Citation

Hara S, Kobayash M, Kuriiwa F, Kurosaki K, Mizukami H. Genom. Data 2017; 12: 74-75.

Affiliation

Department of Legal Medicine, Kanazawa Medical University, Ishikawa 920-0293, Japan.

Copyright

(Copyright © 2017, Elsevier Publishing)

DOI

10.1016/j.gdata.2017.03.007

PMID

28386529

PMCID

PMC5374847

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.

Language: en