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Lessons learned from perinatal exposure to diethylstilbestrol.
1Developmental Endocrinology Section, Laboratory of Toxicology, Environmental Toxicology Program, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. newbold1@niehs.nih.gov
Toxicology and Applied Pharmacology
|August 18, 2004
Summary
Diethylstilbestrol (DES) exposure during development causes reproductive tract abnormalities and tumors. These findings in rodent models inform risks from environmental estrogens at low doses.
Area of Science:
- Reproductive toxicology
- Endocrinology
- Developmental biology
Background:
- Diethylstilbestrol (DES) is a known perinatal carcinogen, causing reproductive tract abnormalities later in life.
- Understanding DES's mechanisms informs risks from environmental estrogens.
- Rodent models are crucial for studying developmental exposure effects.
Observation:
- Developmental exposure to low-dose DES adversely affects fertility and increases tumor incidence in mice.
- These effects occur at environmentally relevant estrogen dose levels.
- Environmental chemicals with weak estrogenic activity mimic DES effects in neonatal mice.
Findings:
- Neonatal exposure to weak environmental estrogens increases benign and malignant tumors, including uterine leiomyomas and adenocarcinomas.
- Cellular and molecular mechanisms underlying DES-induced perinatal carcinogenesis are being elucidated.
- Trans-generational adverse effects are observed in animal models, though mechanisms are unknown.
Implications:
- Findings highlight risks of environmental estrogens at low, relevant doses.
- Advances in genetic and epigenetic mechanisms aid in predicting risks from other environmental estrogens.
- Understanding estrogen's role in development is key to assessing risks of endocrine-disrupting chemicals.