{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T05:07:43Z","timestamp":1770786463015,"version":"3.50.0"},"reference-count":33,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,10,11]],"date-time":"2004-10-11T00:00:00Z","timestamp":1097452800000},"content-version":"vor","delay-in-days":4301,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[1993,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The salicylate trapping method was used to investigate the changes in hydroxyl radical (\u00b7OH) levels in the selectively vulnerable hippocampus compared to the cerebral cortex of gerbils subjected to a 10 min period of near complete forebrain ischemia. Salicylate\u2010derived 2,5\u2010dihydroxybenzoic acid (2,5\u2010DHBA) was measured in sham\u2010operated animals and at 1, 5, and 15 min of reperfusion. A basal level of 2,5\u2010DHBA was also seen in non\u2010ischemic gerbil brain, both in the hippocampus and cortex. The hippocampal basal level was 160% higher than in the cortex (<jats:italic>P<\/jats:italic> &lt; .01). Treatment with the cytochrome P450 inhibitor SKF\u2010525A (50 mg\/kg s.c. 30 min before measurement) did not affect this basal level in either hippocampus or cortex, which argues against a contribution of metabolic salicylate hydroxylation as its source. In contrast, pretreatment with the arachidonic acid cyclo\u2010oxygenase inhibitor ibuprofen (20 mg\/kg s.c.) decreased (\u221268.8%) the level of salicylate hydroxylation in the hippocampus, but not the cortex. In animals subjected to 10 min of forebrain ischemia, a selective increase in 2,5\u2010DHBA was observed in the hippocampus at 1 min of reprerfusion which subsided by 5 min. No increase in salicylate hydroxylation was apparent in the cortex within the same time frame. The increase in \u00b7OH in the hippocampus at 1 min of reperfusion was accompanied by a significant decrease (\u221215%; <jats:italic>P<\/jats:italic> &lt; .03) in the hippocampal levels of vitamin E. No loss of vitamin E was observed in the cortex at the same time. It is hypothesized that the selective ischemic vulnerability of the hippocampus is mechanistically related to a selective post\u2010ischemic burst in \u00b7OH in that region. Moreover, this may be based upon an intrinsically higher level of oxidative stress in that region as a by\u2010product of greater arachidonic acid turnover. \u00a9 1993 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.490340111","type":"journal-article","created":{"date-parts":[[2005,5,25]],"date-time":"2005-05-25T20:18:21Z","timestamp":1117052301000},"page":"107-112","source":"Crossref","is-referenced-by-count":117,"title":["Hydroxyl radical production and lipid peroxidation paralles selective post\u2010ischemic vulnerability in gerbil brain"],"prefix":"10.1002","volume":"34","author":[{"given":"Edward D.","family":"Hall","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. K.","family":"Andrus","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. S.","family":"Althaus","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. 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