TY - JOUR
T1 - Regulated production of free radicals by the mitochondrial electron transport chain
T2 - Cardiac ischemic preconditioning
AU - Matsuzaki, Satoshi
AU - Szweda, Pamela A.
AU - Szweda, Luke I.
AU - Humphries, Kenneth M.
PY - 2009/11/30
Y1 - 2009/11/30
N2 - Excessive production of free radicals by mitochondria is associated with, and likely contributes to, the progression of numerous pathological conditions. Nevertheless, the production of free radicals by the mitochondria may have important biological functions under normal or stressed conditions by activating or modulating redox-sensitive cellular signaling pathways. This raises the intriguing possibility that regulated mitochondrial free radical production occurs via mechanisms that are distinct from pathologies associated with oxidative damage. Indeed, the capacity of mitochondria to produce free radicals in a limited manner may play a role in ischemic preconditioning, the phenomenon whereby short bouts of ischemia protect from subsequent prolonged ischemia and reperfusion. Ischemic preconditioning can thus serve as an important model system for defining regulatory mechanisms that allow for transient, signal-inducing, production of free radicals by mitochondria. Defining how these mechanism(s) occur will provide insight into therapeutic approaches that minimize oxidative damage without altering normal cellular redox biology. The aim of this review is to present and discuss evidence for the regulated production of superoxide by the electron transport chain within the ischemic preconditioning paradigm of redox regulation.
AB - Excessive production of free radicals by mitochondria is associated with, and likely contributes to, the progression of numerous pathological conditions. Nevertheless, the production of free radicals by the mitochondria may have important biological functions under normal or stressed conditions by activating or modulating redox-sensitive cellular signaling pathways. This raises the intriguing possibility that regulated mitochondrial free radical production occurs via mechanisms that are distinct from pathologies associated with oxidative damage. Indeed, the capacity of mitochondria to produce free radicals in a limited manner may play a role in ischemic preconditioning, the phenomenon whereby short bouts of ischemia protect from subsequent prolonged ischemia and reperfusion. Ischemic preconditioning can thus serve as an important model system for defining regulatory mechanisms that allow for transient, signal-inducing, production of free radicals by mitochondria. Defining how these mechanism(s) occur will provide insight into therapeutic approaches that minimize oxidative damage without altering normal cellular redox biology. The aim of this review is to present and discuss evidence for the regulated production of superoxide by the electron transport chain within the ischemic preconditioning paradigm of redox regulation.
KW - Cardiac ischemia
KW - Electron transport chain
KW - Free radicals
KW - Mitochondria
KW - Oxidation and reduction
KW - Preconditioning
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U2 - 10.1016/j.addr.2009.05.008
DO - 10.1016/j.addr.2009.05.008
M3 - Review article
C2 - 19716389
AN - SCOPUS:71549152199
SN - 0169-409X
VL - 61
SP - 1324
EP - 1331
JO - Advanced Drug Delivery Reviews
JF - Advanced Drug Delivery Reviews
IS - 14
ER -