Abstract
Background and purpose. Low molecular weight antioxidants (LMWA), which reflect tissue reducing power, are among the endogenous mechanisms for neutralizing reactive oxygen species (ROS). Ischemic preconditioning (IPC) was associated with decreased oxidative stress. We examined the effect of focal ischemia on LMWA and on prostaglandin E2 (PGE2, a product of arachidonic acid oxidation) in the brain, heart, liver, and lungs of rats subjected to 90 min of ischemia and in IPC rats subjected to similar insult. Methods. Transient right middle cerebral artery occlusion (MCAO) was performed for 90 min and at 0, 5, 30, 60, or 240 min of reperfusion, LMWA and PGE 2 were evaluated by cyclic voltametry (CV) and radioimmunoassay, respectively. IPC was induced by 2 min of MCAO, 24 h prior to the major ischemic episode. Results. LMWA decreased at 5 min of reperfusion in the brain, heart, liver, and lung and rose 4 h later only in the brain. PGE2 levels increased three to fivefold in all tissues examined. Surprisingly, in IPC rats a dramatic increase of LMWA occurred at 5 min of reperfusion in the brain and in the peripheral organs. Uric acid, but not ascorbic, is the major LMWA increased. Conclusions. We propose that after ischemia, ROS rapidly consume the antioxidants reserves in the brain and also in peripheral organs, suggesting that the whole body is under oxidative stress. Moreover, part of the neuroprotection afforded by IPC is mediated by the brain's ability to mobilize antioxidants, especially uric acid, that attenuate the massive ROS-mediated oxidative stress.
| Original language | English |
|---|---|
| Pages (from-to) | 117-124 |
| Number of pages | 8 |
| Journal | Experimental Neurology |
| Volume | 192 |
| Issue number | 1 |
| DOIs | |
| State | Published - Mar 1 2005 |
| Externally published | Yes |
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Keywords
- Ascorbic acid
- Biological oxidation potential
- Brain ischemia
- Reactive oxygen species
- Uric acid
ASJC Scopus subject areas
- Neurology
- Neuroscience(all)
Cite this
Ischemic preconditioning increases antioxidants in the brain and peripheral organs after cerebral ischemia. / Glantz, Lucio; Avramovich, Aharon; Trembovler, Victoria; Gurvitz, Vladimir; Kohen, Ron; Eidelman, Leonid A.; Shohami, Esther.
In: Experimental Neurology, Vol. 192, No. 1, 01.03.2005, p. 117-124.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ischemic preconditioning increases antioxidants in the brain and peripheral organs after cerebral ischemia
AU - Glantz, Lucio
AU - Avramovich, Aharon
AU - Trembovler, Victoria
AU - Gurvitz, Vladimir
AU - Kohen, Ron
AU - Eidelman, Leonid A.
AU - Shohami, Esther
PY - 2005/3/1
Y1 - 2005/3/1
N2 - Background and purpose. Low molecular weight antioxidants (LMWA), which reflect tissue reducing power, are among the endogenous mechanisms for neutralizing reactive oxygen species (ROS). Ischemic preconditioning (IPC) was associated with decreased oxidative stress. We examined the effect of focal ischemia on LMWA and on prostaglandin E2 (PGE2, a product of arachidonic acid oxidation) in the brain, heart, liver, and lungs of rats subjected to 90 min of ischemia and in IPC rats subjected to similar insult. Methods. Transient right middle cerebral artery occlusion (MCAO) was performed for 90 min and at 0, 5, 30, 60, or 240 min of reperfusion, LMWA and PGE 2 were evaluated by cyclic voltametry (CV) and radioimmunoassay, respectively. IPC was induced by 2 min of MCAO, 24 h prior to the major ischemic episode. Results. LMWA decreased at 5 min of reperfusion in the brain, heart, liver, and lung and rose 4 h later only in the brain. PGE2 levels increased three to fivefold in all tissues examined. Surprisingly, in IPC rats a dramatic increase of LMWA occurred at 5 min of reperfusion in the brain and in the peripheral organs. Uric acid, but not ascorbic, is the major LMWA increased. Conclusions. We propose that after ischemia, ROS rapidly consume the antioxidants reserves in the brain and also in peripheral organs, suggesting that the whole body is under oxidative stress. Moreover, part of the neuroprotection afforded by IPC is mediated by the brain's ability to mobilize antioxidants, especially uric acid, that attenuate the massive ROS-mediated oxidative stress.
AB - Background and purpose. Low molecular weight antioxidants (LMWA), which reflect tissue reducing power, are among the endogenous mechanisms for neutralizing reactive oxygen species (ROS). Ischemic preconditioning (IPC) was associated with decreased oxidative stress. We examined the effect of focal ischemia on LMWA and on prostaglandin E2 (PGE2, a product of arachidonic acid oxidation) in the brain, heart, liver, and lungs of rats subjected to 90 min of ischemia and in IPC rats subjected to similar insult. Methods. Transient right middle cerebral artery occlusion (MCAO) was performed for 90 min and at 0, 5, 30, 60, or 240 min of reperfusion, LMWA and PGE 2 were evaluated by cyclic voltametry (CV) and radioimmunoassay, respectively. IPC was induced by 2 min of MCAO, 24 h prior to the major ischemic episode. Results. LMWA decreased at 5 min of reperfusion in the brain, heart, liver, and lung and rose 4 h later only in the brain. PGE2 levels increased three to fivefold in all tissues examined. Surprisingly, in IPC rats a dramatic increase of LMWA occurred at 5 min of reperfusion in the brain and in the peripheral organs. Uric acid, but not ascorbic, is the major LMWA increased. Conclusions. We propose that after ischemia, ROS rapidly consume the antioxidants reserves in the brain and also in peripheral organs, suggesting that the whole body is under oxidative stress. Moreover, part of the neuroprotection afforded by IPC is mediated by the brain's ability to mobilize antioxidants, especially uric acid, that attenuate the massive ROS-mediated oxidative stress.
KW - Ascorbic acid
KW - Biological oxidation potential
KW - Brain ischemia
KW - Reactive oxygen species
KW - Uric acid
UR - http://www.scopus.com/inward/record.url?scp=13444291515&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=13444291515&partnerID=8YFLogxK
U2 - 10.1016/j.expneurol.2004.11.012
DO - 10.1016/j.expneurol.2004.11.012
M3 - Article
C2 - 15698625
AN - SCOPUS:13444291515
VL - 192
SP - 117
EP - 124
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
IS - 1
ER -