Ischemic neuronal cell damage and iron metaoblism

1996 Fiscal Year Final Research Report Summary

• Project/Area Number: 06671421
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Cerebral neurosurgery
• Research Institution: Teikyo Univ.School of Med.
• Principal Investigator: KANEMITSU Hitdeaki Teikyo Univ.School of Med., Dept.of Neurosurgery, Assistant Prof., 医学部, 講師 (10129992)
• Co-Investigator(Kenkyū-buntansha): TAMURA Akira Teikyo Univ.School of Med., Dept.of Neurosurgery, Professor, 医学部, 教授 (80111532)
• Project Period (FY): 1994 – 1996
• Keywords: cerebral ischemia / rat / gerbil / iron / clathrin / transferrin / transferrin receptor / home oxygenase

Research Abstract

We have studied the distribution and the metabolism of iron in rat and gerbil brains following three kinds of cerebral ischemia. One was the focal cerebral ischemia which occluded middle cerebral artery in the rat. Second was the whole cerebral ischemia which was induced by cardiac arrest in the rat. Third was the forebrain ischemia which occulded bilateral common carotid arteries in the gerbil. The methods for the distribution and the metabolism of iron were carried out by Perls' and Gomori methods for iron deposition, immunohistochemistry for clathrin, transferrin and transferrin receptor, and in situ hibridization or in situ reverse transcriptase-polymerase chain reaction (RT-PCR) hybridization for home oxygenase 1 and 2. We could not detect iron deposition in the ischemic group as well as in the normal group. We could not recognized the significant difference between in the ischemic group and in the normal group regarding the immunohistochemistry for clathrin, transferrin and transferrin receptor, and in situ hybridization or in situ RT-PCR hybridization for home oxygnase 1 and 2. These results suggest that the deposition and the metabolism of iron do not plays a direct role of neuronal death following cerebral ischemia.