Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-1-8
pubmed:abstractText
Bisphenol A (BPA), known as an environmental endocrine disruptor, is widely used as a plasticizer. This study aims to investigate whether exposure in utero to BPA alters the architecture, proliferative index, and genomic signature of the rat mammary gland during critical stages of development. Pregnant rats were gavaged with 25 microg BPA/kg body weight (BW; low-dose group) or 250 microg BPA/kg BW (high-dose group) from day 10 post-conception to delivery. Female litters were euthanized at 21, 35, 50, and 100 days, and mammary glands were collected. Analysis of gland morphology was performed from whole-mounted mammary tissue, while proliferative index was determined by detection of bromodeoxyuridine incorporation in the epithelial cells. Genomic profiles were obtained by microarray analysis, and some genes were validated by real-time RT-PCR. BPA exposure induced changes in the mammary gland that were time and dose specific. High-dose exposure resulted in architectural modifications, mainly in the number of undifferentiated epithelial structures of the breast tissue. Proliferative index did not show remarkable differences by the effect of BPA. Low and high doses of BPA changed the gene expression signature of the mammary gland following a different fashion: low dose had the highest effect by 50 days, while high dose had a highest influence on gene expression by 100 days. Both doses presented a significant cluster of up-modulated genes related to the immune system at the age of maximal changes. Moreover, high-dose exposure induced changes in genes related to differentiation suggesting alterations in the normal development of the gland. The increase of undifferentiated structures and the changes in the gene expression profile at different ages suggest that prenatal exposure to BPA can affect the susceptibility of the mammary gland to transformation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1479-6805
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
196
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-12
pubmed:meshHeading
pubmed-meshheading:18180321-Aging, pubmed-meshheading:18180321-Animals, pubmed-meshheading:18180321-Cell Differentiation, pubmed-meshheading:18180321-Cell Division, pubmed-meshheading:18180321-Dose-Response Relationship, Drug, pubmed-meshheading:18180321-Endocrine Disruptors, pubmed-meshheading:18180321-Epithelial Cells, pubmed-meshheading:18180321-Female, pubmed-meshheading:18180321-Gene Expression Profiling, pubmed-meshheading:18180321-Immunity, pubmed-meshheading:18180321-Mammary Glands, Animal, pubmed-meshheading:18180321-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:18180321-Phenols, pubmed-meshheading:18180321-Pregnancy, pubmed-meshheading:18180321-Prenatal Exposure Delayed Effects, pubmed-meshheading:18180321-Rats, pubmed-meshheading:18180321-Rats, Sprague-Dawley, pubmed-meshheading:18180321-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2008
pubmed:articleTitle
Effect of prenatal exposure to the endocrine disruptor bisphenol A on mammary gland morphology and gene expression signature.
pubmed:affiliation
Breast Cancer Research Laboratory, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural