Abstract:
:Maternal hyperhomocysteinemia is one of the common complications of pregnancy that causes offspring cognitive deficits during postnatal development. In the present work, we evaluated the effect of prenatal hyperhomocysteinemia on structural and ultrastructural organization, neuronal and glial cell number, apoptosis (caspase-3 content and activity), inflammatory markers (tumor necrosis factor-α, interleukin-6, and interleukin-1β), and p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation in the offspring brain cortex in early ontogenesis. Wistar female rats received methionine (0.6 g/kg body weight) by oral administration during pregnancy. Histological and biochemical analyses of 5- and 20-day-old pups' cortical tissue were performed. Lysosome accumulation and other neurodegenerative changes in neurons of animals with impaired embryonic development were investigated by electron microscopy. Neuronal staining (anti-NeuN) revealed a reduction in neuronal number, accompanied by increasing of caspase-3 active form protein level and activity. Maternal hyperhomocysteinemia also elevated the number of astroglial and microglial cells and increased expression of interleukin-1β and p38 MAPK phosphorylation, which indicates the development of neuroinflammatory processes.
journal_name
Neurotox Resjournal_title
Neurotoxicity researchauthors
Shcherbitskaia AD,Vasilev DS,Milyutina YP,Tumanova NL,Zalozniaia IV,Kerkeshko GO,Arutjunyan AVdoi
10.1007/s12640-020-00233-wsubject
Has Abstractpub_date
2020-08-01 00:00:00pages
408-420issue
2eissn
1029-8428issn
1476-3524pii
10.1007/s12640-020-00233-wjournal_volume
38pub_type
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