent from ATP-sensitive K+ channels and free radicals.
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This study investigated whether glibenclamide exerts a defibrillatory action and if this action is mediated by a blockade of ATP-sensitive K+ channels (K(ATP)) or by an anti-free radical mechanism. Aerobically perfused isolated rat hearts were subjected to 10 min of pacing-induced ventricular
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