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Effects of chronic carbon monoxide exposure on fetal growth and development in mice
BACKGROUND: Carbon monoxide (CO) is produced endogenously, and can also be acquired from many exogenous sources: ie. cigarette smoking, automobile exhaust. Although toxic at high levels, low level production or exposure lends to normal physiologic functions: smooth muscle cell relaxation, control of...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297534/ https://www.ncbi.nlm.nih.gov/pubmed/22168775 http://dx.doi.org/10.1186/1471-2393-11-101 |
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author | Venditti, Carolina C Casselman, Richard Smith, Graeme N |
author_facet | Venditti, Carolina C Casselman, Richard Smith, Graeme N |
author_sort | Venditti, Carolina C |
collection | PubMed |
description | BACKGROUND: Carbon monoxide (CO) is produced endogenously, and can also be acquired from many exogenous sources: ie. cigarette smoking, automobile exhaust. Although toxic at high levels, low level production or exposure lends to normal physiologic functions: smooth muscle cell relaxation, control of vascular tone, platelet aggregation, anti- inflammatory and anti-apoptotic events. In pregnancy, it is unclear at what level maternal CO exposure becomes toxic to the fetus. In this study, we hypothesized that CO would be embryotoxic, and we sought to determine at what level of chronic CO exposure in pregnancy embryo/fetotoxic effects are observed. METHODS: Pregnant CD1 mice were exposed to continuous levels of CO (0 to 400 ppm) from conception to gestation day 17. The effect on fetal/placental growth and development, and fetal/maternal CO concentrations were determined. RESULTS: Maternal and fetal CO blood concentrations ranged from 1.12- 15.6 percent carboxyhemoglobin (%COHb) and 1.0- 28.6%COHb, respectively. No significant difference was observed in placental histological morphology or in placental mass with any CO exposure. At 400 ppm CO vs. control, decreased litter size and fetal mass (p < 0.05), increased fetal early/late gestational deaths (p < 0.05), and increased CO content in the placenta and the maternal spleen, heart, liver, kidney and lung (p < 0.05) were observed. CONCLUSIONS: Exposure to levels at or below 300 ppm CO throughout pregnancy has little demonstrable effect on fetal growth and development in the mouse. |
format | Online Article Text |
id | pubmed-3297534 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-32975342012-03-09 Effects of chronic carbon monoxide exposure on fetal growth and development in mice Venditti, Carolina C Casselman, Richard Smith, Graeme N BMC Pregnancy Childbirth Research Article BACKGROUND: Carbon monoxide (CO) is produced endogenously, and can also be acquired from many exogenous sources: ie. cigarette smoking, automobile exhaust. Although toxic at high levels, low level production or exposure lends to normal physiologic functions: smooth muscle cell relaxation, control of vascular tone, platelet aggregation, anti- inflammatory and anti-apoptotic events. In pregnancy, it is unclear at what level maternal CO exposure becomes toxic to the fetus. In this study, we hypothesized that CO would be embryotoxic, and we sought to determine at what level of chronic CO exposure in pregnancy embryo/fetotoxic effects are observed. METHODS: Pregnant CD1 mice were exposed to continuous levels of CO (0 to 400 ppm) from conception to gestation day 17. The effect on fetal/placental growth and development, and fetal/maternal CO concentrations were determined. RESULTS: Maternal and fetal CO blood concentrations ranged from 1.12- 15.6 percent carboxyhemoglobin (%COHb) and 1.0- 28.6%COHb, respectively. No significant difference was observed in placental histological morphology or in placental mass with any CO exposure. At 400 ppm CO vs. control, decreased litter size and fetal mass (p < 0.05), increased fetal early/late gestational deaths (p < 0.05), and increased CO content in the placenta and the maternal spleen, heart, liver, kidney and lung (p < 0.05) were observed. CONCLUSIONS: Exposure to levels at or below 300 ppm CO throughout pregnancy has little demonstrable effect on fetal growth and development in the mouse. BioMed Central 2011-12-14 /pmc/articles/PMC3297534/ /pubmed/22168775 http://dx.doi.org/10.1186/1471-2393-11-101 Text en Copyright ©2011 Venditti 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 Venditti, Carolina C Casselman, Richard Smith, Graeme N Effects of chronic carbon monoxide exposure on fetal growth and development in mice |
title | Effects of chronic carbon monoxide exposure on fetal growth and development in mice |
title_full | Effects of chronic carbon monoxide exposure on fetal growth and development in mice |
title_fullStr | Effects of chronic carbon monoxide exposure on fetal growth and development in mice |
title_full_unstemmed | Effects of chronic carbon monoxide exposure on fetal growth and development in mice |
title_short | Effects of chronic carbon monoxide exposure on fetal growth and development in mice |
title_sort | effects of chronic carbon monoxide exposure on fetal growth and development in mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297534/ https://www.ncbi.nlm.nih.gov/pubmed/22168775 http://dx.doi.org/10.1186/1471-2393-11-101 |
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