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Breathing new life into nitric oxide signaling: A brief overview of the interplay between oxygen and nitric oxide

Journal

REDOX BIOLOGY
Volume 5, Issue -, Pages 225-233

Publisher

ELSEVIER
DOI: 10.1016/j.redox.2015.05.002

Keywords

Nitric oxide; Diffusion; Oxygen; Metabolism; Half-life; Signaling

Funding

  1. National Institute of General Medical Sciences of the National Institutes of Health (NIH) [R01GM085232]

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Nitric oxide ((NO)-N-center dot, nitrogen monoxide) is one of the most unique biological signaling molecules associated with a multitude of physiologic and pathological conditions. In order to fully appreciate its numerous roles, it is essential to understand its basic biochemical properties. Most signaling effector molecules such as steroids or proteins have a significant life-span and function through classical receptor-ligand interactions. (NO)-N-center dot, however, is a short-lived free-radical gas that only reacts with two types of molecules under biological conditions; metals and other free radicals. These simple interactions can lead to a myriad of complex intermediates which in turn have their own phenotypic effects. For these reasons, responses to (NO)-N-center dot often appear to be random or contradictory when outcomes are compared across various experimental settings. This article will serve as a brief overview of the chemical, biological, and microenvironmental factors that dictate (NO)-N-center dot signaling with an emphasis on (NO)-N-center dot metabolism. The prominent role that oxygen (dioxygen, O-2) plays in (NO)-N-center dot metabolism and how it influences the biological effects of (NO)-N-center dot will be highlighted. This information and these concepts are intended to help students and investigators think about the interpretation of data from experiments where biological effects of (NO)-N-center dot are being elucidated. (C) 2015 The Author. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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