Brain infarction correlates more closely with acrolein than with reactive oxygen species

Ryotaro Saiki, Hyerim Park, Itsuko Ishii, Madoka Yoshida, Kazuhiro Nishimura, Toshihiko Toida, Hideki Tatsukawa, Soichi Kojima, Yoshihiko Ikeguchi, Anthony E. Pegg, Keiko Kashiwagi, Kazuei Igarashi

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


Although it is thought that the major factor responsible for cell damage is reactive oxygen species (ROS), our recent studies have shown that acrolein is more toxic than ROS. Thus, the relative importance of acrolein and ROS in cell damage during brain infarction was compared using photochemically induced thrombosis model mice. The levels of acrolein-conjugated albumin, and of 4-hydroxynonenal (HNE)-conjugated albumin and 8-OHdG were evaluated as indicators of damage produced by acrolein and ROS, respectively. The increase in acrolein-conjugated albumin was much greater than the increase in HNE-conjugated albumin or 8-OHdG, suggesting that acrolein is more strongly involved in cell damage than ROS during brain infarction. It was also shown that infarction led more readily to RNA damage than to DNA or phospholipid damage. As a consequence, polyamines were released from RNA, and acrolein was produced from polyamines, especially from spermine by spermine oxidase. Production of acrolein from spermine by spermine oxidase was clarified using spermine synthase-deficient Gy mice and transglutaminase 2-knockout mice, in which spermine content is negligible or spermidine/spermine N1-acetyltransferase activity is elevated.

Original languageEnglish (US)
Pages (from-to)1044-1049
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - Jan 28 2011

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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