glutathione reductase/acidente vascular cerebral

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Plasma oxidants and antioxidants in acute ischaemic stroke.

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Plasma levels of the oxidants xanthine oxidase, nitric oxide and malondialdehyde and the antioxidants superoxide dismutase, glutathione peroxidase and glutathione reductase, together with total superoxide scavenger activity and non-enzymatic superoxide scavenger activity, were determined in 19

Lipid peroxidation, hemolysis and antioxidant enzymes of erythrocytes in stroke.

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Erythrocyte membrane lipid peroxidation and consequent percentage hemolysis and related antioxidant enzymes viz., superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase were determined in 16 cases of hemorrhagic stroke and 30 cases of thrombotic stroke. The results obtained

[Oxidative stress as an indicator of metabolic disorders in the pathogenesis of cerebral stroke].

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OBJECTIVE To verify the oxidative stress as an indicator of metabolic disorders in the complex pathogenesis of hemorrhagic and ischemic stroke. METHODS The study included 50 hemorrhagic stroke patients and 50 ischemic stroke patients. A control group consisted of 20 age-matched healthy subjects. In

[Glutathione system in erythrocytes and blood plasma in strokes and dyscirculatory encephalopathy].

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In dyscirculatory encephalopathy and moderate ischemic stroke there are single changes of components of glutathione metabolism. In moderate and severe ischemic stroke frequent and considerable changes have been revealed. Changes in hemorrhagic stroke are also expressed. An increase of activities of

Relationship between estradiol and antioxidant enzymes activity of ischemic stroke.

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Some evidence suggests the neuroprotection of estrogen provided by the antioxidant activity of this compound. The main objective of this study was to determine the level of estradiol and its correlation with the activity of antioxidant enzymes, total antioxidant status and ferritin from ischemic

PON1 55/192 polymorphism, oxidative stress, type, prognosis and severity of stroke.

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We investigated the association of PON1 55/192 polymorphisms with type, severity and prognosis of stroke and oxidative markers. Paraoxonase1 (PON1), Glutathione Reductase (GSH-Rd) and Malondialdehyde (MDA) levels were measured at day 1 and at day 5 following the onset of stroke. Genotypes were

Riboflavin status in acute ischaemic stroke.

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BACKGROUND There is experimental evidence that riboflavin (vitamin B2) supplementation reduces oxidative damage and cerebral oedema following acute stroke. OBJECTIVE To measure riboflavin levels in acute stroke before and after supplementation with this vitamin. METHODS Ninety-six acute ischaemic

B-group vitamin supplementation mitigates oxidative damage after acute ischaemic stroke.

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Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately following acute stroke and that endogenous antioxidant defences are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of B-group vitamins

Type 2 diabetic patients with ischemic stroke: decreased insulin sensitivity and decreases in antioxidant enzyme activity are related to different stroke subtypes.

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We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke

Zinc stimulates the production of toxic reactive oxygen species (ROS) and inhibits glutathione reductase in astrocytes.

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The release of zinc (Zn) from glutamatergic synapses contributes to the neuropathology of ischemia, traumatic brain injury, and stroke. Astrocytes surround glutamatergic synapses and are vulnerable to the toxicity of Zn, which impairs their antioxidative glutathione (GSH) system and elevates the

Antioxidant supplementation with or without B-group vitamins after acute ischemic stroke: a randomized controlled trial.

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BACKGROUND Evidence shows that there is a rapid increase in the production of markers of oxidative damage immediately after acute ischemic stroke and that endogenous antioxidant defenses are rapidly depleted, thus permitting further tissue damage. Several studies point to an antioxidant effect of

Hesperidin ameliorates functional and histological outcome and reduces neuroinflammation in experimental stroke.

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Incidence of stroke is considered to be a major cause of death throughout the world. The middle cerebral artery occlusion (MCAO) for 2h followed by 22h of reperfusion model was used in male Wistar rats to study the protection of stroke by hesperidin. Hesperidin administration (50mg/kg b.wt.) once

Ameliorative stroke of selenium against toxicological effects of mercuric chloride in liver of freshwater catfish Heteropneustes fossilis (Bloch).

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Mercury, a prevalent and unrelenting toxin, occurs in a variety of forms in freshwater as well as, in marine life. Mercury is an important inducer of oxidative stress in fish leading to formation of reactive oxygen species. Selenium is an essential micronutrient for animals and has antagonistic

Ischemic and oxidative damage to the hypothalamus may be responsible for heat stroke.

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The hypothalamus may be involved in regulating homeostasis, motivation, and emotional behavior by controlling autonomic and endocrine activity. The hypothalamus communicates input from the thalamus to the pituitary gland, reticular activating substance, limbic system, and neocortex. This allows the

A comparative study of PNIPAM nanoparticles of curcumin, demethoxycurcumin, and bisdemethoxycurcumin and their effects on oxidative stress markers in experimental stroke.

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Oxidative stress and inflammatory damage play an important role in cerebral ischemic pathogenesis and may represent a target for treatment. The development of new strategies for enhancing drug delivery to the brain is of great importance in diagnostics and therapeutics of central nervous diseases.

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