Spermidine/spermine N1-acetyl transferase activity in rat brain following transient focal cerebral ischemia and reperfusion

Yat Ching Tong, Juei Tang Cheng, Wang Chuan Wan

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)


The polyamine system is very sensitive to different pathological states of brain and is perturbed after central nervous system (CNS) injury. Spermidine/Spermine N1-acetyl transferase (SSAT) is the key enzyme responsible for interconversion of spermine and spermidine to spermidine and putrescine respectively. In the present study, SSAT activity was evaluated in the rat CNS, following transient focal cerebral ischemia and reperfusion. The middle cerebral artery (MCA) was occluded for 2 h in male spontaneously hypertensive rats by an intraluminal suture technique. Animals were sacrificed at 3-24 h reperfusion following the MCA occlusion and SSAT activity was assayed in cortex and striatum. Results showed that SSAT activity was significantly increased at 12 h reperfusion in cortex and at 9, 12 and 18 h reperfusion in striatum following ischemia compared to sham or contralateral controls. These results demonstrate that polyamine catabolism in the rat CNS is altered following MCA occlusion. In the in vitro ischemia study, SSAT activity was evaluated in primary cortical neuronal cultures at 6-24 h re-oxygenation intervals following oxygen-glucose deprivation for 1 h, and the results from this group show that the enzyme activity increased by about 62% (P < 0.05) at 24 h re-oxygenation. This study suggests that the increased SSAT activity may contribute to the increase in putrescine during the post-ischemic period.

Original languageEnglish
Pages (from-to)17-20
Number of pages4
JournalNeuroscience Letters
Issue number1
Publication statusPublished - 2001 Mar 2

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Spermidine/spermine N<sup>1</sup>-acetyl transferase activity in rat brain following transient focal cerebral ischemia and reperfusion'. Together they form a unique fingerprint.

Cite this