Gene expression in rat striatum following carbon monoxide poisoning

Shuichi Hara , Masamune Kobayash , Fumi Kuriiwa , Kunihiko Kurosaki , Hajime Mizukami
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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.

一氧化碳中毒后大鼠纹状体的基因表达
一氧化碳(CO)中毒导致脑损伤,可通过氢治疗来减轻[1],[2],氢是一种选择性清除羟基自由基(OH)的清除剂[3]。这表明OH在一氧化碳中毒引起的脑损伤中起作用。研究表明,严重一氧化碳中毒导致血中碳氧血红蛋白(COHb)水平升高后,大鼠纹状体中OH的生成明显增强。70%是由3000 ppm CO引起的,但同样严重的CO中毒,由于1000 ppm CO,血液COHb水平约为50%[4]。有趣的是,5% O2引起的缺氧与3000 ppm CO相当,产生的•OH比3000 ppm CO少得多[4]。此外,cAMP的产生与OH的产生并行[5]可能有助于OH的产生[6]。缺氧以外的其他机制可能导致CO中毒脑损伤[7]。为了寻找其机制,我们研究了1000ppm CO、3000ppm CO和5% O2对大鼠纹状体基因表达的影响。所有阵列数据已存入Gene Expression Omnibus (GEO)数据库,登录号为GSE94780。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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