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Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture.
The generation of hydrogen peroxide (H2O2) and the derivative free hydroxyl radical (. OH) in cultures of mouse cells grown in the presence of visible light and ambient oxygen was shown previously to be implicated in chromatid damage. Furthermore, chromosome alterations appear to be associated with...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
1985
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1977259/ https://www.ncbi.nlm.nih.gov/pubmed/2415146 |
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author | Jones, G. M. Sanford, K. K. Parshad, R. Gantt, R. Price, F. M. Tarone, R. E. |
author_facet | Jones, G. M. Sanford, K. K. Parshad, R. Gantt, R. Price, F. M. Tarone, R. E. |
author_sort | Jones, G. M. |
collection | PubMed |
description | The generation of hydrogen peroxide (H2O2) and the derivative free hydroxyl radical (. OH) in cultures of mouse cells grown in the presence of visible light and ambient oxygen was shown previously to be implicated in chromatid damage. Furthermore, chromosome alterations appear to be associated with the spontaneous neoplastic transformation of mouse cells in culture. An attempt was made in this study to reduce the incidence of chromosomal aberrations and delay or prevent the onset of spontaneous neoplastic transformation of freshly isolated mouse cells, both fibroblasts and epidermal keratinocytes, by adding catalase to the culture medium, shielding the cultures from wavelengths less than 500 nm and providing a gas phase of 0-1% O2. These conditions significantly decreased the incidence of chromosomal aberrations in both cell types, and in fibroblasts prevented tumourigenicity in non-irradiated syngeneic mice, and increased latent periods for tumour development in X-irradiated mice. The epidermal keratinocytes were particularly resistant to spontaneous neoplastic transformation under all conditions tested. These observations on the protective effect of extracellular catalase suggest that H2O2, a normal metabolite, and/or the derivative .OH can directly or indirectly produce genetic damage and neoplastic transformation in mouse fibroblasts. |
format | Text |
id | pubmed-1977259 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1985 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-19772592009-09-10 Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. Jones, G. M. Sanford, K. K. Parshad, R. Gantt, R. Price, F. M. Tarone, R. E. Br J Cancer Research Article The generation of hydrogen peroxide (H2O2) and the derivative free hydroxyl radical (. OH) in cultures of mouse cells grown in the presence of visible light and ambient oxygen was shown previously to be implicated in chromatid damage. Furthermore, chromosome alterations appear to be associated with the spontaneous neoplastic transformation of mouse cells in culture. An attempt was made in this study to reduce the incidence of chromosomal aberrations and delay or prevent the onset of spontaneous neoplastic transformation of freshly isolated mouse cells, both fibroblasts and epidermal keratinocytes, by adding catalase to the culture medium, shielding the cultures from wavelengths less than 500 nm and providing a gas phase of 0-1% O2. These conditions significantly decreased the incidence of chromosomal aberrations in both cell types, and in fibroblasts prevented tumourigenicity in non-irradiated syngeneic mice, and increased latent periods for tumour development in X-irradiated mice. The epidermal keratinocytes were particularly resistant to spontaneous neoplastic transformation under all conditions tested. These observations on the protective effect of extracellular catalase suggest that H2O2, a normal metabolite, and/or the derivative .OH can directly or indirectly produce genetic damage and neoplastic transformation in mouse fibroblasts. Nature Publishing Group 1985-10 /pmc/articles/PMC1977259/ /pubmed/2415146 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article Jones, G. M. Sanford, K. K. Parshad, R. Gantt, R. Price, F. M. Tarone, R. E. Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
title | Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
title_full | Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
title_fullStr | Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
title_full_unstemmed | Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
title_short | Influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
title_sort | influence of added catalase on chromosome stability and neoplastic transformation of mouse cells in culture. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1977259/ https://www.ncbi.nlm.nih.gov/pubmed/2415146 |
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