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Journal ArticleDOI

Protective effect of L-cysteine and glutathione on rat brain Na+,K+-ATPase inhibition induced by free radicals.

TLDR
It is suggested that the antioxidant action of Cys and GSH may be due to the binding of free radicals to sulfhydryl groups of the molecule, so that free radicals cannot induce Na+,K+-ATPase inhibition.
Abstract
The aim of this study was to investigate whether the preincubation of brain homogenates with L-phenylalanine (Phe), L-cysteine (Cys) or reduced glutathione (GSH) could reverse the free radical effects on Na+,K+-ATPase activity. Two well established systems were used for the production of free radicals: 1) FeSO4 (84 microM) plus ascorbic acid (400 microM) and 2) FeSO4, ascorbic acid and H2O2 (1 mM) for 10 min at 37 degrees C in homogenates of adult rat whole brain. Changes in brain Na+,K+-ATPase activity and total antioxidant status (TAS) were studied in the presence of each system separately, with or without Phe, Cys or GSH. TAS value reflects the amount of free radicals and the capacity of the antioxidant enzymes to limit the free radicals in the homogenate. Na+,K+-ATPase was inhibited by 35-50% and TAS value was decreased by 50-60% by both systems of free radical production. The enzymatic inhibition was completely reversed and TAS value increased by 150-180% when brain homogenates were preincubated with 0.83 mM Cys or GSH. However, this Na+,K+-ATPase inhibition was not affected by 1.80 mM Phe, which produced a 45-50% increase in TAS value. It is suggested that the antioxidant action of Cys and GSH may be due to the binding of free radicals to sulfhydryl groups of the molecule, so that free radicals cannot induce Na+,K+-ATPase inhibition. Moreover, Cys and GSH could regulate towards normal values the neural excitability and metabolic energy production, which may be disturbed by free radical action on Na+,K+-ATPase.

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Protective effect of L-cysteine and glutathione on the modulated suckling rat brain Na+, K+, -ATPase and Mg2+ -ATPase activities induced by the in vitro galactosaemia

TL;DR: Gal and its derivatives may produce free radicals in the suckling rat brain, reported for first time, and the addition of the above antioxidants may reduce the consequences of brain Mg2+ -ATPase activation by Gal and Galtol in galactokinase deficiency galactosaemia.
Journal ArticleDOI

In vivo and in vitro effects of cadmium on adult rat brain total antioxidant status, acetylcholinesterase, (Na+,K+)-ATPase and Mg2+-ATPase activities: protection by L-cysteine

TL;DR: Cd can influence in a different way the examined enzyme activities after short- and long-term administration, and Cd may modulate brain cholinergic mechanism(s), neural excitability and metabolic energy production, and L-cysteine can have a protective antioxidant effect on the oxidative stress of the brain induced by Cd.
Journal ArticleDOI

The neuroprotective effect of curcumin and Nigella sativa oil against oxidative stress in the pilocarpine model of epilepsy: a comparison with valproate.

TL;DR: The promising anticonvulsant and potent antioxidant effects of curcumin and NSO are reflected in reducing oxidative stress, excitability and the induction of seizures in epileptic animals and improving some of the adverse effects of antiepileptic drugs.
Journal ArticleDOI

Protective role of Panax ginseng extract standardized with ginsenoside Rg3 against acrylamide-induced neurotoxicity in rats.

TL;DR: It could be concluded that Panax ginseng extract exhibited a protective action against ACR toxicity and it is worth noting that treatment with Panax Ginseng Extract before or at the same time as ACR treatment was more effective than when administered after ACRtreatment.
References
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Journal ArticleDOI

Activity-Dependent Energy Metabolism in Rat Posterior Pituitary Primarily Reflects Sodium Pump Activity

TL;DR: This report provides evidence that the increase in glucose utilization evoked by functional activation in neural tissue is due to the opening of Na+ channels and activation of Na+, K+ -ATPase activity.
Journal ArticleDOI

Oxidative stress: Free radical production in neural degeneration

TL;DR: The oxidative stress theory of neurodegeneration, on excitotoxin-induced cell damage and on impairment of mitochondrial function are focused on as three major noxae being the most likely causes of cell death either independently or in connection with each other.
Journal ArticleDOI

Aromatic hydroxylation and nitration of phenylalanine and tyrosine bY peroxynitrite Evidence for hydroxyl radical production from peroxynitrite

TL;DR: It is found that incubation of phenylalanine with peroxynitrite leads to a small amount of p‐, m‐ and o‐tyrosine, specific products of attack by this radical, and formation of nitro‐aromatic compounds may be a useful marker of peroxlynitrite generation in biological systems.
Journal ArticleDOI

Glutathione contents of tissues in the aging mouse.

G A Hazelton, +1 more
- 15 Apr 1980 - 
TL;DR: Results extend the previous results and indicate that a general characteristic of aging tissues may be a decrease in GSH concentrations, consistent with the hypothesis that the reducing potential of tissues decreases in senescence.
Journal ArticleDOI

Glial cell function: Active control of extracellular K+ concentration

TL;DR: The glial cell Na+ K+-ATPase was always more active, and markedly more sensitive to variations in the K+ ion concentration than the neuronal ATPase, which support the idea that control of the extracellular K- ion concentration in the CNS is at least in part dependent on the metabolically coupled sodium-potassium pump of the glia.
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