Abstract | BACKGROUND AND PURPOSE: METHODS: A unilateral infarction was induced in mouse brain by photoinduction after injection of Rose Bengal. The volume of the infarction was analyzed using the public domain National Institutes of Health image program. Protein-conjugated acrolein levels at the locus of infarction and in cells were measured by Western blotting. Levels of polyamines were measured by high-performance liquid chromatography. RESULTS: When the size of brain infarction was decreased by N(1), N(4), N(8)-tribenzylspermidine, a channel blocker of the NMDA receptors, levels of Ca(2+) and protein-conjugated acrolein (PC-Acro) were reduced, while levels of polyamines were increased at the locus of infarction. When cell growth of mouse mammary carcinoma FM3A cells and neuroblastoma Neuro2a cells was inhibited by Ca(2+), the level of polyamines decreased, while that of PC-Acro increased. It was also shown that Ca(2+) toxicity was decreased in an acrolein toxicity decreasing FM3A mutant cells recently isolated. In addition, 20-40 μM Ca(2+) caused the release of polyamines from ribosomes. The results indicate that acrolein is produced from polyamines released from ribosomes through Ca(2+) increase. CONCLUSION:
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Authors | Mizuho Nakamura, Takeshi Uemura, Ryotaro Saiki, Akihiko Sakamoto, Hyerim Park, Kazuhiro Nishimura, Yusuke Terui, Toshihiko Toida, Keiko Kashiwagi, Kazuei Igarashi |
Journal | Atherosclerosis
(Atherosclerosis)
Vol. 244
Pg. 131-7
(Jan 2016)
ISSN: 1879-1484 [Electronic] Ireland |
PMID | 26630182
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- Reactive Oxygen Species
- Receptors, N-Methyl-D-Aspartate
- Acrolein
- Calcium
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Topics |
- Acrolein
(metabolism)
- Animals
- Blotting, Western
- Brain
(metabolism, pathology)
- Brain Infarction
(metabolism, pathology)
- Calcium
(metabolism)
- Cell Line, Tumor
- Disease Models, Animal
- Male
- Mice
- Mice, Inbred C57BL
- Reactive Oxygen Species
(metabolism)
- Receptors, N-Methyl-D-Aspartate
(metabolism)
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