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J Reprod Immunol. 2011 Jun;90(1):14-20. doi: 10.1016/j.jri.2011.04.005. Epub 2011 May 31.

Blastocyst implantation is vulnerable to stress-induced rises in endogenous estrogens and also to excretions of estrogens by proximate males.

Author information

1
Department of Psychology, Neuroscience & Behaviour, McMaster University, Hamilton, Ontario, L8S 4K1, Canada. decatanz@mcmaster.ca

Abstract

Although estrogens help to prepare the uterus for blastocyst implantation, small elevations above optimal levels can prevent implantation. In diverse mammals, stressors including extreme temperatures, physical restraint, environment changes, and predator exposure can impede implantation. This can be mimicked by treating inseminated females with exogenous estrogens. Peri-implantation stressors can elevate estradiol levels, while exogenous estrogen antibodies can mitigate the influences of stress on implantation. Another stimulus that disrupts implantation is exposure to novel males (the "Bruce effect"). This effect, best known in mice, is mediated by chemical factors in male urine. Although a longstanding hypothesis relates the Bruce effect to the female's olfactory memory trace of the sire and reaction to odors of novel males, evidence increasingly supports an alternative hypothesis that implicates males' excreted estrogens. Male urine contains substantial amounts of unconjugated estradiol, and males actively deliver urine toward females which impinges on their nasal region. The Bruce effect can be diminished by drug treatment of males that reduces urinary estradiol, and by treatment of females with estrogen antibodies. Tritiated estradiol ((3)H-E(2)) systemically delivered to male mice was evident in their urine. When (3)H-E(2) was given intra-nasally to inseminate females, it was found in their circulation and in diverse tissues, with greatest radioactivity in the uterus. Accordingly, evidence indicates that males' excreted estradiol can arrive at the female reproductive tract, where it can disrupt implantation through known mechanisms.

PMID:
21632121
DOI:
10.1016/j.jri.2011.04.005
[Indexed for MEDLINE]

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