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Reactive oxygen species and the modulation of stroke.
Free Radic Biol Med. 2005 Jun 01; 38(11):1433-44.FR

Abstract

Reactive oxygen species and oxidative state are slowly gaining acceptance in having a physiological relevance rather than just being the culprits in pathophysiological processes. The control of the redox environment of the cell provides for additional regulation in relation to critical cellular signal transduction pathways. Conversely, aberrant regulation of oxidative state manifesting as oxidative stress can predispose a cell to adverse outcome. The PI3-kinase/Akt pathway is one such pathway that is partially regulated via oxidative state and, in an oxidative stress paradigm such as ischemic reperfusion injury, may be inactivated, which can lead to potentiation and or exacerbation of cell death. Activation of NF(kappa)B has also been associated with oxidative stress. The role of NF(kappa)B in neuronal cell death is widely debated, with major studies highlighting both a pro- and an antiapoptotic role for NF(kappa)B with the outcome being region, stimulus, dose, and duration specific. This review hopes to make clear that oxidative state plays a key role in the regulation and control of numerous signal transduction pathways in the cell and that elucidating the mechanisms behind oxidative stress-mediated neuronal cell death is important in identifying potential putative targets for the treatment of neuropathologies such as stroke.

Authors+Show Affiliations

Centre for Functional Genomics & Human Disease, Monash Institute of Reproduction and Development, Monash University, Melbourne, VIC 3168, Australia. peter.crack@med.monash.edu.auNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

15890617

Citation

Crack, Peter J., and Juliet M. Taylor. "Reactive Oxygen Species and the Modulation of Stroke." Free Radical Biology & Medicine, vol. 38, no. 11, 2005, pp. 1433-44.
Crack PJ, Taylor JM. Reactive oxygen species and the modulation of stroke. Free Radic Biol Med. 2005;38(11):1433-44.
Crack, P. J., & Taylor, J. M. (2005). Reactive oxygen species and the modulation of stroke. Free Radical Biology & Medicine, 38(11), 1433-44.
Crack PJ, Taylor JM. Reactive Oxygen Species and the Modulation of Stroke. Free Radic Biol Med. 2005 Jun 1;38(11):1433-44. PubMed PMID: 15890617.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen species and the modulation of stroke. AU - Crack,Peter J, AU - Taylor,Juliet M, PY - 2004/12/09/received PY - 2005/01/10/revised PY - 2005/01/21/accepted PY - 2005/5/14/pubmed PY - 2005/10/7/medline PY - 2005/5/14/entrez SP - 1433 EP - 44 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 38 IS - 11 N2 - Reactive oxygen species and oxidative state are slowly gaining acceptance in having a physiological relevance rather than just being the culprits in pathophysiological processes. The control of the redox environment of the cell provides for additional regulation in relation to critical cellular signal transduction pathways. Conversely, aberrant regulation of oxidative state manifesting as oxidative stress can predispose a cell to adverse outcome. The PI3-kinase/Akt pathway is one such pathway that is partially regulated via oxidative state and, in an oxidative stress paradigm such as ischemic reperfusion injury, may be inactivated, which can lead to potentiation and or exacerbation of cell death. Activation of NF(kappa)B has also been associated with oxidative stress. The role of NF(kappa)B in neuronal cell death is widely debated, with major studies highlighting both a pro- and an antiapoptotic role for NF(kappa)B with the outcome being region, stimulus, dose, and duration specific. This review hopes to make clear that oxidative state plays a key role in the regulation and control of numerous signal transduction pathways in the cell and that elucidating the mechanisms behind oxidative stress-mediated neuronal cell death is important in identifying potential putative targets for the treatment of neuropathologies such as stroke. SN - 0891-5849 UR - https://www.unboundmedicine.com/medline/citation/15890617/Reactive_oxygen_species_and_the_modulation_of_stroke_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(05)00037-7 DB - PRIME DP - Unbound Medicine ER -