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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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Exogenous oxidants activate nuclear factor kappa B through Toll-like receptor 4 stimulation to maintain inflammatory phenotype in macrophage.

TL;DR: The results support the involvement of TLR4 mediated oxidant‐induced inflammatory phenotype through NF‐&kgr;B activation in macrophages and suggest exogenous oxidants may play a role in activating inflammatory phenotypes that propagate and maintain chronic disease states.
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A tutorial on oxidative stress and redox signaling with application to exercise and sedentariness

TL;DR: Exercise training appears to optimize the redox environment by dramatically enhancing the capacity of the cell to neutralize ROS while regularly creating oxidative environments in which membrane and secretory proteins can be synthesized.
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Modulation of membrane lipid composition and homeostasis in salmon hepatocytes exposed to hypoxia and perfluorooctane sulfonamide, given singly or in combination.

TL;DR: The data show that hypoxia may, singly or in combination with PFOSA produce deleterious health, physiological and developmental consequences through the alteration of membrane lipid profile in organisms.
References
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Journal ArticleDOI

Superoxide Dismutase AN ENZYMIC FUNCTION FOR ERYTHROCUPREIN (HEMOCUPREIN)

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Journal ArticleDOI

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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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