ArticleNeurotoxicity research2017
Effects of Hydroxyurea Exposure on the Rat Cerebellar Neuroepithelium: an Immunohistochemical and Electron Microscopic Study Along the Anteroposterior and Mediolateral Axes.
Article in Neurotoxicity research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- An immunocytochemical approach to the analysis of the cell division cycle in the rat cerebellar neuroepithelium.Cell cycle (Georgetown, Tex.) · 2020Article
- Patterns of Apoptosis and Autophagy Activation After Hydroxyurea Exposure in the Rat Cerebellar External Granular Layer: an Immunoperoxidase and Ultrastructural Analysis.Neurotoxicity research · 2020Article
- Hydroxyurea Exposure and Development of the Cerebellar External Granular Layer: Effects on Granule Cell Precursors, Bergmann Glial and Microglial Cells.Neurotoxicity research · 2019Article
- An Animal Model for Assessing the Effects of Hydroxyurea Exposure Suggests That the Administration of This Agent to Pregnant Women and Young Infants May Not Be as Safe as We Thought.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We present a histological study of the cell death of cerebellar neuroepithelial neuroblasts following treatment with the cytotoxic agent hydroxyurea (HU) during the embryonic life. Pregnant rats were treated with a single dose of HU (300 mg/kg) at embryonic days 13, 14, or 15 of gestation, and their fetuses were studied from 5 to 35 h after treatment to elucidate the mechanisms of HU-induced fetotoxicity. Quantification of several parameters such as the density of pyknotic, mitotic, and PCNA-immunoreactive cells indicated that HU compromises the survival of the cerebellar neuroepithelium neuroblasts. On the other hand, our light and electron microscopic investigations during the course of prenatal development indicated that HU leads to two types of cell death: apoptosis and cells presenting cytoplasmic vacuolization, altered organelles, and a recognizable cell nucleus. Both modalities of cell death resulted in a substantial loss of cerebellar neuroepithelium cells. Current results suggest that HU exposure during gestation is toxic to the cerebellar neuroepithelium. Moreover, they allow to examine the mechanisms of HU-induced toxicity during the early development of the central nervous system. Our data also suggest that it is essential to avoid underestimating the adverse effects of HU when administered during early prenatal life.
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