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Therapeutic treatment with ascorbate rescues mice from heat stroke-induced death by attenuating systemic inflammatory response and hypothalamic neuronal damage.

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The impact of ascorbate on oxidative stress-related diseases is moderate because of its limited oral bioavailability and rapid clearance. However, recent evidence of the clinical benefit of parenteral vitamin C administration has emerged, especially in critical care. Heatstroke is defined as a form

Ascorbate status and fibrinogen concentrations after cerebrovascular accident.

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Leucocyte ascorbate (LA) and serum ascorbate (SA) were measured in patients who had sustained an acute cerebrovascular accident. There was a significant fall in LA and Sa within 24 hours of the incident and this persisted for several weeks. The "stress" of the event resulted in a rise in serum

Ascorbate and malondialdehyde in stroke patients.

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It is believed that free radical formation and subsequent oxidative damage in the form of lipid peroxidation may be a factor in the cerebral damage secondary to the ischaemia of a cerebrovascular accident (CVA). Total serum ascorbate and malondialdehyde (MDA) were measured in 45 patients with CVA on

[Blood cell aggregation and oxidative stress in pathogenesis of ischemic stroke].

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Rheologic properties of blood cells and a state of oxidative-reductive processes and blood systems have been studied in 75 patients in acute period of ischemic stroke. The signs of oxidative stress development and simultaneous augmentation of blood cells aggregation were found. Shifts of

A cerebroprotective dose of intravenous citrate/sorbitol-stabilized dehydroascorbic acid is correlated with increased cerebral ascorbic acid and inhibited lipid peroxidation after murine reperfused stroke.

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OBJECTIVE Oxidative damage has been implicated in the pathogenesis of cerebral ischemia. We previously demonstrated that exogenously supplied dehydroascorbic acid (DHA), an oxidized, blood-brain barrier transportable form of the antioxidant ascorbic acid (AA), improves outcome after experimental

Role of the antioxidant ascorbate in hibernation and warming from hibernation.

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Ground squirrels tolerate up to 90% reductions in cerebral blood flow during hibernation as well as rapid reperfusion upon periodic arousal from torpor without apparent neurological damage. Thus, hibernation is studied as a model of tolerance to cerebral ischemia and other types of brain injury.

Effects of vitamin C and aspirin in ischemic stroke-related lipid peroxidation: results of the AVASAS (Aspirin Versus Ascorbic acid plus Aspirin in Stroke) Study.

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A condition of oxidative stress is known to occur in ischemic stroke, the current therapeutic intervention of which is largely limited to thrombolysis. To assess the effect of vitamin C - in conjunction to aspirin - in ischemic stroke-related lipid peroxidation, we measured plasma levels of

Oxidative stress induced by ascorbate causes neuronal damage in an in vitro system.

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Of particular physiological interest, ascorbate, the ionized form of ascorbic acid, possesses strong reducing properties. However, it has been shown to induce oxidative stress and lead to apoptosis under certain experimental conditions. Ascorbate in the brain is released during hypoxia, including

Prolyl hydroxylase domain inhibitors: can multiple mechanisms be an opportunity for ischemic stroke?

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Stroke and cerebrovascular disease are now the fifth most common cause of death behind other diseases such as heart, cancer and respiratory disease and accounts for approximately 40-50 fatalities per 100,000 people each year in the United States. Currently the only therapy for acute stroke, is

Ascorbate attenuates atrial pacing-induced peroxynitrite formation and electrical remodeling and decreases the incidence of postoperative atrial fibrillation.

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Atrial fibrillation (AF), the most common chronic arrhythmia, increases the risk of stroke and is an independent predictor of mortality. Available pharmacological treatments have limited efficacy. Once initiated, AF tends to self-perpetuate, owing in part to electrophysiological remodeling in the

NXY-059, a Failed Stroke Neuroprotectant, Offers No Protection to Stem Cell-Derived Human Neurons.

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BACKGROUND Developing new medicines is a complex process where understanding the reasons for both failure and success takes us forward. One gap in our understanding of most candidate stroke drugs before clinical trial is whether they have a protective effect on human tissues. NXY-059 is a spin-trap

Plasma antioxidants and cognitive performance in middle-aged and older adults: results of the Austrian Stroke Prevention Study.

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OBJECTIVE To study the association between cognitive status and plasma concentrations of various antioxidants in middle-aged and older individuals without neuropsychiatric disease. METHODS Evaluation of cross-sectional data from a cohort study. METHODS The Austrian Stroke Prevention Study. METHODS A

Involvement of oxidative stress in ascorbate-induced proapoptotic death of PC12 cells.

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Ascorbate is a reducing agent, but it is also known to oxidize cellular components under specific conditions. The mechanism of this oxidative action, however, is not well established. Ascorbate treatment increased lipid peroxide content in PC12 cells, but did not increase quantities of lipid

Induction of DNA Hydroxymethylation Protects the Brain After Stroke.

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Background and Purpose- Epigenetics play a significant role in brain pathologies. We currently evaluated the role of a recently discovered brain-enriched epigenetic modification known as 5-hydroxymethylcytosine (5hmC) in regulating transcriptomic and pathogenic mechanisms after focal ischemic

Vitamin C function in the brain: vital role of the ascorbate transporter SVCT2.

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Ascorbate (vitamin C) is a vital antioxidant molecule in the brain. However, it also has a number of other important functions, participating as a cofactor in several enzyme reactions, including catecholamine synthesis, collagen production, and regulation of HIF-1 alpha. Ascorbate is transported

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