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Bibliographic Record
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- Material Type
- 文書・図像類
- Author/Editor
- 西川, 拓朗
- Author Heading
- 西川, 拓朗 ニシカワ, タクロウ
- Publication, Distribution, etc.
- Alternative Title
- Prevention of benzene (or radiation) induced acute myeloid leukemia (or bone marrow failure) by myeloperoxidase inhibitor
- Text Language Code
- jpn
- Target Audience
- 一般
- Note (General)
- 2012-2013年度科学研究費助成事業（若手研究（B））研究成果報告書 課題番号：24790602 研究代表者：西川拓朗（鹿児島大学・医学部・歯学部附属病院・助教）ベンゼンの骨髄毒性とミエロペルオキシダーゼ（MPO）の関係を明らかにするためにヒト骨髄細胞株にベンゼン代謝物の一つであるベンゼントリオール（BT）を曝露し、MPO阻害化、非阻害化における遺伝子の発現変動をマイクロアレイ法で網羅的に、アポトーシス誘導はフローサイトメモリー法で解析した。BT曝露でアポトーシスが生じ、1213遺伝子の発現が変動し、アポトーシス、抗アポトーシス、細胞増殖、炎症、細胞周期関連遺伝子の発現が上昇した。しかし、MPO阻害で、これら遺伝子の発現変動、アポトーシス誘導は劇的に抑制された。MPOはベンゼン骨髄毒性のリスク評価や予防における分子マーカーとなり得る。While it is known that benzene induces myeloid leukemia in humans, the mechanism has yet to be clarified. Previously, we suggested that myeloperoxidase (MPO) was the key enzyme because it promotes generation of powerful oxidant hypochlorous acid which reacting with DNA. In our study, using a whole-human-genome oligonucleotide microarray, we analyzed the genome-wide expression profiles of HL60 human promyelocytic cell lines exposed to 1,2,4-benzenetriol (BT) with or without MPO inhibition. The microarray analysis revealed that 4h exposure to BT changed the expressionin HL60 cells of 1213 genes associated with transcription, RNA metabolic processes, immuneresponse, apoptosis, cell death, and biosynthetic processes, and that these changes were dramatically lessened by MPO-specific inhibition. Gene expression profiles along with GO and KEGG pathway annotation analysis suggest that there maybe a role for MPO as an examination marker or in prophylaxis forchemical carcinogenesis.