Perinatal Asphyxia and Brain Development: Mitochondrial Damage Without Anatomical or Cellular Losses
| العنوان: | Perinatal Asphyxia and Brain Development: Mitochondrial Damage Without Anatomical or Cellular Losses |
|---|---|
| المؤلفون: | Antonio Galina, Ana Paula Miranda Mendonça, Danielle Rayêe, Clara Rodrigues-Ferreira, Anna Carolina Carvalho da Fonseca, Paula Ribeiro Paes Pereira, Diego Szczupak, Marcus F. Oliveira, Flavia Regina Souza Lima, Thaia Silva-Rodrigues, Daniela Uziel, Roberto Lent, Jean Pierre Mendes Lima |
| المصدر: | Biochimica et Biophysica Acta (BBA) - Bioenergetics. 1859:e75 |
| بيانات النشر: | Elsevier BV, 2018. |
| سنة النشر: | 2018 |
| مصطلحات موضوعية: | 0301 basic medicine, Biochemistry, chemistry.chemical_compound, 0302 clinical medicine, Medicine, Cells, Cultured, Evans Blue, Membrane Potential, Mitochondrial, Neurons, Brain Mass, Brain, Organ Size, Cell Hypoxia, Mitochondria, medicine.anatomical_structure, Neurology, Blood-Brain Barrier, Cerebral cortex, Mitochondrial Membranes, Lactates, Female, medicine.symptom, Cell Respiration, Calcium buffering, Neuroscience (miscellaneous), Biophysics, Citrate (si)-Synthase, Permeability, Andrology, Asphyxia, 03 medical and health sciences, Cellular and Molecular Neuroscience, Animals, Rats, Wistar, Fetus, business.industry, Cell Biology, Hypoxia (medical), medicine.disease, Survival Analysis, Perinatal asphyxia, 030104 developmental biology, Animals, Newborn, chemistry, Astrocytes, Energy Metabolism, business, 030217 neurology & neurosurgery, Ex vivo |
| الوصف: | Perinatal asphyxia remains a significant cause of neonatal mortality and is associated with long-term neurodegenerative disorders. In the present study, we evaluated cellular and subcellular damages to brain development in a model of mild perinatal asphyxia. Survival rate in the experimental group was 67%. One hour after the insult, intraperitoneally injected Evans blue could be detected in the fetuses' brains, indicating disruption of the blood-brain barrier. Although brain mass and absolute cell numbers (neurons and non-neurons) were not reduced after perinatal asphyxia immediately and in late brain development, subcellular alterations were detected. Cortical oxygen consumption increased immediately after asphyxia, and remained high up to 7 days, returning to normal levels after 14 days. We observed an increased resistance to mitochondrial membrane permeability transition, and calcium buffering capacity in asphyxiated animals from birth to 14 days after the insult. In contrast to ex vivo data, mitochondrial oxygen consumption in primary cell cultures of neurons and astrocytes was not altered after 1% hypoxia. Taken together, our results demonstrate that although newborns were viable and apparently healthy, brain development is subcellularly altered by perinatal asphyxia. Our findings place the neonate brain mitochondria as a potential target for therapeutic protective interventions. |
| تدمد: | 0005-2728 |
| DOI: | 10.1016/j.bbabio.2018.09.224 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::90000c5d47aafccce88ae47a2427037d https://doi.org/10.1016/j.bbabio.2018.09.224 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....90000c5d47aafccce88ae47a2427037d |
| قاعدة البيانات: | OpenAIRE |
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