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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Endocrine disrupting chemicals (EDCs) and sex steroid receptors
Julianne M Hall1, Kenneth S Korach2
1Quinnipiac University Frank H. Netter MD School of Medicine, Hamden, CT, United States.
Abstract:
Sex-steroid receptors (SSRs) are essential mediators of estrogen, progestin, and androgen signaling that are critical in vast aspects of human development and multi-organ homeostasis. Dysregulation of SSR function has been implicated in numerous pathologies including cancers, obesity, Type II diabetes mellitus, neuroendocrine disorders, cardiovascular disease, hyperlipidemia, male and female infertility, and other reproductive disorders. Endocrine disrupting chemicals (EDCs) modulate SSR function in a wide variety of cell and tissues. There exists strong experimental, clinical, and epidemiological evidence that engagement of EDCs with SSRs may disrupt endogenous hormone signaling leading to physiological abnormalities that may manifest in disease. In this chapter, we discuss the molecular mechanisms by which EDCs interact with estrogen, progestin, and androgen receptors and alter SSR functions in target cells. In addition, the pathological consequences of disruption of SSR action in reproductive and other organs by EDCs is described with an emphasis on underlying mechanisms of receptors dysfunction.
Insights
Endocrine disrupting chemicals (EDCs) interfere with sex-steroid receptors (SSRs), impacting hormone signaling. This disruption can lead to various diseases affecting development, homeostasis, and reproductive health.
Area of Science:
- Endocrinology and Molecular Biology
- Reproductive Health and Toxicology
Background:
- Sex-steroid receptors (SSRs) mediate critical estrogen, progestin, and androgen signaling pathways.
- Dysfunctional SSRs are linked to numerous diseases, including cancers, metabolic disorders, and reproductive issues.
- Endocrine disrupting chemicals (EDCs) are environmental agents known to interfere with SSR function.
Purpose of the Study:
- To elucidate the molecular mechanisms by which EDCs interact with SSRs.
- To describe the pathological consequences of EDC-induced SSR disruption.
- To emphasize the underlying mechanisms of receptor dysfunction.
Main Methods:
- Review of experimental, clinical, and epidemiological evidence on EDC-SSR interactions.
- Analysis of molecular mechanisms of EDC engagement with estrogen, progestin, and androgen receptors.
- Description of pathological outcomes in reproductive and other organs due to SSR dysfunction.
Main Results:
- EDCs modulate SSR function across various cell types and tissues.
- EDC interaction with SSRs disrupts endogenous hormone signaling, causing physiological abnormalities.
- Disruption of SSR action by EDCs leads to dysfunction in target cells and organs.
Conclusions:
- EDCs pose a significant threat to endocrine homeostasis by interfering with SSR signaling.
- Understanding EDC-SSR interactions is crucial for addressing associated pathologies.
- Further research into receptor dysfunction mechanisms is warranted to mitigate health risks.
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