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#hormone disruption

2 public questions tagged with this topic.

Teratogens

Low-dose exposure to endocrine disruptors causes:

Classical toxicology assumes monotonic high dose effects, but endocrine disruptors exhibit non-monotonic U-shaped responses where low prenatal doses program lasting changes without acute lethality. During sensitive windows, low-level exposure alters DNA methylation, histone marks in hormone-responsive tissues, increasing estrogen receptor number or altering metabolic set points. Phenotypic consequences emerge long after chemical clearance at puberty or adulthood as infertility, obesity, metabolic syndrome, behavioral alterations, increased tumor susceptibility. This developmental origin paradigm indicates low-dose gestational exposure causes late-life disabilities rather than immediate toxicity, explaining adult diseases originating from fetal endocrine disruption.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: Low-dose disruptors late-life disabilities.

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Teratogens

Which endocrine disruptor mimics estrogen?

Among classic endocrine disruptors, diethylstilbestrol most clearly exemplifies synthetic estrogen mimicry. DES contains stilbene backbone with phenolic groups spatially resembling estradiol enabling high-affinity agonism at estrogen receptors alpha and beta, activating transcription of estrogen-dependent genes in uterus, vagina and mammary tissue. While BPA binds estrogen receptors with much lower potency and atrazine elevates estrogen indirectly via aromatase induction, DES directly substitutes estrogen, causing persistent estrogenization of developing Mullerian ducts. Cyclopamine targets hedgehog signaling, not estrogen. Consequently DES stands as archetypal estrogen-mimicking teratogen with potent hormonal activity.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: DES mimics estrogen endocrine disruption.

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