Endocrine Toxicology Flashcards
(75 cards)
What are common toxic agents for endocrine toxicity?
Cadmium, lead, TCDD, PCBs, perchlorate, bisphenol A, phthalates, PFOS, PBDEs, arsenic.
What is the mechanism of TCDD-induced endocrine toxicity?
Activates AhR, disrupts thyroid and pituitary hormone signaling.
What is the mechanism of perchlorate endocrine toxicity?
Inhibits thyroid-iodide symporter, reducing thyroid hormone production, causing goiter.
What is the mechanism of bisphenol A toxicity?
Mimics estrogen, disrupts endocrine signaling, affecting reproduction and metabolism. Increases LH secretion in adult male rats.
Also possible thyroid disrupting chemical. Potentially blocks T3 action by atagonizing receptor.
What are biomarkers for endocrine toxicity?
Altered hormone levels (TSH, cortisol, insulin), thyroid size, blood glucose.
What are testing methods for endocrine toxicity?
Hormone assays, histopathological examination, EDSTAC tier 1/2 studies.
If a chemical exhibits the potential to interact with the estrogen, androgen, or thyroid hormone systems, it proceeds to Tier 2.
What are endpoints for endocrine toxicity?
Goiter, diabetes mellitus, pituitary dysfunction, adrenal hyperplasia.
How does cadmium cause endocrine toxicity?
Inhibits LH/FSH secretion, affecting pituitary and adrenal function.
What is the role of PCBs in endocrine toxicity?
Disrupt thyroid hormone homeostasis via AhR activation.
How do phthalates cause endocrine toxicity?
Act as anti-androgens, impairing testicular development and function.
How does TCDD (dioxin) mechanistically disrupt thyroid function? (Domain II)
TCDD activates AhR, inducing UGT1A1, increasing thyroid hormone (T4) glucuronidation and excretion, leading to reduced T4 levels (DABT_Study_Notes.xlsx, Endocrine Tox; Web: NIH, 2025).
What is the endocrine target of polychlorinated biphenyls (PCBs)? (Domain II)
PCBs target thyroid hormone receptors, acting as agonists or antagonists, disrupting T3/T4 signaling and neurodevelopment (DABT_Study_Notes.xlsx, Endocrine Tox; Chemical Carcinogenesis).
How do polybrominated diphenyl ethers (PBDEs) cause endocrine toxicity? (Domain II)
PBDEs mimic thyroid hormones, binding to transthyretin, displacing T4, and reducing circulating T4 levels (DABT_Study_Notes.xlsx, Endocrine Tox; Web: EPA, 2024).
What mechanism underlies perchlorate’s thyroid toxicity? (Domain II)
Perchlorate inhibits sodium-iodide symporter (NIS), reducing iodide uptake, impairing thyroid hormone synthesis (DABT_Study_Notes.xlsx, Endocrine Tox; Web: NIH, 2025).
How does bisphenol A (BPA) disrupt estrogen signaling? (Domain II)
BPA binds estrogen receptors (ERα/ERβ), acting as a weak agonist, altering gene expression in reproductive tissues (DABT_Study_Notes.xlsx, Endocrine Tox; Web: PubMed, 2024).
What is the endocrine target of phthalates like DEHP? (Domain II)
Phthalates target testicular Leydig cells, reducing testosterone synthesis, leading to reproductive developmental defects (DABT_Study_Notes.xlsx, Endocrine Tox; Web: NIH, 2025).
How does atrazine mechanistically cause endocrine disruption? (Domain II)
Atrazine upregulates aromatase (CYP19), increasing estrogen synthesis, disrupting gonadal development in amphibians (DABT_Study_Notes.xlsx, Endocrine Tox; Web: EPA, 2024).
What mechanism does methoxychlor use to disrupt endocrine function? (Domain II)
Methoxychlor’s metabolite HPTE binds estrogen receptors, acting as an agonist, altering uterine and ovarian function (DABT_Study_Notes.xlsx, Endocrine Tox; Web: PubMed, 2024).
How does vinclozolin affect the androgen system? (Domain II)
Vinclozolin’s metabolites bind androgen receptors as antagonists, inhibiting testosterone-dependent gene expression (DABT_Study_Notes.xlsx, Endocrine Tox; Web: NIH, 2025).
What is the endocrine target of DDT and its metabolite DDE? (Domain II)
DDT/DDE target estrogen receptors, acting as agonists, and androgen receptors, acting as antagonists, disrupting reproductive function (DABT_Study_Notes.xlsx, Endocrine Tox; Web: EPA, 2024).
How does perfluorooctanoic acid (PFOA) cause endocrine toxicity? (Domain II)
PFOA activates PPARα, altering lipid metabolism and thyroid hormone homeostasis, reducing T4 levels (DABT_Study_Notes.xlsx, Endocrine Tox; Web: NIH, 2025).
What mechanism underlies cadmium’s endocrine disruption? (Domain II)
Cadmium mimics estrogen by binding ERα, altering gene expression in breast and uterine tissues (DABT_Study_Notes.xlsx, Endocrine Tox; Web: PubMed, 2024).
How does lead (Pb) affect the hypothalamic-pituitary-adrenal (HPA) axis? (Domain II)
Lead increases cortisol secretion by disrupting ACTH feedback, targeting adrenal glands, causing stress response dysregulation (DABT_Study_Notes.xlsx, Endocrine Tox; Principles & Mechanisms).
What is the endocrine target of arsenic exposure? (Domain II)
Arsenic targets glucocorticoid receptors, inhibiting cortisol signaling, affecting glucose metabolism (DABT_Study_Notes.xlsx, Endocrine Tox; Web: NIH, 2025).