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Journal ArticleDOI

Redox environment of the cell as viewed through the redox state of the glutathione disulfide/glutathione couple.

Freya Q. Schafer, +1 more
- 01 Jun 2001 - 
- Vol. 30, Iss: 11, pp 1191-1212
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TLDR
Estimates can be used to more fully understand the redox biochemistry that results from oxidative stress, which hopefully will provide a rationale and understanding of the cellular mechanisms associated with cell growth and development, signaling, and reductive or oxidative stress.
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This article is published in Free Radical Biology and Medicine.The article was published on 2001-06-01. It has received 4274 citations till now. The article focuses on the topics: RoGFP & Redox.

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Citations
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Specific inhibition of hypoxia inducible factor 1 exaggerates cell injury induced by in vitro ischemia through deteriorating cellular redox environment.

TL;DR: Investigation of the effects of inhibiting HIF‐1 on cellular redox status in SH‐SY5Y cells exposed to hypoxia or oxygen and glucose deprivation (OGD), coupled with cell death analyses, suggest that maintenance of cellularRedox status by Hif‐1 protects cells from hypoxic and ischemia mediated injuries.
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Mitochondrial Glutathione: Recent Insights and Role in Disease

TL;DR: The participation of mGSH as a contributor to disease progression in pathologies as diverse as Alzheimer’s disease, alcoholic and non-alcoholic steatohepatitis, or diabetic nephropathy is highlighted and the involvement of mitochondrial ROS in the signaling of new prescribed drugs and in other pathologies is still being revealed.
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Carbon-Dot-Based Nanosensors for the Detection of Intracellular Redox State.

TL;DR: In vitro cell assays demonstrate the feasibility of using carbon-dot-based nanosensors in evaluating the intracellular redox state of different cells.
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GSH-targeted nanosponges increase doxorubicin-induced toxicity "in vitro" and "in vivo" in cancer cells with high antioxidant defenses

TL;DR: Doxorubicin-loaded GSH-NS, in the cancer cells with high GSH content, inhibited clonogenic growth, cell viability, topoisomerase II activity and induced DNA damage with higher effectiveness than free drug, and reduced the development of human tumor in xenograft models more thanfree drug.
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Effect of vanillic acid on COQ6 mutants identified in patients with coenzyme Q10 deficiency

TL;DR: Treatment with two hydroxylated analogues of 4-hydroxybenzoic acid, namely, vanillic acid or 3-4-hydroxylation of the quinone ring of coenzyme Q, restored the respiratory growth of yeast Δcoq6 cells expressing the mutant huCOQ6-isoa proteins and could represent an interesting therapeutic option for COQ6 patients.
References
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Journal ArticleDOI

Induction of apoptotic program in cell-free extracts : requirement for datp and cytochrome c

TL;DR: Cells undergoing apoptosis in vivo showed increased release of cy tochrome c to their cytosol, suggesting that mitochondria may function in apoptosis by releasing cytochrome c.
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The Pecking Order of Free Radicals and Antioxidants: Lipid Peroxidation, α-Tocopherol, and Ascorbate

TL;DR: In this article, the authors used one-electron reduction potentials to predict a pecking order, or hierarchy, for free radical reactions, which is in agreement with experimentally observed free radical electron (hydrogen atom) transfer reactions.
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Oxidative stress as a mediator of apoptosis

TL;DR: Thomas Buttke and Paul Sandstrom suggest that eukaryotic cells may benefit from this perilous existence by invoking oxidative stress as a common mediator of apoptosis.
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Antioxidant and Redox Regulation of Gene Transcription

TL;DR: The efficacy of different antioxidants to favorably influence the molecular mechanisms implicated in human disease should be a critical determinant of its selection for clinical studies.
Journal ArticleDOI

Oxidized redox state of glutathione in the endoplasmic reticulum

TL;DR: Results suggest that the demonstrated preferential transport of GSSG compared to GSH into the ER lumen may contribute to this redox compartmentation.
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