glutathione/hypoxia

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The potential protective roles of zinc, selenium and glutathione on hypoxia-induced TRPM2 channel activation in transfected HEK293 cells.

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Hypoxia induces cell death through excessive production of reactive oxygen species (ROS) and calcium (Ca²⁺) influx in cells and TRPM2 cation channel is activated by oxidative stress. Zinc (Zn), selenium (Se), and glutathione (GSH) have antioxidant properties in several cells and

EFFECT OF POMEGRANATE (Punica granatum L) JUICE ON CHANGES IN TISSUE GLUTATHIONE LEVELS OF RATS EXPOSED TO HIGH ALTITUDE HYPOXIA.

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Oxidative stress due to excessive production of free radicals in living organisms during exposure to hypobaric hypoxia is well documented. In search of a suitable antioxidant from natural sources, in the present study effect of pomegranate (Punica granatum, family Punicaceae) juice (PG) was

Extracellular reduced glutathione increases neuronal vulnerability to combined chemical hypoxia and glucose deprivation.

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In addition to its intracellular antioxidant role, reduced glutathione (GSH) is released by CNS cells and may mediate or modulate excitatory neurotransmission. Although extracellular GSH levels rise in the ischemic cortex, its effect on the viability of energy-compromised neurons has not been

A hypoxia efficient imidazole-based Ru(II) arene anticancer agent resistant to deactivation by glutathione.

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A slow hydrolyzing imidazole-based Ru(II)-arene complex [(L)Ru(II)(η(6)-p-cym)(Cl)](PF6) (1) with excellent stability in the extracellular chloride concentration shows better activity under hypoxia and strong resistance to glutathione (GSH) in vitro under hypoxic conditions. 1 arrests the cell cycle

Impairment of synaptic transmission by transient hypoxia in hippocampal slices: improved recovery in glutathione peroxidase transgenic mice.

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There is increasing evidence that oxygen free radicals contribute to ischemic brain injury. It is unclear, however, to what extent specific antioxidant enzymes can prevent or reverse the impairment of synaptic function caused by transient hypoxia. In this study, we investigated in transgenic (Tg)

Seasonal- and temperature-dependent variation in CNS ascorbate and glutathione levels in anoxia-tolerant turtles.

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We determined the ascorbic acid (ascorbate) and glutathione (GSH) contents of eight regions of the CNS from anoxia-tolerant turtles collected in summer and in winter. Ascorbate was of special interest because it is found in exceptionally high levels in the turtle CNS. The temperature-dependence of

Brain peroxidative and glutathione status after moderate hypoxia in normal weight and intra-uterine growth-restricted newborn piglets.

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In order to investigate the pathogenetic factors causing the relatively frequent occurrence of brain injury in intrauterine growth-restricted newborns, lipid peroxidation products (TBAR), glutathione (GSH, GSSG) and in vitro production of reactive oxygen species (chemiluminescence, stimulated lipid

[Glutathione, a biochemical indicator for different types of cellular stress. The change in the GSH level in the brain of rats with hypoxia].

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By the ligation of left vertebral artery in some white, adult WISTAR rats, of 150-200 g, anaesthetized with ether, a cerebral hypoxia of 10 minutes was induced. After beheading, there was determined the level of SH-neproteic groups and glutathione (GSH) in the whole heparinized blood and there was

Alteration in Downstream Hypoxia Gene Signaling in Neonatal Glutathione Peroxidase Overexpressing Mouse Brain after Hypoxia-Ischemia.

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We have previously shown that glutathione peroxidase (GPx) overexpressing mice (hGPx-tg) have reduced brain injury after neonatal hypoxia-ischemia (HI) as a consequence of reduced hydrogen peroxide accumulation. However, this protection is reversed with hypoxia preconditioning, raising the question

Delayed hypothermia prevents decreases in N-acetylaspartate and reduced glutathione in the cerebral cortex of the neonatal pig following transient hypoxia-ischaemia.

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The effects of normothermia and delayed hypothermia on the levels of N-acetylaspartate (NAA), reduced glutathione (GSH) and the activities of mitochondrial complex I, II-III, IV and citrate synthase were measured in brain homogenates obtained from anaesthetized neonatal pigs following transient in

Purification and properties of the glutathione S-transferases from the anoxia-tolerant turtle, Trachemys scripta elegans.

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Glutathione S-transferases (GSTs) play critical roles in detoxification, response to oxidative stress, regeneration of S-thiolated proteins, and catalysis of reactions in nondetoxification metabolic pathways. Liver GSTs were purified from the anoxia-tolerant turtle, Trachemys scripta elegans.

Intermittent hypoxia, brain glyoxalase-1 and glutathione reductase-1, and anxiety-like behavior in mice.

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OBJECTIVE Sleep apnea has been associated with anxiety, but the mechanisms of the sleep apnea-anxiety relationship are unresolved. Sleep apnea causes oxidative stress, which might enhance anxiety-like behavior in rodents. To clarify the apnea-anxiety connection, we tested the effect of intermittent

Measurement of fetal plasma levels of glutathione S-transferase B1 as an indicator of damage to the liver caused by hypoxia in utero.

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Glutathione S-transferase B1 (GST B1) concentration in blood and amniotic fluid from fetuses investigated for a variety of conditions including rhesus (Rh) allo-immunisation was assessed for its usefulness as a measure of liver damage caused by hypoxia in utero. The concentration in blood from the

Melatonin affects conjugation of 4-hydroxynonenal with glutathione in liver of pacu, a hypoxia-tolerant fish.

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In cytosol from liver of pacu, Piaractus mesopotamicus, a hypoxia-tolerant fish that dwells in Pantanal, we found an enzyme activity capable of modulating the alkenal 4-hydroxy-2-nonenal (HNE) by conjugating it with glutathione (GST-HNE activity). HNE is a downstream metabolite from the oxidation of

Purification and properties of glutathione reductase from liver of the anoxia-tolerant turtle, Trachemys scripta elegans.

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Belépés Regisztrálás

Glutathione reductase (GR) is a homodimeric flavoprotein that catalyzes the reduction of oxidized glutathione (GSSG) using NADPH as a cofactor. The enzyme is a major component of cellular defense mechanisms against oxidative injury. In this study, GR was purified from the liver of the

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