نتایج جستجو برای: gsh depletion

تعداد نتایج: 71935  

2013
Koji Aoyama Toshio Nakaki

Glutathione (GSH) was discovered in yeast cells in 1888. Studies of GSH in mammalian cells before the 1980s focused exclusively on its function for the detoxication of xenobiotics or for drug metabolism in the liver, in which GSH is present at its highest concentration in the body. Increasing evidence has demonstrated other important roles of GSH in the brain, not only for the detoxication of x...

Journal: :Environmental Health Perspectives 1997
S A Golladay S H Park A E Aust

This study investigated glutathione (GSH) homeostasis in human lung epithelial cells (A549) exposed to crocidolite. Exposure of A549 cells to 3 micrograms/cm2 crocidolite resulted in a decrease in intracellular reduced glutathione by 36% without a corresponding increase in GSH disulfide. After a 24-hr exposure to crocidolite, 75% of the intracellular GSH lost was recovered in the extracellular ...

Journal: :Oncology reports 2013
Woo Hyun Park Suhn Hee Kim

Gallic acid (GA) is involved in various biological processes such as cell growth inhibition and apoptosis through changes in reactive oxygen species (ROS). In the present study, we investigated the effects of MAPK (MEK, JNK or p38) inhibitors on cell death in GA-induced A549 lung cancer cells in relation to ROS and glutathione (GSH). Treatment with 100 µM GA inhibited the growth of A549 cells a...

Journal: :Free radical research 2004
Yoshihiro Higuchi Tanihiro Yoshimoto

Glutamate and buthionine sulfoximine (BSO) both reduce intracellular glutathione (GSH) concentration but by different mechanisms, and thereby induce cell death in C6 rat glioma cells. The effects of lipid peroxidation on chromosomal DNA damage during the GSH depletion-induced cell death were assessed. Polyunsaturated fatty acids (PUFA), such as arachidonic acid (AA), gamma-linolenic acid and li...

2013
BRADLEY A. ARRICK CARL F. NATHAN ZANVIL A. COHN

A preliminary account of this work was presented at the 66th Annual Meeting of the Federation of American Societies for Experimental Biology, April 1982. Dr. Nathan is an Irma T. Hirschl Career Scientist. Address reprint requests to Dr. Arrick. Received for publication 23 June 1982 and in revised form 18 October 1982. with BSO alone results in near-complete GSH depletion without loss of cell vi...

Journal: :The Journal of infectious diseases 2002
Pia Villa Alessandra Saccani Antonio Sica Pietro Ghezzi

Neutrophils have a dual role in sepsis-defending against infection and mediating organ failure. Because glutathione (GSH) is lower in sepsis, the hypothesis that GSH depletion might impair the migratory response of neutrophils to infection was tested. In a mouse model of polymicrobial sepsis induced by cecal ligation and puncture, GSH depletion inhibited peritoneal neutrophil infiltration, incr...

Journal: :The Journal of biological chemistry 2000
J Choi R M Liu R K Kundu F Sangiorgi W Wu R Maxson H J Forman

Human immunodeficiency virus (HIV) progressively depletes GSH content in humans. Although the accumulated evidence suggests a role of decreased GSH in the pathogenesis of HIV, significant controversy remains concerning the mechanism of GSH depletion, especially in regard to envisioning appropriate therapeutic strategies to help compensate for such decreased antioxidant capacity. Tat, a transact...

Journal: :Toxicological sciences : an official journal of the Society of Toxicology 2005
Rita Loch-Caruso Brad L Upham Craig Harris James E Trosko

Previous studies have shown that the insecticide lindane (gamma-hexachlorocyclohexane) induces a biphasic inhibition of gap junction intercellular communication that is accompanied by oxidative stress. The present study investigates the hypothesis that depletion of cellular glutathione (GSH) is a mechanistic link between lindane-induced oxidative stress and inhibition of myometrial gap junction...

Journal: :The Journal of pharmacology and experimental therapeutics 1997
T Oguro E Kaneko S Numazawa S Imaoka Y Funae T Yoshida

Both trans- and cis-stilbene oxide (TSO and CSO) markedly induced heme oxygenase-1 (HO-1) at the transcriptional level in rat liver. HO-1 induction by TSO and CSO was preceded by glutathione (GSH) depletion in the liver. Pretreatment of rats with buthionine sulfoximine (BSO), an inhibitor of GSH biosynthesis, enhanced GSH depletion evoked by either TSO or CSO and augmented the increase in HO-1 ...

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