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glutathione/треска

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Glutathione biosynthesis in the aging adult yellow-fever mosquito [Aedes aegypti (Louisville)].

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Our previous findings [Hazelton & Lang (1978) Fed. Proc. Fed. Am. Soc. Exp. Biol. 37(6), 2378 (abstr.)] demonstrated a senescence-specific decrease in glutathione (GSH) concentration in the yellow-fever mosquito Aedes aegypti (Louisville)]. As a possible mechanism for this change, GSH biosynthesis

Effect of glutathione depletion, hyperthermia, and a 100-mT static magnetic field on an hsp70/luc reporter system.

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Heat shock proteins, in particular hsp70, are induced under conditions of cellular stress. It has been reported that environmental stimuli such as hyperthermia, oxidative stress, and exposure to magnetic fields increase levels of hsp70. It has also been reported that hyperthermia in combination with

Glutathione-S-Transferase Variants are not Associated With Increased Carotid Intima-Media Thickness in Turkish Familial Mediterranean Fever Patients.

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UNASSIGNED This study aims to evaluate the carotid intima-media thickness (CIMT) in patients diagnosed with Familial Mediterranean fever (FMF) and investigate whether there is a relationship between glutathione-S-transferase (GST) gene polymorphisms and CIMT. UNASSIGNED Sixty FMF patients (17 males,

Malignant hyperthermia (MH): porcine erythrocyte damage from oxidation and glutathione peroxidase deficiency.

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Malignant hyperthermia (MH) is a severe familial disease in both the pig and the human, with 70% fatality when fully expressed in humans. MH produces rapid elevation of temperature in response to stresses, of which there are two general kinds: Societal or emotional stress, and chemical stressors.

Lipid peroxide levels in a murine adenocarcinoma exposed to hyperthermia: the role of glutathione depletion.

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Increased lipid peroxide levels were obtained 1 h after a 60-min 43 degrees C hyperthermia treatment of a solid murine C3H mammary adenocarcinoma, grown subcutaneously in the hind paws of mice. Previous work from our group revealed that this heat treatment depletes the intracellular glutathione

Glutathione S-transferase activities in the yellow-fever mosquito [Aedes aegypti (Louisville)] during growth and aging.

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Our previous findings [Hazelton & Lang (1978) Fed. Proc. Fed. Am. Soc. Exp. Biol. 37(6), 2378 (abstr.)] demonstrated aging-specific changes in glutathione concentrations in the yellow-fever mosquito [Aedes aegypti (Louisville)]. A possible mechanism could be increased utilization via glutathione

Influence of hypoxia and hyperthermia upon peroxidative and glutathione status in growth-restricted newborn piglets.

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Normal weight (NW) and spontaneously intra-uterine growth-restricted newborn piglets (IUGR) were submitted to 1 hour hypoxia and hyperthermia followed by 3 hours reoxygenation. Glutathione (GSH, GSSG), lipid peroxidation products (TBAR) and cytochrome P450 dependent production of reactive oxygen

Failure of chronic glutathione elevation to reduce cytotoxicity produced by exposure to cis-diamminedichloroplatinum(II), ionizing radiation, or hyperthermia.

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Chinese hamster ovary (CHO) cells cultured in vitro were continuously exposed to increasing concentrations of diethylmaleate (DEM). Chronic exposure of these cells (designated CHO/DEM) to 80 microM diethylmaleate resulted in an increase in cystine transport, a decrease in glutathione inhibition of

New Insights into the Role of Glutathione in the Mechanism of Fever.

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Glutathione is one of the most important and potent antioxidants. The development of pharmacological compounds that can either increase or decrease glutathione concentrations has allowed investigation into the role of glutathione in various biological processes, including immune responses. Recent

Buthionine sulfoximine, a glutathione depletor, attenuates endotoxic fever and reduces IL-1β and IL-6 level in rats.

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The aim of our study was to investigate the effect of buthionine sulfoximine (BSO) - a glutathione depletor - on a course of endotoxic fever and IL-1β and IL-6 production. Male Wistar rats were subjected to intraperitoneal injection of lipopolysaccharide (LPS) from E. coli (50μg/kg, ip) to provoke

Genetic polymorphisms of paraoxonase1 192 and glutathione peroxidase1 197 enzymes in familial Mediterranean fever.

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Familial Mediterranean fever (FMF) is an autosomal recessive disorder and is the most frequent of the periodic febrile inflammatory syndromes. The pathogenesis of the disease is not completely understood, even though the FMF gene has been identified. Oxidative stress and inflammation may play a role

Glutathione deficiency attenuates endotoxic fever in rats.

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OBJECTIVE Glutathione constitutes the first line of the cellular defence mechanism against oxidative stress, and according to published data it is required by a number of factors that are involved in fever mechanism. The aim of the present study was to investigate whether or not glutathione

Involvement of superoxide dismutase and glutathione peroxidase in attenuation of radiation-induced hyperthermia by interleukin-1 alpha in rats.

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Pretreatment with recombinant human interleukin-1 alpha (rhIL-1 alpha) 20 h before irradiation attenuates radiation-induced hyperthermia. Experiments were conducted to determine the role of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) in rhIL-1

Enhancement of melphalan-induced gastrointestinal toxicity in mice treated with regional hyperthermia and BSO-mediated glutathione depletion.

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Both hyperthermia and glutathione depletion have been shown to increase the antineoplastic activity of melphalan. Investigations were carried out to define the toxicity and activity of melphalan given in conjunction with local (right hind limb) hyperthermia and L-buthionine-SR-sulphoximine

Protection against 3,4-methylenedioxymethamphetamine-induced neurodegeneration produced by glutathione depletion in rats is mediated by attenuation of hyperthermia.

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3,4-Methylenedioxymethamphetamine (MDMA) administration produces neurotoxic degeneration of serotonin terminals in rat brain. These effects occur only after systemic administration and not after central injection, suggesting that peripheral metabolism, possibly hepatic, is required for toxicity.
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