| Apoptosis in the subependyma of young adult rats after single and fractionated doses of X-rays. | |
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MedLine Citation:
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PMID: 9205079 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Ionizing radiation is commonly used in the treatment of brain tumors but can cause significant damage to surrounding normal brain. The pathogenesis of this damage is uncertain, and understanding the response of potential target cell populations may provide information useful for developing strategies to optimize therapeutic irradiation. In the mammalian forebrain, the subependyma is a mitotically active area that is a source of oligodendrocytes and astrocytes, and it has been hypothesized that depletion of cells from this region could play a role in radiation-induced white matter injury. Using a distinct morphological pattern of nuclear fragmentation and an immunohistochemical method to specifically label the 3'-hydroxyl termini of DNA strand breaks (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling), we quantified apoptosis in the subependyma in the young adult rat brain after single and fractionated doses of X-rays. Significant increases in apoptotic index (percentage of cells showing apoptosis) were detected 3 h after irradiation, and the peak apoptotic index was detected at 6 h. Six h after irradiation, the dose response for apoptosis was characterized by a steep increase in apoptotic index between 0.5 and 2.0 Gy and a plateau from 2-30 Gy. The fraction of cells susceptible to apoptosis was estimated to be about 40%, and treatment of rats with cycloheximide inhibited apoptosis. When daily 1.5-Gy fractions of X-rays were administered, the first three fractions were equally effective at decreasing the cell population via apoptosis. There was no additional apoptosis or decrease in cellularity in spite of one to four additional doses of X-rays. Those data suggested some input of cells into the subependymal population during fractionated treatment, and subsequent studies showed that there was a significant rise in 5-bromo-2' deoxyuridine labeling index 2-3 days after irradiation, indicating increased cellular proliferation. The proliferative response after depletion of cells via apoptosis may represent the recruitment of a relatively quiescent stem cell population. It is possible that the radiation response of subependymal stem cells and not the apoptotic-sensitive population per se are critical elements in the response of the brain to radiation injury. |
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Authors:
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C Shinohara; G T Gobbel; K R Lamborn; E Tada; J R Fike |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Cancer research Volume: 57 ISSN: 0008-5472 ISO Abbreviation: Cancer Res. Publication Date: 1997 Jul |
Date Detail:
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Created Date: 1997-07-25 Completed Date: 1997-07-25 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2984705R Medline TA: Cancer Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 2694-702 Citation Subset: IM |
Affiliation:
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Brain Tumor Research Center, Department of Neurological Surgery, School of Medicine, University of California, San Francisco 94143-0520, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis* Biological Markers / analysis Cell Division / radiation effects Corpus Callosum / chemistry, radiation effects Dose-Response Relationship, Radiation Ependyma / chemistry, radiation effects* Glial Fibrillary Acidic Protein / analysis Immunohistochemistry Intermediate Filament Proteins / analysis Lectins / analysis Male Nerve Tissue Proteins* Nucleotidases / analysis Plant Lectins* Rats Rats, Inbred F344 Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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CA 13525/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Glial Fibrillary Acidic Protein; 0/Intermediate Filament Proteins; 0/Lectins; 0/Nerve Tissue Proteins; 0/Plant Lectins; 0/Ricinus communis agglutinin-1; 0/nestin; EC 3.1.3.-/Nucleotidases; EC 3.1.3.6/3'-nucleotidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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