Loading…
The male mammary gland: A target for the xenoestrogen bisphenol A
► Male CD-1 mice lack nipples but retain mammary epithelium throughout their lifetime. ► The male mammary gland is histologically indistinguishable from the female gland. ► Adult male mammary epithelium expresses estrogen receptor α. ► Developmental exposure to low doses of BPA alters male mammary g...
Saved in:
Published in: | Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2013-06, Vol.37, p.15-23 |
---|---|
Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | ► Male CD-1 mice lack nipples but retain mammary epithelium throughout their lifetime. ► The male mammary gland is histologically indistinguishable from the female gland. ► Adult male mammary epithelium expresses estrogen receptor α. ► Developmental exposure to low doses of BPA alters male mammary gland morphology. ► The morphological effects are seen in adulthood and are dose-dependent.
Males of some strains of mice retain their mammary epithelium even in the absence of nipples. Here, we have characterized the mammary gland in male CD-1 mice both in whole mounts and histological sections. We also examined the effects of bisphenol A (BPA), an estrogen mimic that alters development of the female mouse mammary gland. BPA was administered at a range of environmentally relevant doses (0.25–250μg/kg/day) to pregnant and lactating mice and then the mammary glands of male offspring were examined at several periods in adulthood. We observed age- and dose-specific effects on mammary gland morphology, indicating that perinatal BPA exposures alter the male mammary gland in adulthood. These results may provide insight into gynecomastia, the most common male breast disease in humans, where proliferation of the mammary epithelium leads to breast enlargement. |
---|---|
ISSN: | 0890-6238 1873-1708 |
DOI: | 10.1016/j.reprotox.2013.01.002 |