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pmid:28386529

Gene expression in rat striatum following carbon monoxide poisoning.

Shuichi Hara · Masamune Kobayash · Fumi Kuriiwa · Kunihiko Kurosaki · Hajime Mizukami

Genomics data · 2017 doi:10.1016/j.gdata.2017.03.007

Paper

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Experiment

partial

Data

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Analysis

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Execution

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Gene expression in rat striatum following carbon monoxide poisoning.
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10.1016/j.gdata.2017.03.007
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Shuichi Hara
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Masamune Kobayash
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Fumi Kuriiwa
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Kunihiko Kurosaki
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Hajime Mizukami
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Genomics data
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2017
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.
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