uu.seUppsala University Publications
Change search
ReferencesLink to record
Permanent link

Direct link
Increased expression of genes encoding proangiogenic and vasoconstriction factors in the cardiac tissues of rats following long‑term exposure to bisphenol A
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences. (Drug Safety and Toxicology)
(English)Manuscript (preprint) (Other academic)
National Category
Environmental Health and Occupational Health
URN: urn:nbn:se:uu:diva-160661OAI: oai:DiVA.org:uu-160661DiVA: diva2:452344
Available from: 2011-10-28 Created: 2011-10-28 Last updated: 2012-01-03
In thesis
1. Experimental Studies of Endocrine Disrupting Compounds in Vascular Cells and Tissues
Open this publication in new window or tab >>Experimental Studies of Endocrine Disrupting Compounds in Vascular Cells and Tissues
2011 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Epidemiological evidence suggest that exposure to endocrine disrupting compounds (EDCs) is a risk factor for diseases that involves the cardiovascular system but we know little about the mechanisms whereby these compounds can cause injury in the vasculature. The aim of this thesis was to characterize the effects and mechanisms of some EDCs in vascular cells and highly vascularized tissues.

Elevated exposure to environmental EDCs is associated with an increased risk for cardiovascular diseases. In vitro studies demonstrated that the environmental EDCs, 1-nitropyrene, PCB126 and bisphenol A, caused distinct changes in primary human endothelial cells. 1‑Nitropyrene induced cell stress and DNA damage, PCB126 caused changes that indicate endothelial dysfunction and vasoconstriction, and BPA induced changes that indicate angiogenesis and vasoconstriction. Further studies demonstrated that long-term exposure of rats to BPA induced changes in rat cardiac tissues in vivo similar to those observed in human endothelial cells in vitro. The type of cellular alterations that were demonstrated is known to play to play a role in cardiovascular disease in humans. These findings suggest that environmental EDCs can cause damage to the human endothelium that may contribute to the development of cardiovascular disease.

The beneficial effects of the pharmaceutical EDC tamoxifen in breast cancer treatment are compromised by an increased risk for bleedings, hyperplasia, and cancer in the endometrium. Ex vivo studies identified the glandular and surface epithelia as potential target sites for tamoxifen adduct formation and tamoxifen-induced cell stress the human endometrium. No signs of tamoxifen-induced changes were detected in the blood vessels. The results suggest that bioactivation of tamoxifen and subsequent cell injury in endometrial epithelial cells may play a role for tamoxifen’s side effects in the endometrium.

Taken together, this thesis provide evidence that may help understanding how exposure to EDCs can increase the risk for diseases in that involves the cardiovascular system.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2011. 61 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Pharmacy, ISSN 1651-6192 ; 150
Endocrine disrupting compounds, endothelium, vascular toxicity
National Category
Pharmaceutical Sciences
Research subject
urn:nbn:se:uu:diva-160662 (URN)978-91-554-8217-6 (ISBN)
Public defence
2011-12-17, B21, Uppsala Biomedical Centre, Husargatan 3, Uppsala, 09:15 (Swedish)
Available from: 2011-11-25 Created: 2011-10-28 Last updated: 2012-01-03Bibliographically approved

Open Access in DiVA

No full text

Search in DiVA

By author/editor
Andersson, Helén
By organisation
Department of Pharmaceutical Biosciences
Environmental Health and Occupational Health

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Total: 152 hits
ReferencesLink to record
Permanent link

Direct link