Document Detail

Cyclophosphamide-induced agenesis of cerebral aqueduct resulting in hydrocephalus in mice.
MedLine Citation:
PMID:  17457626     Owner:  NLM     Status:  MEDLINE    
The present work was undertaken to reveal the mechanism of cerebral aqueduct agenesis found to result in hydrocephalus following intrauterine exposure to model teratogen, cyclophosphamide, in murine fetuses. A single dose of 10-mg/kg body weight cyclophosphamide was injected intaperitoneally to pregnant mice on day 10, 11 or 12 of gestation. Fetuses were collected through abdominal incision on day 18 and studied for various malformations of brain and cranium including hydrocephalus. Incomplete development and failure of canalization of the cerebral aqueduct were detected when serial sections of brain in coronal and transverse planes were studied under the microscope. Biotechnological investigations such as % DNA fragmentation, % viable cell count and cell proliferation assay were carried out on brain cells for further studies. Agenesis and non-canalization of the cerebral aqueduct resulted in increased pressure of CSF, which led to rupture of the aqueduct complicated by leakage and accumulation of CSF in brain substance forming a cavity containing CSF parallel and lateral to the unopened part of the cerebral aqueduct. Incomplete development along with non-canalization of the cerebral aqueduct resulted in blockage of CSF flow through the ventricles that manifest as internal hydrocephalus. External hydrocephalus on the other hand was detected where the CSF accumulated in the cavity formed inside the brain substance and established communication with the CSF in the subarachnoid space. Cyclophosphamide induced inhibition of mitosis and cell differentiation of ependymal cells reflecting a decreased % viable cell count and cell proliferation assay along with augmentation of apoptosis of brain cells quantified as increased % DNA fragmentation count, which were identified as the contributing factors underlying the agenesis and incomplete development of the cerebral aqueduct. The study also suggests that cell survival, proliferation, migration or differentiation of ependymal cells might have been affected, and we speculate that CSF may have an inducing role in the development and canalization of the cerebral aqueduct.
Prakash; Gajendra Singh; Sukh Mahendra Singh
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication     Date:  2007-04-25
Journal Detail:
Title:  Neurosurgical review     Volume:  30     ISSN:  0344-5607     ISO Abbreviation:  Neurosurg Rev     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-06-11     Completed Date:  2007-07-30     Revised Date:  2009-07-29    
Medline Journal Info:
Nlm Unique ID:  7908181     Medline TA:  Neurosurg Rev     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  245-51; discussion 251     Citation Subset:  IM    
Department of Anatomy, Centre for Basic Sciences, Kasturba Medical College, Bejai, Mangalore, Karnataka, 575004, India.
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MeSH Terms
Apoptosis / drug effects
Cell Count
Cell Differentiation / drug effects
Cell Movement / drug effects
Cell Proliferation / drug effects
Cell Survival / drug effects
Cerebral Aqueduct / abnormalities*
Cerebral Ventricles / cytology,  drug effects
DNA Fragmentation / drug effects
Ependyma / cytology
Hydrocephalus / cerebrospinal fluid,  chemically induced*
Reg. No./Substance:
0/Teratogens; 50-18-0/Cyclophosphamide
Retraction In:
Bertalanffy H, Bozinov O, Krayenbühl N. Neurosurg Rev. 2009 Apr;32(2):253   [PMID:  19225817 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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