{"title":"Gene expression in rat striatum following carbon monoxide poisoning","authors":"Shuichi Hara , Masamune Kobayash , Fumi Kuriiwa , Kunihiko Kurosaki , Hajime Mizukami","doi":"10.1016/j.gdata.2017.03.007","DOIUrl":null,"url":null,"abstract":"<div><p>Carbon monoxide (CO) poisoning causes brain damage, which is attenuated by treatment with hydrogen <span>[1]</span>, <span>[2]</span>, a scavenger selective to hydroxyl radical (<img>OH) [3]. This suggests a role of <img>OH in brain damage due to CO poisoning. Studies have shown strong enhancement of <img>OH production in rat striatum by severe CO poisoning with a blood carboxyhemoglobin (COHb) level ><!--> <!-->70% due to 3000<!--> <!-->ppm CO, but not less severe CO poisoning with a blood COHb level at approximately 50% due to 1000<!--> <!-->ppm CO [4]. Interestingly, 5% O<sub>2</sub> causes hypoxia comparable with that by 3000<!--> <!-->ppm CO and produces much less <sup>•</sup>OH than 3000<!--> <!-->ppm CO does [4]. In addition, cAMP production in parallel with <img>OH production <span>[5]</span> might contribute to <img>OH production <span>[6]</span>. It is likely that mechanisms other than hypoxia contribute to brain damage due to CO poisoning <span>[7]</span>. To search for the mechanisms, we examined the effects of 1000<!--> <!-->ppm CO, 3000<!--> <!-->ppm CO and 5% O<sub>2</sub> on gene expression in rat striatum. All array data have been deposited in the Gene Expression Omnibus (GEO) database under accession number GSE94780.</p></div>","PeriodicalId":56340,"journal":{"name":"Genomics Data","volume":"12 ","pages":"Pages 74-75"},"PeriodicalIF":0.0000,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gdata.2017.03.007","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genomics Data","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2213596017300491","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
Abstract
Carbon monoxide (CO) poisoning causes brain damage, which is attenuated by treatment with hydrogen [1], [2], a scavenger selective to hydroxyl radical (OH) [3]. This suggests a role of OH in brain damage due to CO poisoning. Studies have shown strong enhancement of OH production in rat striatum by severe CO poisoning with a blood carboxyhemoglobin (COHb) level > 70% due to 3000 ppm CO, but not less severe CO poisoning with a blood COHb level at approximately 50% due to 1000 ppm CO [4]. Interestingly, 5% O2 causes hypoxia comparable with that by 3000 ppm CO and produces much less •OH than 3000 ppm CO does [4]. In addition, cAMP production in parallel with OH production [5] might contribute to OH production [6]. It is likely that mechanisms other than hypoxia contribute to brain damage due to CO poisoning [7]. To search for the mechanisms, we examined the effects of 1000 ppm CO, 3000 ppm CO and 5% O2 on gene expression in rat striatum. All array data have been deposited in the Gene Expression Omnibus (GEO) database under accession number GSE94780.