Histopathological changes in the brain of mouse fetuses by etoposide-administration
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- Nam Chunja
- Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
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- Woo Gye-Hyeong
- Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
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- Uetsuka Koji
- Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
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- Nakayama Hiroyuki
- Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
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- Doi Kunio
- Department of Veterinary Pathology, Graduate School of Agricultural and Life Sciences, The University of Tokyo
Bibliographic Information
- Other Title
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- Etoposideに起因されるマウスの胎仔の脳の組織病理学的な変化
Abstract
Etoposide (VP-16), a topoisomerase II inhibitor, is an anti-tumor agent which causes embryotoxicity, exencephaly, encephalocele, anophthalmia and major skeletal malformations of fetuses when administered to dams of rodents. We examined VP-16-induced histopathological changes in the brain of mouse fetuses. Pregnant mice were intraperitoneally treated with VP-16 (4 mg/kg) on 12th day of gestation (GD 12), and fetuses were collected from 1 to 48 hours after treatment (HAT). A moderate decrease of mitotic figures of neuroepithelial cells was observed in the telencephalic wall at 4 HAT. A moderate to marked increase of pyknotic neuroepithelial cells was detected in the brain of VP-16-treated fetuses, and being most prominent from 8 to 24 HAT. These pyknotic cells were also positively stained by TUNEL and cleaved caspase-3 immunostain. It was suggested that excessive neuronal apoptosis was induced in the brain of mouse fetuses treated with VP-16 on GD 12.
Journal
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- Annual Meeting of the Japanese Society of Toxicology
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Annual Meeting of the Japanese Society of Toxicology 32 (0), 16-16, 2005
The Japanese Society of Toxicology
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Details 詳細情報について
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- CRID
- 1390001205658580608
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- NII Article ID
- 130007003554
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- Data Source
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- JaLC
- CiNii Articles
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- Abstract License Flag
- Disallowed