Role of mitochondrial permeability transition in fetal brain damage in rats
Autor: | Atsuko Oya, Hidehiko Miyake, Yoshinari Taniuchi, Akihito Nakai, Yukino Shibazaki, Toshiyuki Takeshita |
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Rok vydání: | 2004 |
Předmět: |
medicine.medical_specialty
Central nervous system Ischemia Apoptosis Brain damage Mitochondrion Fetal Hypoxia Mitochondrial Membrane Transport Proteins Ion Channels Brain Ischemia Mitochondrial membrane transport protein Developmental Neuroscience Pregnancy Cyclosporin a Internal medicine medicine Animals Rats Wistar Cerebral Cortex biology Mitochondrial Permeability Transition Pore medicine.disease Rats Endocrinology medicine.anatomical_structure Neurology Mitochondrial permeability transition pore In utero Reperfusion Injury Pediatrics Perinatology and Child Health Cyclosporine biology.protein Brain Damage Chronic Female Neurology (clinical) medicine.symptom Energy Metabolism Mitochondrial Swelling Neuroscience |
Zdroj: | Pediatric Neurology. 30:247-253 |
ISSN: | 0887-8994 |
Popis: | Recirculation after transient in utero ischemia has previously been found to be accompanied by delayed deterioration of cellular bioenergetic state and of mitochondrial function in the fetal rat brain. Our objective was to assess whether the delayed deterioration is a result of the activation of mitochondrial permeability transition which is observed ultrastructurally as mitochondrial swelling. The respiratory activities and ultrastructure of isolated mitochondria and the cellular bioenergetic state in fetal rat brain were examined at the end of 30 minutes of in utero ischemia and after 1, 2, 3 and 4 hours of recirculation. Cyclosporin A, a potent and virtually specific mitochondrial permeability transition blocker, or vehicle was administered 1 hour after recirculation. In the vehicle-treated animals, the transient ischemia was associated with a delayed deterioration of cellular bioenergetic state and mitochondrial activities at 4 hours of recirculation. The number of swollen mitochondria increased markedly after 4 hours of recirculation. The deterioration and the swelling were prevented by cyclosporin A. The present study indicates that cyclosporin A treatment improves recovery of fetal brain energy metabolism and inhibits the mitochondrial swelling after transient in utero ischemia. The results suggest that mitochondria and mitochondrial permeability transition may be involved in the development of ischemic brain damage in the immature rat. |
Databáze: | OpenAIRE |
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