Toxic acrolein production due to Ca2+ influx by the NMDA receptor during stroke
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- 作者：Mizuho Nakamuraa ; Takeshi Uemuraa ; Ryotaro Saikia ; b ; Akihiko Sakamotoc ; Hyerim Parkb ; Kazuhiro Nishimurab ; Yusuke Teruic ; Toshihiko Toidab ; Keiko Kashiwagic ; Kazuei Igarashia ; b ; iga16077@faculty.chiba-u.jp" class="auth_mail" title="E-mail the corresponding author
- 关键词：Acrolein ; Ca2+ ; Polyamines ; Ribosomes ; Reactive oxygen species ; Brain infarction
- 刊名：Atherosclerosis
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：244
- 期：Complete
- 页码：131-137
- 全文大小：2042 K
文摘
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Size of brain infarction was decreased by TB34, a channel blocker of NMDA receptors.
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Levels of Ca2+ and protein-conjugated acrolein (PC-Acro) were reduced by TB34.
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Polyamines decreased and PC-Acro increased by Ca2+ in cell culture systems.
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20 to 40 μM Ca2+ caused the release of polyamines from ribosomes in vitro.
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Acrolein is produced from polyamines released from ribosomes through Ca2+ increase.