期刊
JOURNAL OF EXPERIMENTAL BIOLOGY
卷 207, 期 18, 页码 3221-3231出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jeb.01022
关键词
brain; ischemia; oxidative stress; antioxidant
类别
资金
- NHLBI NIH HHS [P01 HL4244] Funding Source: Medline
Despite numerous defenses, the brain is vulnerable to oxidative stress resulting from ischemia/reperfusion. Excitotoxic stimulation of superoxide and nitric oxide production leads to formation of highly reactive products, including peroxynitrite and hydroxyl radical, which are capable of damaging lipids, proteins and DNA. Use of transgenic mutants and selective pharmacological antioxidants has greatly increased understanding of the complex interplay between substrate deprivation and ischemic outcome. Recent evidence that reactive oxygen/nitrogen species play a critical role in initiation of apoptosis, mitochondrial permeability transition and poly(ADP-ribose) polymerase activation provides additional mechanisms for oxidative damage and new targets for post-ischemic therapeutic intervention. Because oxidative stress involves multiple post-ischemic cascades leading to cell death, effective prevention/ treatment of ischemic brain injury is likely to require intervention at multiple effect sites.
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