Abstract:
:1-beta-D-Arabinofuranosylcytosine (Ara-C), a cytidine analogue cytotoxic to proliferating cells, has a teratogenic effect in the brain of experimental animals and causes neural cell apoptosis in vitro and in vivo. In the present study, pregnant rats were injected with Ara-C on Day 13 of gestation and the fetal brain was collected from 1 to 48 h after treatment. Histopathological examinations revealed marked induction of apoptotic cell death and decrease of mitosis in neuroepithelial cells in the brain of Ara-C-treated fetus, and these changes were most prominent from 9 to 12 h. Expression of p53 protein, which mediates apoptosis and cell cycle arrest after DNA damage, was elevated remarkably and peaked at 3 h. p21, a cyclin-dependent kinase inhibitor responsible for p53-mediated cell cycle arrest, showed intense overexpression in protein and mRNA levels following the increase of p53 protein. The mRNA expressions of other p53 transcriptional target genes, bax, cyclinG1, and fas, also significantly increased and peaked at around 9 h. In conclusion, prenatal treatment of Ara-C is thought to induce apoptosis and inhibition of cell proliferation mediated by p53 and its target genes in the fetal brain.
journal_name
Neurotoxicol Teratoljournal_title
Neurotoxicology and teratologyauthors
Yamauchi H,Katayama K,Ueno M,Uetsuka K,Nakayama H,Doi Kdoi
10.1016/j.ntt.2004.03.010subject
Has Abstractpub_date
2004-07-01 00:00:00pages
579-86issue
4eissn
0892-0362issn
1872-9738pii
S0892036204000522journal_volume
26pub_type
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journal_title:Neurotoxicology and teratology
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