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Beyond oxidative stress: an immunologist’s guide to reactive oxygen species

Carl Nathan, +1 more
- 01 May 2013 - 
- Vol. 13, Iss: 5, pp 349-361
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TLDR
ROS chemistry and their pleiotropy make them difficult to localize, to quantify and to manipulate — challenges the authors must overcome to translate ROS biology into medical advances.
Abstract
Reactive oxygen species (ROS) react preferentially with certain atoms to modulate functions ranging from cell homeostasis to cell death. Molecular actions include both inhibition and activation of proteins, mutagenesis of DNA and activation of gene transcription. Cellular actions include promotion or suppression of inflammation, immunity and carcinogenesis. ROS help the host to compete against microorganisms and are also involved in intermicrobial competition. ROS chemistry and their pleiotropy make them difficult to localize, to quantify and to manipulate — challenges we must overcome to translate ROS biology into medical advances.

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Nanodevices for studying nano-pathophysiology.

TL;DR: Nano-scaled devices, including liposomes, nanoparticles and polymeric nanoassemblies, such as polymeric micelles and vesicles, which can precisely control their structure and functions for specifically interacting with cells and tissues are reviewed.
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Plasma membrane order and fluidity are diversely triggered by elicitors of plant defence

TL;DR: The ROS-dependent increase of plasma membrane order is a generic event triggered by elicitors of plant defence, whereas fluidity enhancement is specifically triggered by cryptogein, a sterol-carrier elicitin.
Journal ArticleDOI

Alteration of Nrf2 and Glutamate Cysteine Ligase expression contribute to lesions growth and fibrogenesis in ectopic endometriosis.

TL;DR: expression of the transcription factor NRF2 and its effector GCL are both profoundly deregulated in endometriotic lesions towards increased growth and fibrogenetic processes, and Alteration of Nrf2 and Glutamate Cysteine Ligase expression contribute to locally increased oxidative stress in ectopic lesion of endometiosis.
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Mechanistic Investigation on Oxidative Degradation of ROS-Responsive Thioacetal/Thioketal Moieties and Their Implications

TL;DR: In this article, a mechanism for the oxidative cleavage of thioacetal/thioketal moieties was proposed, where the thiolate components are converted to the corresponding disulfide product along with the formation of the respective aldehydes and ketones.
Journal ArticleDOI

Redox signaling at the crossroads of human health and disease

TL;DR: The roles of ROS as multifaceted physiological modulators to mediate redox signaling and sustain redox homeostasis are revealed and two different therapeutic strategies to treat redox‐relevant diseases are suggested.
References
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Journal ArticleDOI

Superoxide Dismutase AN ENZYMIC FUNCTION FOR ERYTHROCUPREIN (HEMOCUPREIN)

TL;DR: The demonstration that O2·- can reduce ferricytochrome c and tetranitromethane, and that superoxide dismutase, by competing for the superoxide radicals, can markedly inhibit these reactions, is demonstrated.
Journal ArticleDOI

Myeloid-derived suppressor cells as regulators of the immune system.

TL;DR: The origin, mechanisms of expansion and suppressive functions of MDSCs, as well as the potential to target these cells for therapeutic benefit are discussed.
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Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?

TL;DR: It is argued that modulating the unique redox regulatory mechanisms of cancer cells might be an effective strategy to eliminate these cells.
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A role for mitochondria in NLRP3 inflammasome activation

TL;DR: It is shown that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome, and may explain the frequent association of mitochondrial damage with inflammatory diseases.
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Biological defense mechanisms. The production by leukocytes of superoxide, a potential bactericidal agent.

TL;DR: O(2) (-) is made by leukocytes under circumstances which suggest that it may be involved in bacterial killing, and is identified as the agent responsible for the leukocyte-mediated reduction of cytochrome c.
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