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Published on: June 7, 2012
Genetic variation in physiological sensitivity to estrogen in mice
J L Spearow1, P O'Henley, P Doemeny
1Section of Neurobiology, Physiology and Behavior, University of California at Davis, 95616, USA. jlspearow@ucdavis.edu
Summary
Genetic variation significantly impacts how mice respond to estrogenic compounds. CD-1 mice show resistance to reproductive disruption, unlike other strains, due to higher detoxification enzyme activity.
Area of Science:
- Endocrinology
- Toxicology
- Genetics
Background:
- Endocrine-disrupting chemicals (EDCs) pose risks to reproductive health.
- Estrogenic agents can disrupt normal development.
- Understanding genetic variation in sensitivity is crucial for risk assessment.
Purpose of the Study:
- To investigate genetic differences in susceptibility to estrogenic endocrine disruption in male mice.
- To identify mouse strains with varying sensitivity to estradiol (E2).
Main Methods:
- Juvenile male mice of different strains were exposed to increasing doses of estradiol (E2).
- Reproductive parameters including testes weight, vesicular gland weight, and spermatogenesis were assessed.
- Testicular estrone sulfotransferase (EST) activity was measured.
Main Results:
- Significant (greater than 16-fold) differences in E2 susceptibility were observed between mouse strains.
- CD-1 mice were highly resistant to E2-induced inhibition of reproductive parameters.
- Low doses of E2 eliminated spermatid maturation in C17/Jls and C57BL/6J strains.
- CD-1 mice exhibited higher testicular EST activity, suggesting a role in estrogen detoxification.
Conclusions:
- Genetic variation profoundly influences sensitivity to estrogenic endocrine disruption.
- Higher testicular EST activity in CD-1 mice contributes to their resistance.
- Future studies should consider genetic background in animal models for EDC risk assessment.
