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DABT 2025 > Reproductive Toxicology > Flashcards

Reproductive Toxicology Flashcards

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1
Q

What are common toxic agents for reproductive toxicity?

A

Diethylstilbestrol, cadmium, cyclophosphamide, ethanol, thalidomide, TCDD, vinclozolin, busulfan, retinoids, flutamide.

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2
Q

What is the mechanism of diethylstilbestrol toxicity?

A

Acts as a xenoestrogen, disrupts hormonal signaling, causing vaginal adenocarcinoma.

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3
Q

What is the mechanism of thalidomide reproductive toxicity?

A

Disrupts angiogenesis and redox signaling, leading to limb defects (phocomelia).

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4
Q

What is the mechanism of TCDD reproductive toxicity?

A

Activates AhR, delays pubertal landmarks and impairs fertility.

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5
Q

What are biomarkers for reproductive toxicity?

A

Anogenital distance, serum hormone levels (LH, FSH, testosterone), organ weights (testes, ovaries).

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6
Q

What are testing methods for reproductive toxicity?

A

Pubertal male/female rat assays, uterotrophic assay, Hershberger assay, segment I-III tests.

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7
Q

What are endpoints for reproductive toxicity?

A

Cryptorchidism, hypospadias, reduced sperm production, sterility, fetal death.

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8
Q

How does cadmium cause reproductive toxicity?

A

Disrupts testicular function, reduces sperm count via oxidative stress.

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9
Q

What is the role of ethanol in reproductive toxicity?

A

Causes fetal alcohol syndrome, impairing gonadal development.

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10
Q

How is cyclophosphamide toxic to reproduction?

A

Alkylates DNA, destroys germ cells, causing infertility.

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11
Q

How does ethanol mechanistically cause developmental toxicity in the fetus? (Domain II)

A

Ethanol crosses the placenta, inducing oxidative stress and apoptosis in neural crest cells, leading to craniofacial defects and fetal alcohol syndrome (DABT_Study_Notes.xlsx, Repro Tox; Web: NIH, 2025).

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12
Q

What is the reproductive target of diethylstilbestrol (DES) toxicity? (Domain II)

A

DES targets the female reproductive tract, acting as an estrogen receptor agonist, causing vaginal adenocarcinoma in exposed offspring (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).

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13
Q

How does thalidomide induce teratogenicity? (Domain II)

A

Thalidomide inhibits cereblon-mediated angiogenesis, disrupting limb bud development, resulting in phocomelia (DABT_Study_Notes.xlsx, Repro Tox; Web: PubMed, 2024).

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14
Q

What mechanism underlies valproic acid’s developmental toxicity? (Domain II)

A

Valproic acid inhibits histone deacetylase (HDAC), altering gene expression, causing neural tube defects (DABT_Study_Notes.xlsx, Repro Tox; Web: NIH, 2025).

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15
Q

How does isotretinoin (Accutane) cause reproductive toxicity? (Domain II)

A

Isotretinoin, a retinoid, disrupts retinoic acid signaling, targeting craniofacial and neural development, leading to severe teratogenicity (DABT_Study_Notes.xlsx, Repro Tox; Web: FDA, 2024).

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16
Q

What reproductive target is affected by methylmercury toxicity? (Domain II)

A

Methylmercury targets the fetal brain, causing neuronal apoptosis via oxidative stress, leading to developmental neurotoxicity (DABT_Study_Notes.xlsx, Repro Tox; Document: Neuro Tox).

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17
Q

How does lead mechanistically impair male reproductive function? (Domain II)

A

Lead disrupts the hypothalamic-pituitary-gonadal axis, reducing testosterone and impairing spermatogenesis in Leydig cells (DABT_Study_Notes.xlsx, Repro Tox; Document: Principles & Mechanisms).

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18
Q

What is the mechanism of cyclophosphamide’s reproductive toxicity? (Domain II)

A

Cyclophosphamide, an alkylating agent, forms DNA adducts in germ cells, causing testicular and ovarian toxicity (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).

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19
Q

How does nicotine affect fetal development? (Domain II)

A

Nicotine activates nAChR, disrupting placental vascularization, leading to low birth weight and neurodevelopmental deficits (DABT_Study_Notes.xlsx, Repro Tox; Document: Neuro Tox).

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20
Q

What reproductive target is affected by polychlorinated biphenyls (PCBs)? (Domain II)

A

PCBs target the hypothalamic-pituitary axis, altering gonadotropin release, causing reduced fertility and neurodevelopmental delays (DABT_Study_Notes.xlsx, Repro Tox; Document: Neuro Tox).

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21
Q

How does cocaine induce developmental toxicity? (Domain II)

A

Cocaine inhibits dopamine reuptake, causing vasoconstriction, reducing placental blood flow, and leading to low birth weight (DABT_Study_Notes.xlsx, Repro Tox; Document: Neuro Tox).

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22
Q

What is the mechanism of carbamazepine’s teratogenicity? (Domain II)

A

Carbamazepine inhibits folate metabolism, disrupting neural tube closure, leading to spina bifida (DABT_Study_Notes.xlsx, Repro Tox; Web: PubMed, 2024).

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23
Q

How does methotrexate cause reproductive toxicity? (Domain II)

A

Methotrexate inhibits folate synthesis, targeting rapidly dividing embryonic cells, causing miscarriage and congenital malformations (DABT_Study_Notes.xlsx, Repro Tox; Web: NIH, 2025).

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24
Q

What reproductive target is affected by phenytoin toxicity? (Domain II)

A

Phenytoin targets the fetal palate, disrupting folate metabolism, leading to cleft palate and heart defects (DABT_Study_Notes.xlsx, Repro Tox; Web: FDA, 2024).

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25
How does bisphenol A (BPA) mechanistically affect reproduction? (Domain II)
BPA mimics estrogen, binding ERα, disrupting ovarian folliculogenesis and reducing fertility (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
26
What is the mechanism of tetrachloroethylene’s reproductive toxicity? (Domain II)
Tetrachloroethylene, a PPARα agonist, disrupts steroidogenesis, targeting testicular function and reducing sperm quality (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
27
How does arsenic induce reproductive toxicity? (Domain II)
Arsenic generates ROS, targeting testicular germ cells, causing reduced sperm motility and infertility (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
28
What reproductive target is affected by cadmium toxicity? (Domain II)
Cadmium targets Sertoli cells, inducing ROS and disrupting tight junctions, leading to testicular atrophy (DABT_Study_Notes.xlsx, Repro Tox; Document: Principles & Mechanisms).
29
How does hexachlorobenzene cause developmental toxicity? (Domain II)
Hexachlorobenzene disrupts thyroid hormone homeostasis, targeting fetal neurodevelopment, causing cognitive deficits (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
30
What is the mechanism of vinyl chloride’s reproductive toxicity? (Domain II)
Vinyl chloride forms DNA adducts, targeting germ cells, causing reduced fertility and increased miscarriage risk (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
31
How does benzo[a]pyrene affect reproductive function? (Domain II)
Benzo[a]pyrene, a PAH, forms DNA adducts via CYP1A1 metabolism, targeting ovarian follicles, causing premature ovarian failure (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
32
What reproductive target is affected by TCDD (dioxin) toxicity? (Domain II)
TCDD activates AhR, targeting prostate development, causing reduced prostate weight and fertility (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
33
How does chlorpyrifos mechanistically cause reproductive toxicity? (Domain II)
Chlorpyrifos inhibits acetylcholinesterase, disrupting gonadotropin release, targeting sperm production (DABT_Study_Notes.xlsx, Repro Tox; Document: Principles & Mechanisms).
34
What is the mechanism of phenobarbital’s developmental toxicity? (Domain II)
Phenobarbital activates CAR, enhancing thyroid hormone clearance, targeting fetal brain development, causing cognitive delays (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
35
How does cyclophosphamide affect female reproductive function? (Domain II)
Cyclophosphamide alkylates DNA in ovarian granulosa cells, causing follicular atresia and premature ovarian failure (DABT_Study_Notes.xlsx, Repro Tox; Document: Chemical Carcinogenesis).
36
What factors are critical in designing a reproductive toxicity study? (Domain I.A)
Study design includes dose selection, exposure timing (e.g., pre-mating, gestation), and endpoints like fertility and fetal viability, per OECD Test No. 416, using GLP-compliant models (ABT Handbook, Domain I.A; Web: OECD, 2024).
37
How does ethanol cause developmental toxicity mechanistically? (Domain II)
Ethanol disrupts neural crest cell migration via oxidative stress and apoptosis, leading to fetal alcohol syndrome with craniofacial defects (ABT Handbook, Domain II.A; Document: Neuro Tox; Web: NIH, 2025).
38
What endpoints identify reproductive hazards in acute toxicity studies? (Domain III.A)
Endpoints include reduced sperm count, ovarian dysfunction, and embryo lethality, assessed via histopathology and hormone levels, per OECD Test No. 421 (ABT Handbook, Domain III.A; Web: OECD, 2024).
39
How is occupational exposure to phthalates assessed for reproductive toxicity? (Domain III.B)
Exposure is measured via urinary metabolites (e.g., MEHP) using GC-MS, correlating with reduced testosterone and fertility (ABT Handbook, Domain III.B; Web: ATSDR, 2024).
40
How does diethylstilbestrol (DES) induce reproductive toxicity? (Domain II)
DES acts as an estrogen mimic, binding ERα, disrupting vaginal epithelium development, and causing adenocarcinoma (ABT Handbook, Domain II.D; Document: Chemical Carcinogenesis; Web: NIH, 2025).
41
How are in vitro models used to study developmental toxicity? (Domain I.B)
Embryonic stem cell tests (EST) assess differentiation inhibition, predicting teratogenicity per ECVAM guidelines (ABT Handbook, Domain I.B; Web: ECHA, 2024).
42
What susceptibility factors influence lead’s reproductive toxicity? (Domain II)
Genetic polymorphisms (e.g., ALAD) and age increase susceptibility to lead’s effects on sperm motility and miscarriage risk (ABT Handbook, Domain II.C; Document: Principles & Mechanisms; Web: NIH, 2025).
43
How is dose-response assessment applied to bisphenol A (BPA) reproductive toxicity? (Domain III.C)
BMD models quantify reduced fertility from BPA, establishing NOAEL for safe exposure levels (ABT Handbook, Domain III.C; Web: EPA, 2023).
44
How are reproductive risks from pesticides characterized in risk assessment? (Domain III.D)
Risks (e.g., chlorpyrifos-induced sperm damage) are characterized using MOE and hazard quotients, integrating animal and human data (ABT Handbook, Domain III.D; Web: EPA, 2024).
45
How does applied toxicology address public health concerns from teratogens? (Domain IV)
Biomonitoring (e.g., folate levels) and epidemiology guide thalidomide restrictions, protecting fetal health (ABT Handbook, Domain IV.A; Web: FDA, 2024).
46
How is the OECD 414 study designed for regulatory compliance? (Domain I.A)
OECD 414 assesses prenatal developmental toxicity in rodents, dosing during organogenesis, evaluating fetal malformations, per GLP (ABT Handbook, Domain I.A; Web: OECD, 2024).
47
What mechanistic role does oxidative stress play in cadmium-induced testicular toxicity? (Domain II)
Cadmium induces ROS, disrupting Sertoli cell function, leading to impaired spermatogenesis (ABT Handbook, Domain II.A; Document: Principles & Mechanisms; Web: ATSDR, 2024).
48
How are reproductive endpoints interpreted in multigeneration studies? (Domain I.C)
Endpoints like litter size and gonadal histopathology are analyzed, integrating systemic effects, per OECD 416 (ABT Handbook, Domain I.C; Web: NIH, 2025).
49
What biomarkers assess reproductive exposure to mercury? (Domain III.B)
Mercury levels in hair and blood correlate with reduced fertility, measured via AAS (ABT Handbook, Domain III.B; Document: Neuro Tox; Web: EPA, 2023).
50
How does atrazine cause reproductive toxicity, and what is its AOP? (Domain II)
Atrazine inhibits GnRH release, reducing LH and testosterone, impairing spermatogenesis via hypothalamic-pituitary-gonadal axis disruption (ABT Handbook, Domain II.D; Web: PubMed, 2024).
51
How are in silico models used to predict reproductive toxicity? (Domain I.B)
QSAR models predict estrogenic activity of chemicals, guiding safer pesticide development (ABT Handbook, Domain I.B; Web: ECHA, 2024).
52
What genetic factors influence susceptibility to vinclozolin’s reproductive toxicity? (Domain II)
Polymorphisms in AR increase vinclozolin’s anti-androgenic effects, reducing anogenital distance (ABT Handbook, Domain II.C; Web: NIH, 2025).
53
How is the benchmark dose applied to organophosphate reproductive effects? (Domain III.C)
BMD models reduced fertility from chlorpyrifos, establishing a POD for safe exposure (ABT Handbook, Domain III.C; Document: Neuro Tox; Web: EPA, 2023).
54
How does weight of evidence integrate data for reproductive risk characterization? (Domain III.D)
WoE uses in vitro (EST), in vivo (OECD 416), and human data, applying Bradford Hill criteria to assess causation (ABT Handbook, Domain III.D; Web: ECHA, 2024).
55
How does applied toxicology evaluate reproductive risks from plastics? (Domain IV)
Epidemiological studies assess BPA’s role in infertility, developing safer plastic regulations (ABT Handbook, Domain IV.A; Web: FDA, 2024).
56
What statistical methods analyze reproductive toxicity study results? (Domain I.C)
ANOVA compares litter parameters, and logistic regression models dose-response for malformations (ABT Handbook, Domain I.C; Web: PubMed, 2024).
57
How does thalidomide cause developmental toxicity? (Domain II)
Thalidomide inhibits angiogenesis via cereblon binding, causing limb defects (ABT Handbook, Domain II.A; Document: Chemical Carcinogenesis; Web: NIH, 2025).
58
How are reproductive hazards from solvents identified in regulatory studies? (Domain III.A)
Hazards (e.g., toluene-induced fetal loss) are identified via OECD Test No. 422, focusing on fertility endpoints (ABT Handbook, Domain III.A; Web: OECD, 2024).
59
What exposure metrics assess DEHP’s reproductive effects? (Domain III.B)
DEHP exposure (mg/kg/day) is measured via urinary metabolites, correlating with testicular atrophy (ABT Handbook, Domain III.B; Web: ATSDR, 2024).
60
How does nicotine’s toxicity affect reproductive function mechanistically? (Domain II)
Nicotine disrupts placental vascularization via nAChR activation, causing low birth weight (ABT Handbook, Domain II.E; Document: Neuro Tox; Web: PubMed, 2024).
61
How are alternative testing methods validated for reproductive toxicity? (Domain I.A)
Zebrafish embryo assays validate teratogenicity against rodent data, ensuring reliable predictions (ABT Handbook, Domain I.A; Web: ECHA, 2024).
62
What role do species differences play in retinoid teratogenicity? (Domain II)
Rabbits are more sensitive to retinoid-induced neural tube defects than rats due to RAR expression differences (ABT Handbook, Domain II.B; Web: NIH, 2025).
63
How is the margin of safety calculated for pesticide reproductive toxicity? (Domain III.D)
MOS is NOAEL (from OECD 416) divided by human exposure, ensuring safe chlorpyrifos use (ABT Handbook, Domain III.D; Web: EPA, 2024).
64
How does applied toxicology address reproductive risks in occupational settings? (Domain IV)
OSHA PELs and PPE mitigate DBCP exposure, reducing sterility risks (ABT Handbook, Domain IV.C; Web: CDC, 2024).
65
What is the role of endocrine disruption in reproductive toxicity? (Domain II)
Endocrine disruptors (e.g., DDT) alter steroidogenesis, reducing fertility via ER and AR pathways (ABT Handbook, Domain II.A; Document: Chemical Carcinogenesis; Web: NIH, 2025).
66
How are reproductive study results communicated to regulatory bodies? (Domain I.C)
Results are reported in OECD 416-compliant formats, with fertility and fetal data for EPA submissions (ABT Handbook, Domain I.C; Web: EPA, 2024).
67
How does methoxychlor’s mechanism cause reproductive toxicity? (Domain II)
Methoxychlor mimics estrogen, binding ERα, disrupting ovarian folliculogenesis (ABT Handbook, Domain II.E; Document: Chemical Carcinogenesis; Web: ATSDR, 2024).
68
What ecotoxicological endpoints are relevant for reproductive toxicity? (Domain III.A)
Fish reproductive impairment from atrazine is assessed via OECD Test No. 229, indicating environmental hazards (ABT Handbook, Domain III.A; Web: OECD, 2024).
69
How is internal reproductive exposure to cadmium measured? (Domain III.B)
Cadmium levels in testicular tissue are measured via ICP-MS, correlating with infertility (ABT Handbook, Domain III.B; Document: Principles & Mechanisms; Web: EPA, 2023).
70
How does valproic acid’s toxicity affect fetal development? (Domain II)
Valproic acid inhibits HDAC, causing neural tube defects via altered gene expression (ABT Handbook, Domain II.A; Document: Risk Assessment; Web: PubMed, 2024).
71
How is the therapeutic index used for retinoid developmental effects? (Domain III.C)
TI compares therapeutic doses to those causing teratogenicity, ensuring safe isotretinoin use (ABT Handbook, Domain III.C; Web: FDA, 2024).
72
How does applied toxicology mitigate reproductive risks from consumer products? (Domain IV)
BPA bans in baby bottles reduce developmental exposure, protecting fetal health (ABT Handbook, Domain IV.C; Web: ECHA, 2024).
73
What are the limitations of in vitro reproductive toxicity assays? (Domain I.B)
In vitro assays lack placental metabolism, limiting prediction of in vivo teratogenicity (ABT Handbook, Domain I.B; Web: ECHA, 2024).
74
How does vinyl chloride’s reproductive toxicity inform risk assessment? (Domain III.D)
Vinyl chloride’s testicular toxicity is assessed via dose-response models, setting safe exposure limits (ABT Handbook, Domain III.D; Document: Chemical Carcinogenesis; Web: EPA, 2023).
75
What is the role of omics in studying reproductive toxicity mechanisms? (Domain II)
Proteomics identifies disrupted pathways (e.g., steroidogenesis) in phthalate-induced testicular injury (ABT Handbook, Domain II.F; Web: PubMed, 2024).
76
How are reproductive effects of air pollutants assessed in epidemiology? (Domain IV)
Studies correlate PM2.5 exposure with low birth weight, guiding WHO AQG levels (ABT Handbook, Domain IV.E; Web: WHO, 2024).
77
What analytical methods characterize test agents for reproductive studies? (Domain I.A)
HPLC analyzes chemical stability (e.g., ICH Q3A[R2]) for reproductive studies, ensuring accurate dosing (ABT Handbook, Domain I.A; Web: FDA, 2024).
78
How does endosulfan’s mechanism cause reproductive toxicity? (Domain II)
Endosulfan inhibits testosterone synthesis, reducing sperm count via aromatase upregulation (ABT Handbook, Domain II.D; Document: Neuro Tox; Web: NIH, 2025).
79
What is the role of PBPK modeling in reproductive dose-response assessment? (Domain III.C)
PBPK models predict BPA’s placental transfer, refining dose-response for developmental effects (ABT Handbook, Domain III.C; Web: EPA, 2023).
80
How does applied toxicology address emerging reproductive risks from nanomaterials? (Domain IV)
Nanosilver’s testicular toxicity is evaluated via in vitro studies, developing safety standards (ABT Handbook, Domain IV.B; Web: NIH, 2025).
81
How are systemic and local reproductive effects distinguished in study interpretation? (Domain I.C)
Systemic effects (e.g., lead infertility) involve hormonal disruption, while local effects (e.g., cadmium testicular damage) are tissue-specific (ABT Handbook, Domain I.C; Web: ATSDR, 2024).
82
What factors increase reproductive susceptibility to pesticides? (Domain II)
Genetic polymorphisms (e.g., PON1) and prenatal exposure increase chlorpyrifos-induced developmental toxicity (ABT Handbook, Domain II.C; Document: Neuro Tox; Web: ATSDR, 2024).
83
How is the precautionary principle applied to reproductive risk management? (Domain III.D)
Conservative exposure limits for phthalates are set when data is uncertain, prioritizing fetal safety (ABT Handbook, Domain III.D; Web: ECHA, 2024).
84
What clinical signs indicate reproductive toxicity in poisoning incidents? (Domain IV)
Signs include amenorrhea or reduced libido, guiding treatments like chelation for lead exposure (ABT Handbook, Domain IV.K; Web: NIH, 2025).
85
How does green chemistry reduce reproductive toxicity risks in product design? (Domain IV)
Safer plasticizers (e.g., replacing DEHP) reduce testicular toxicity in consumer products (ABT Handbook, Domain IV.G; Web: EPA, 2023).
86
What are the regulatory standards for reproductive toxicity testing? (Domain IV)
EPA and OECD require two-generation studies (e.g., OECD 416) for pesticides, ensuring reproductive safety (ABT Handbook, Domain IV.L; Web: EPA, 2024).

DABT 2025 (16 decks)

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