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Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3
BACKGROUND: The presence of cancer makes it difficult to predict the progress of pregnancy and can be deleterious to the maternal-foetal relationship. Apoptosis may affect a range of placental functions and result in the retardation of foetal growth. In this work, we investigated the placental alter...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2006
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534057/ https://www.ncbi.nlm.nih.gov/pubmed/16800886 http://dx.doi.org/10.1186/1471-2407-6-168 |
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author | Toledo, Mércia Tancredo Ventrucci, Gislaine Marcondes, Maria Cristina Cintra Gomes |
author_facet | Toledo, Mércia Tancredo Ventrucci, Gislaine Marcondes, Maria Cristina Cintra Gomes |
author_sort | Toledo, Mércia Tancredo |
collection | PubMed |
description | BACKGROUND: The presence of cancer makes it difficult to predict the progress of pregnancy and can be deleterious to the maternal-foetal relationship. Apoptosis may affect a range of placental functions and result in the retardation of foetal growth. In this work, we investigated the placental alterations produced by tumour growth and the effects on the expression of apoptotic factors in placental tissue. METHODS: Adult female Wistar rats (90 days old, n = 54) were allocated to control (C), tumour-bearing (W), or ascitic fluid-injected (A) groups and were killed on the 16(th), 19(th )or 21(st )day of pregnancy. Placental tissues were analysed using biochemical and histochemical assays. RESULTS: The placental protein content and glutathione-S-transferase activity were decreased in groups W and A. Histochemical analysis showed an increase in the number of cells with cleaved PARP, caspase 3 and cytochrome-c in groups W and A, indicating that the tumour growth clearly damaged placental tissue and affected the levels of apoptotic factors. These results were confirmed by western blotting. CONCLUSION: Since trophoblastic cells are responsible for maintaining a normal placental function, the uncontrolled death of these cells in response to tumour cell growth or substances derived from ascitic fluid could have a negative impact on foetal development. Further knowledge of these events may help to preserve the foetus and placenta during development. |
format | Text |
id | pubmed-1534057 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-15340572006-08-09 Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 Toledo, Mércia Tancredo Ventrucci, Gislaine Marcondes, Maria Cristina Cintra Gomes BMC Cancer Research Article BACKGROUND: The presence of cancer makes it difficult to predict the progress of pregnancy and can be deleterious to the maternal-foetal relationship. Apoptosis may affect a range of placental functions and result in the retardation of foetal growth. In this work, we investigated the placental alterations produced by tumour growth and the effects on the expression of apoptotic factors in placental tissue. METHODS: Adult female Wistar rats (90 days old, n = 54) were allocated to control (C), tumour-bearing (W), or ascitic fluid-injected (A) groups and were killed on the 16(th), 19(th )or 21(st )day of pregnancy. Placental tissues were analysed using biochemical and histochemical assays. RESULTS: The placental protein content and glutathione-S-transferase activity were decreased in groups W and A. Histochemical analysis showed an increase in the number of cells with cleaved PARP, caspase 3 and cytochrome-c in groups W and A, indicating that the tumour growth clearly damaged placental tissue and affected the levels of apoptotic factors. These results were confirmed by western blotting. CONCLUSION: Since trophoblastic cells are responsible for maintaining a normal placental function, the uncontrolled death of these cells in response to tumour cell growth or substances derived from ascitic fluid could have a negative impact on foetal development. Further knowledge of these events may help to preserve the foetus and placenta during development. BioMed Central 2006-06-26 /pmc/articles/PMC1534057/ /pubmed/16800886 http://dx.doi.org/10.1186/1471-2407-6-168 Text en Copyright © 2006 Toledo et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Toledo, Mércia Tancredo Ventrucci, Gislaine Marcondes, Maria Cristina Cintra Gomes Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 |
title | Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 |
title_full | Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 |
title_fullStr | Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 |
title_full_unstemmed | Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 |
title_short | Cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved PARP, cytochrome-c and caspase 3 |
title_sort | cancer during pregnancy alters the activity of rat placenta and enhances the expression of cleaved parp, cytochrome-c and caspase 3 |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1534057/ https://www.ncbi.nlm.nih.gov/pubmed/16800886 http://dx.doi.org/10.1186/1471-2407-6-168 |
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