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Mechanisms of cell death governed by the balance between nitrosative and oxidative stress

Mechanisms of cell death governed by the balance between nitrosative and oxidative stress
Mechanisms of cell death governed by the balance between nitrosative and oxidative stress
Many cellular functions in physiology are regulated by the direct interaction of NO with target biomolecules. In many pathophysiologic and toxicologic mechanisms, NO first reacts with oxygen, superoxide or other nitrogen oxides to subsequently elicit indirect effects. The balance between nitrosative stress and oxidative stress within a specific biological compartment can determine whether the presence of NO will be ultimately deleterious or beneficial. Nitrosative stress can be defined primarily through reactions mediated by N2O3, a reactive nitrogen oxide species generated by high fluxes of NO in an aerobic environment. In contrast, oxidative stress is mediated primarily by superoxide and peroxides. In addition to reactive oxygen species, several reactive nitrogen oxide species such as peroxynitrite, nitroxyl, and nitrogen dioxide can also impose oxidative stress to a cell. We here describe how the mechanisms of cell death are interwoven in the balance between the different chemical intermediates involved in nitrosative and oxidative stress.
0077-8923
209-221
Espey, Michael Graham
be05250f-de20-48c2-bc05-924c1f572a7c
Miranda, Katrina M.
128fa814-eb00-472f-a5e7-5657e59ac9b9
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Fukuto, Jon
b49c4f1a-3095-4154-821f-c3eee66d668b
Grisham, Mathew B.
f7558662-f6c3-483f-87eb-499eb69698c3
Vitek, Michael P.
4d4f625e-4ba9-4bb7-be48-03bf29b26ef9
Wink, David A.
008b5aec-8c2b-4035-8912-fb6fd530413c
Espey, Michael Graham
be05250f-de20-48c2-bc05-924c1f572a7c
Miranda, Katrina M.
128fa814-eb00-472f-a5e7-5657e59ac9b9
Feelisch, Martin
8c1b9965-8614-4e85-b2c6-458a2e17eafd
Fukuto, Jon
b49c4f1a-3095-4154-821f-c3eee66d668b
Grisham, Mathew B.
f7558662-f6c3-483f-87eb-499eb69698c3
Vitek, Michael P.
4d4f625e-4ba9-4bb7-be48-03bf29b26ef9
Wink, David A.
008b5aec-8c2b-4035-8912-fb6fd530413c

Espey, Michael Graham, Miranda, Katrina M., Feelisch, Martin, Fukuto, Jon, Grisham, Mathew B., Vitek, Michael P. and Wink, David A. (2000) Mechanisms of cell death governed by the balance between nitrosative and oxidative stress. Annals of the New York Academy of Sciences, 899, 209-221. (doi:10.1111/j.1749-6632.2000.tb06188.x). (PMID:10863541)

Record type: Article

Abstract

Many cellular functions in physiology are regulated by the direct interaction of NO with target biomolecules. In many pathophysiologic and toxicologic mechanisms, NO first reacts with oxygen, superoxide or other nitrogen oxides to subsequently elicit indirect effects. The balance between nitrosative stress and oxidative stress within a specific biological compartment can determine whether the presence of NO will be ultimately deleterious or beneficial. Nitrosative stress can be defined primarily through reactions mediated by N2O3, a reactive nitrogen oxide species generated by high fluxes of NO in an aerobic environment. In contrast, oxidative stress is mediated primarily by superoxide and peroxides. In addition to reactive oxygen species, several reactive nitrogen oxide species such as peroxynitrite, nitroxyl, and nitrogen dioxide can also impose oxidative stress to a cell. We here describe how the mechanisms of cell death are interwoven in the balance between the different chemical intermediates involved in nitrosative and oxidative stress.

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Published date: January 2000
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 337874
URI: http://eprints.soton.ac.uk/id/eprint/337874
ISSN: 0077-8923
PURE UUID: 7ad4d653-aaa6-4fb5-b42d-b6b9c5360482
ORCID for Martin Feelisch: ORCID iD orcid.org/0000-0003-2320-1158

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Date deposited: 22 Jun 2012 15:55
Last modified: 15 Mar 2024 03:41

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Contributors

Author: Michael Graham Espey
Author: Katrina M. Miranda
Author: Martin Feelisch ORCID iD
Author: Jon Fukuto
Author: Mathew B. Grisham
Author: Michael P. Vitek
Author: David A. Wink

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