کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1931279 | 1050547 | 2011 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Brain infarction correlates more closely with acrolein than with reactive oxygen species Brain infarction correlates more closely with acrolein than with reactive oxygen species](/preview/png/1931279.png)
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.
Research highlights
► Acrolein is more strongly involved in cell damage than reactive oxygen species (ROS).
► Infarction led more readily to RNA damage than to DNA or phospholipid damage.
► Acrolein was mainly produced by spermine oxidase from spermine which was released from RNA.
► ROS mainly functions at the level of RNA degradation rather than phospholipid degradation.
Journal: Biochemical and Biophysical Research Communications - Volume 404, Issue 4, 28 January 2011, Pages 1044–1049