Peripheral oxidative biomarkers constitute a valuable indicator of the severity of oxidative brain damage in acute cerebral infarction

Oxidative stress contributes to post-ischemic brain damage. We assessed the correlation between plasma 8-hydroxy-2′-deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, and progressive brain damage in rats subjected to transient or permanent ischemia. Male Wistar rats were subjected to perm...

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Published in:	Brain research Vol. 1025; no. 1; pp. 43 - 50
Main Authors:	Liu, Hao, Uno, Masaaki, Kitazato, Keiko T., Suzue, Atsuhiko, Manabe, Shiji, Yamasaki, Hiroyuki, Shono, Masayuki, Nagahiro, Shinji
Format:	Journal Article
Language:	English
Published:	London Elsevier B.V 29-10-2004 Amsterdam Elsevier New York, NY
Subjects:	8-OHdG Acute Disease Animals Biological and medical sciences Biological marker Biomarkers - metabolism Brain - metabolism Cerebral Infarction - metabolism Cerebral ischemia Deoxyguanosine - analogs & derivatives Deoxyguanosine - metabolism Hypoxia, Brain - metabolism Male Medical sciences Neurology Oxidation-Reduction Oxidative stress Oxidative Stress - physiology Rat Rats Rats, Wistar Severity of Illness Index Vascular diseases and vascular malformations of the nervous system Biological marker Oxidative stress Cerebral ischemia Rat 8-OHdG Cerebral infarction Vertebrata Mammalia Ischemia Animal Rodentia Encephalon
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Summary:	Oxidative stress contributes to post-ischemic brain damage. We assessed the correlation between plasma 8-hydroxy-2′-deoxyguanosine (8-OHdG), as a marker of oxidative DNA damage, and progressive brain damage in rats subjected to transient or permanent ischemia. Male Wistar rats were subjected to permanent- and 0.5-, 1-, 2-h middle cerebral artery occlusion (MCAO). At various times thereafter, the infarct volume, 8-OHdG levels in plasma and brain tissue, DNA fragmentation, and immunohistochemical observations on their brains were recorded and compared. At 12 h after 2-h MCAO–reperfusion, the cortical infarct volume was increased; it peaked at 24 h. DNA degeneration expanded from the caudate putamen into the cortical region at 12 h. 8-OHdG-containing cells in the cortical infarct zone were observed at 12 h, the number of 8-OHdG-positive cells was highest at 24 h and they co-localized with DNA single-strand breaks. Plasma 8-OHdG significantly increased at 12 h, and peaked at 24 h after reperfusion (1.1±0.7 ng/ml (mean±S.D.); controls 0.3±0.1; p<0.01). This increase was in step with increased infarct volume, DNA degradation, and reflected immunohistochemical findings in the cortical region but not the caudate putamen. In the permanent MCAO model, plasma 8-OHdG levels were associated with the brain contents of 8-OHdG. Plasma 8-OHdG and the cortical infarct volume were lower in the 0.5- and 1-h than the 2-h MCAO model. Our findings suggest that 8-OHdG as a peripheral biomarker may be an indicator of oxidative brain damage in acute cerebral infarction.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0006-8993 1872-6240
DOI:	10.1016/j.brainres.2004.07.071