Journal
NEUROSCIENCE LETTERS
Volume 405, Issue 3, Pages 172-174Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2006.06.058
Keywords
lipid peroxidation; neuroprostanes; isoprostanes; ethanol; withdrawal; docosahexaenoic acid
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Funding
- NCI NIH HHS [CA77839] Funding Source: Medline
- NIAAA NIH HHS [AA15145-01] Funding Source: Medline
- NIDDK NIH HHS [DK48831] Funding Source: Medline
- NIEHS NIH HHS [ES13125] Funding Source: Medline
- NIGMS NIH HHS [GM15431] Funding Source: Medline
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Ethanol withdrawal is a serious clinical problem owing in part to over stimulation of ionotropic glutamate receptors in the brain and is linked to elevated oxidative damage. In this study, we tested the hypothesis that lipid peroxidation is elevated in the brain tissue of rats fed an ethanol-containing diet for 6 weeks followed by 24 h of withdrawal. We measured F-2-isoprostanes (IsoPs), as products of arachidonic acid (20:4, n - 6) oxidation and F-4-neuroprostanes (NeuroPs), as products of docosahexaenoic acid (22:6, it - 3; DHA) oxidation. Levels of NeuroPs were significantly elevated in the cerebral cortex (97%) and brainstem (68%) of animals undergoing ethanol withdraw versus control. In contrast, elevations in IsoP content (39%) occurred only in the cerebellum of animals in withdrawal versus control animals. These data demonstrate that DHA, versus arachidonic acid, is particularly vulnerable to oxidative damage in ethanol withdrawal. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
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