2000 Fiscal Year Final Research Report Summary
A Research for Prophylaxis of Ischemia-Reperfusion Damage in the Brain of Neonates during Perinatal Period.
| Project/Area Number |
11671608
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | NAGOYA UNIVERSITY |
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Principal Investigator |
ITAKURA Atsuo SCHOOL OF MEDICINE, NAGOYA UNIVERSITY, ASSISTANT PROFESSOR, 医学部, 講師 (70262897)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUTANI Shigehiko SCHOOL OF MEDICINE, NAGOYA UNIVERSITY, PROFESSOR, 医学部, 教授 (00159162)
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| Project Period (FY) |
1999 – 2000
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| Keywords | HNE / PSN / Ishemic-reperfusion damage in brain |
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| Research Abstract |
Four-hydroxynonenal (HNE) has been proposed as an important marker of radical-induced lipid peroxidation. To assess the occurrence of lipid peroxidation and subsequent neuronal cell death in perinatal brain was the principal objective of this study. Immunochemical studies using an antibody against HNE-modified protein were performed in controls aged from 20 weeks of gestation to 64 years, and patients with pontosubicular neuron necrosis (PSN). Immunohistochemical study showed developmental and aging changes of positive staining in Purkinje cells and pontine neurons (27 weeks - 7 months, 50, 64 years). In addition, karyorrhectic cells in pontine nuclei with PSN were positively stained. Immunoblotting revealed that the 75-kDa protein, which was speculated as mitochondrial complex-1 protein, was the most intensely expressed among multiple immunoreactive proteins. Our results indicated the presence of oxidative stress in the perinatal neuron, and this oxidative stress may contribute to karyorrhectic death.
In addition fetal endothelial cells incubated in hypoxic condition increased the expression of angiotensin-converting enzyme which is a key enzyme of regulation of blood perfusion in fetus. In a next project we will research to elucidate the relation between rennin-angiotensin system and ischmic-reperfusion damage in the fetal brain.
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