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PMCOL 303 > Final exam select topics-endocrinetox > Flashcards

Final exam select topics-endocrinetox Flashcards

1
Q

what is FeBAD

A

fetal basis of adult disease (changes in early life may not manifest until much later)

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2
Q

what are the endocrine effects of most pesticides

A

estrogenic or antiestrogenic or antriestrogenic

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3
Q

what is the deal with polyfluoroalkyl compounds (PFAs)

A

they have high energy CF bonds which resist degradation

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4
Q

what is the structure of PFAs like

A

many CF bonds (hydrophobic core) then hydrophobic tail of carboxylic acid or sulfonic acid

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5
Q

what is the half life of PFAs in humans

A

4-5 years!

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6
Q

what makes BPA bad when it should be a polymrt

A

some polymers are unbound so can leach out

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7
Q

what does BPA do to humans

A

alter sexual development, brain and behavioural abnormalities, obesity, sterility, miscarriage

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8
Q

what is another name for brominated flame retardants

A

polybrominated biphenyls

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9
Q

what are some things that polybrominated biphenyls/ brominated flame retardants do

A

they are endocrine disrupting and neurotoxicity so linked to T2DM and metabolic syndrome

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10
Q

what shape is the polybrominated biphenyls/ brominated flame retardants curve

A

U shape

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11
Q

where is polybrominated biphenyls/ brominated flame retardants found in humans

A

adipose and breast milk

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12
Q

why are these curves not like the classic dose response curve (3)

A
  • properties of receptor
  • 2 separate processes that appear to be a single one (multiple binding sites)
  • desensitization and high doses
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13
Q

what are 3 types of receptors that EDCs often mess with

A

NRs for estrogen and androgens and aryl hydrocarbon receptor

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14
Q

what are 2 types of ERs + where do they bind

A

alpha and beta, to same response element but diff affinities

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15
Q

what are 6 EDC gene transcription mechanisms

A
  • direct recruitment of coactivators
  • direct recruitment of corepressors
  • change conformation of NR so it binds coactivators another NR needs
  • synergism or inhibition b/w 2 NRs bound to neighboring NREs (altering DNA conformation bc they bind so close)
  • competition between 2 NR for NRE
  • activation of one NR may promote degradation of another (proteosome activation)
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16
Q

what is the ERE

A

estrogen response element, BPs that receptor recognizes

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17
Q

what happens with alpha ER knockout

A

increased insulin resistance and impaired glucose tolerance

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18
Q

what may alpha ER control

A

food intake

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19
Q

how can ER increase maturation of adipocytes

A

alpha and beta ER are on preadipocytes

20
Q

what does BPA do to body weight

A

increases adipocyte differentiation so more

21
Q

what does octylphenol do

A

increase adipocyte resistin production

22
Q

what is resistin

A

peptide hormone with high levels in fat people-linked to insulin resistance

23
Q

how can BPA cause hyperinsulinemia

A

effects on ER alpha in the pancreas

24
Q

what kind of curve does BPA make

A

inverted U shape

25
Q

what does BPA seem to mimic

A

estradiol

26
Q

which ER receptor is responsible for BPA insulin and stuff

A

ER alpha

27
Q

what causes non classical ER effects

A

GPR30

28
Q

what is GPR30

A

G protein receptor that binds estrogen (Gs)

29
Q

what binds to GPR30 and what affinities

A

BPA and estrogen at same agonist affinities

30
Q

what happens with GPR30 knockout

A

impaired glucose tolerance and decrease bone growth

31
Q

what is the main thing that happens in epigenetic changes

A

changes in methylation patterns

32
Q

what does methylation do to transcription

A

usually inhibits

33
Q

what can happen with mis-methylated genes

A

DNA being inappropiately sliced or activated

34
Q

what are the 2 points when methylation can be effected

A

after cell is first produced (no previous methylation) and after its normally methylated (later in life)

35
Q

which generation (F) can changes in methylatin occur into to say its transgenerational

A

F3

36
Q

what are 4 ways that obesogens can work

A
  • direct acting on fat cells
  • indirectly by affecting satiety or appetite
  • favor storage of calories
  • interacts with estrogen receptors, RXR-PPARgamma heteromers
37
Q

what happens with PPARgamma stimulation

A

lipogenesis, lipid uptake, increase appetite

38
Q

what is the mechanism of tributyl tin

A

decreases aromatase activity and increases testosterone levels AND PPARgamma and RXR receptor agonists

39
Q

what can tributyl tin do to fish

A

turn girls into boys

40
Q

what does tributyl tin do to multipotent stromal cells

A

makes the stem cells differentiate more into adipocytes rather than bone

41
Q

what compound causes stem cells differentiate more into adipocytes rather than bone

A

tributyl tin

42
Q

what is fabp4

A

marker for early adipocyte differentiation, fatty acid binding protein

43
Q

what is a marker for early adipocyte differentiation

A

fabp4

44
Q

what does tributyl tin do to fabp4

A

pushes stem cells into adipocyte pathway

45
Q

how can we block tributyl tin from pushing stem cells into adipocyte pathway

A

PPARgamma antagnoinsts

PMCOL 303 (25 decks)

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