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Glutathione: overview of its protective roles, measurement, and biosynthesis.

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TLDR
The purpose here is to provide a brief overview of some of the important aspects of glutathione metabolism as part of this special issue that will provide a more comprehensive review of the state of knowledge regarding this essential molecule.
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This article is published in Molecular Aspects of Medicine.The article was published on 2009-02-01 and is currently open access. It has received 1576 citations till now. The article focuses on the topics: Glutathione.

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Citations
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Journal ArticleDOI

Glutathione metabolism in cancer progression and treatment resistance.

TL;DR: Recent studies that focus on deciphering the role of GSH in tumor initiation and progression as well as mechanisms underlying how GSH imparts treatment resistance to growing cancers are discussed.
Journal ArticleDOI

Apoptosis and glutathione: beyond an antioxidant

TL;DR: This work reformulates emerging paradigms of apoptotic cell death into current understanding of cell death mechanisms and suggests that GSH depletion and post-translational modifications of proteins through glutathionylation are critical regulators of apoptosis.
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Glutathione: new roles in redox signaling for an old antioxidant

TL;DR: This review will be focused on the role of GSH in cell signaling by analysing the more recent advancements about its capability to modulate nitroxidative stress, autophagy, and viral infection.
Journal ArticleDOI

Chemistry and biochemistry of lipid peroxidation products.

TL;DR: New advances regarding apoptosis induction, survival/proliferation processes and autophagy regulated by 4-hydroxynonenal, a major product of omega-6 fatty acid peroxidation, in relationship with detoxication mechanisms are related.
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The Redox Stress Hypothesis of Aging

TL;DR: The main objective of this review is to examine the role of endogenous reactive oxygen/nitrogen species (ROS) in the aging process and proposes the "redox stress hypothesis", which proposes that aging-associated functional losses are primarily caused by a progressive pro-oxidizing shift in the redox state of the cells, which leads to the overoxidation of redox-sensitive protein thiols and the consequent disruption of theredox-regulated signaling mechanisms.
References
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Journal ArticleDOI

Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.

TL;DR: This review provides a comprehensive summary on the chemical properties of 4-hydroxyalkenals and malonaldehyde, the mechanisms of their formation and their occurrence in biological systems and methods for their determination, as well as the many types of biological activities described so far.
Journal ArticleDOI

Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain

TL;DR: It is postulate that Keap1 and Nrf2 constitute a crucial cellular sensor for oxidative stress, and together mediate a key step in the signaling pathway that leads to transcriptional activation by this novel NRF2 nuclear shuttling mechanism.
Journal ArticleDOI

Regulation of glutathione synthesis

TL;DR: Dysregulation of GSH synthesis is increasingly being recognized as contributing to the pathogenesis of many pathological conditions, including diabetes mellitus, pulmonary fibrosis, cholestatic liver injury, endotoxemia and drug-resistant tumor cells.
Book ChapterDOI

Assay of glutathione, glutathione disulfide, and glutathione mixed disulfides in biological samples.

TL;DR: The sum of the reduced and oxidized forms of glutathione can be determined by using a kinetic assay in which catalytic amounts of GSH or GSSG and glutATHione reductase bring about the continuous reduction of 5,5′-dithiobis(2-nitrobenzoic acid) (DTNB) by nicotinamide adenine dinucleotide phosphate (NADPH).
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