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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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Journal ArticleDOI

Oxidative Stress Enhances Dendritic Cell Responses to Plasmodium falciparum

TL;DR: It is proposed that oxidative stress during malaria contributes to the inflammatory response by enhancing the magnitude of DC and CD4+ T cell responses without changing the quality.
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Reliability of ROS and RNS detection in hematopoietic stem cells--potential issues with probes and target cell population.

TL;DR: The limitations of the commonly used techniques for detection of ROS and RNS, and the problem of heterogeneity of the cell population used in redox studies, are discussed, which can result in inaccurate conclusions regarding the redox biology of HSCs.
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The ROS derived mitochondrial respirstion not from NADPH oxidase plays key role in Celastrol against angiotensin II-mediated HepG2 cell proliferation

TL;DR: Celastrol has the potential for use in liver cancer therapy through its underlying mechanism of causing cell apoptosis through inhibiting mitochodrial respiratory function and boosting the expression levels of AngII type 2 (AT2) receptor without influencing NADPH oxidase activity.
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Esomeprazole alleviates the damage to stress ulcer in rats through not only its antisecretory effect but its antioxidant effect by inactivating the p38 MAPK and NF-κB signaling pathways

TL;DR: This study provides some evidence that the esomeprazole pretreatment exerts gastroprotective effects in WIR-induced stress ulcer through not only its antisecretory effect but also its antioxidant effect by inactivating the p38 MAPK and NF-κB signaling pathways.
Journal ArticleDOI

The Role of Selenium in Oxidative Stress and in Nonthyroidal Illness Syndrome (NTIS): An Overview.

TL;DR: This review summarizes the main advances on oxidative stress with a focus on selenium metabolism and transport and thyroid-related disorders are discussed, considering that the thyroid gland contains the highest seenium amount per gram of tissue, for future possible therapeutic implication.
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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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