Molecular neurobiology, 2018-02, Vol.55 (2), p.980-988
2018
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- Autor(en) / Beteiligte
- Titel
- Maternal Hypermethioninemia Affects Neurons Number, Neurotrophins Levels, Energy Metabolism, and Na+,K+-ATPase Expression/Content in Brain of Rat Offspring
- Ist Teil von
- Molecular neurobiology, 2018-02, Vol.55 (2), p.980-988
- Ort / Verlag
- New York: Springer US
- Erscheinungsjahr
- 2018
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- In the current study, we verified the effects of maternal hypermethioninemia on the number of neurons, apoptosis, nerve growth factor, and brain-derived neurotrophic factor levels, energy metabolism parameters (succinate dehydrogenase, complex II, and cytochrome c oxidase), expression and immunocontent of Na + ,K + -ATPase, edema formation, inflammatory markers (tumor necrosis factor-alpha and interleukin-6), and mitochondrial hydrogen peroxide levels in the encephalon from the offspring. Pregnant Wistar rats were divided into two groups: the first one received saline (control) and the second group received 2.68 μmol methionine/g body weight by subcutaneous injections twice a day during gestation (approximately 21 days). After parturition, pups were killed at the 21st day of life for removal of encephalon. Neuronal staining (anti-NeuN) revealed a reduction in number of neurons, which was associated to decreased nerve growth factor and brain-derived neurotrophic factor levels. Maternal hypermethioninemia also reduced succinate dehydrogenase and complex II activities and increased expression and immunocontent of Na + ,K + -ATPase alpha subunits. These results indicate that maternal hypermethioninemia may be a predisposing factor for damage to the brain during the intrauterine life.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0893-7648eISSN: 1559-1182DOI: 10.1007/s12035-017-0383-zTitel-ID: cdi_proquest_miscellaneous_1861472446
- Format
- –
- Schlagworte
- Amino Acid Metabolism, Inborn Errors - chemically induced, Amino Acid Metabolism, Inborn Errors - metabolism, Animals, Apoptosis, Biomedical and Life Sciences, Biomedicine, Body weight, Brain, Brain - metabolism, Brain injury, Brain-derived neurotrophic factor, Cell Biology, Cell Count, Cytochrome-c oxidase, Dehydrogenase, Dehydrogenases, Edema, Energy metabolism, Energy Metabolism - physiology, Female, Gestation, Glycine N-Methyltransferase - deficiency, Glycine N-Methyltransferase - metabolism, Growth factors, Hydrogen peroxide, Inflammation, Interleukin 6, Metabolism, Methionine, Mitochondria, Na+/K+-exchanging ATPase, Nerve growth factor, Nerve Growth Factors - metabolism, Neurobiology, Neurology, Neurons, Neurons - metabolism, Neurosciences, Neurotrophic factors, Offspring, Oxidation-Reduction, Parturition, Pregnancy, Prenatal Exposure Delayed Effects - metabolism, Rats, Rats, Wistar, Rodents, Sodium-Potassium-Exchanging ATPase - metabolism, Succinate dehydrogenase, Tumor necrosis factor-α