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ANAT322 > neuroendocrine disrupting chemicals > Flashcards

neuroendocrine disrupting chemicals Flashcards

1
Q

what is an endocrine disruptor?

A

exogenous substance/mixture that alters the function of the endocrine system and causes adverse health effect

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2
Q

why is DDT bad?

A

it mimics estrogen effects and reduces fertility

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3
Q

what are the effects of EDCs on animals sex and reproduction?

A

changes in sex determination, sexual dysfunctions, changes in mate preference

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4
Q

what is bisphenol A

A

BPA: plasticizer that interferes with sex hormones signaling

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5
Q

what are similarities between hormones and endocrine disruptors?

A

act via hormone receptors, act at low doses, blood levels do not always reflect activity, non-linear dose-response relationships, tissue-specific, timing-specific

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6
Q

differences between hormones and endocrine disruptors

A

EDs:
cause abnormal receptor function, can bioaccumulate, interferes with programming processes

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7
Q

why are fetal exposures to EDC’s most dangerous?

A

change in amount or timing of hormones during featus development can have cause behavior, immune function, neurological, gender development problems

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8
Q

which receptor activity do EDCs interact with

A

nuclear receptors (for steroid hormones)

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9
Q

where in the world are EDCs concentrations in wildlife tissue the highest?

A

in regions of high chemical use (north America) (BDE-209)

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10
Q

what EDCs are good at extinguishing fires? where do we find them most?

A

PFAS / PFOS.
they can not be metabolized.
found in europe and waters most.

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11
Q

name examples of products and the toxic chemical in them

A

body lotion: parabens
cologne: phthalates
bug spray: DEET

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12
Q

how do EDCs affect germ cells and what is the effect on reproduction and sex determination?

A

causes germ-cell re-methylation ->altered testis transcriptome -> spermatogenic defect & epigenetic changes transferred to offspring

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13
Q

what did they conclude when they found testis containing oocytes (vitellogenin) in male fishes?

A

something in the water is oestrogenic

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14
Q

how were starling birds affected by being fed contaminated worms?

A

increased volume of the HVC and more complex songs -> more attractive

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15
Q

7 systems targeted by EDCs

A

immune
reproductive
thyroid
bones
neurodevelopmental
hormone
metabolism

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16
Q

what are organotins? give an example and its effect

A

they are biocides, found in anti-fouling paint. tribytylin is one that increases adipocyte differentiation and adipose tissue amount.

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17
Q

how can BPA affect insulin effect?

A

can affect insulin itself, insulin receptor, downstream compound like P13-kinase, PDK, GLUT4, and affect glucose uptake itself

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18
Q

definition of metabolic syndrome

A

refers to central (abdominal) obesity, insulin resistance, glucose intolerance, dyslipidemia/oxidized low density lipoprotein (LDL), increased triglyceride/reduced high density lipoprotein (HDL) levels, elevated blood pressure, endothelial dysfunctions and atherogenesis

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19
Q

how to EDs contribute to metabolic syndrome?

A

inflammatory processes via cytokines/adipokines and
producing the effects of metabolic imbalance

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20
Q

what are the risk factors of metabolic syndrome?

A

obesity, diabetes, hypertension, decreased HDL, elevated triglyceride levels, hypercoagulable states

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21
Q

what is phthalate?

A

plasticizer

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22
Q

what was DES originally used for? what is it? what were its effects?

A

avoiding miscarriages.
synthetic estrogen.
causes: reproductive malformations, infertility, testicular/vaginal cancers, obesity, metabolic disorders, by causing epigenetic changes during development

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23
Q

where is the organotin compound tributylin found? through what receptor do they act?

A

in agriculture and marine paints.
organotin arePPAR and RXR agonists

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24
Q

more specifically how does tributylin act?

A

inhibits the activity of 11beta-hydroxysteroid dehydrogenase, resulting in an increase in local active glucocorticoids levels.
also inhibits aromatase activity and downregulates ER

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25
Q

how may EDCs cause obesity?

A

by directly inducing mitochondrial dysfunction

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26
Q

EDC-induced changes in adipose tissue can promote what else?

A

carcinogenesis, by fucking up cell survival signals

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27
Q

what is the most affected adipose tissue signaling pathway?

A

INSULIN pathway

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28
Q

how does low dose carcinogen EDCs affect adult stem cells vs uterus stem cells?

A

tissue-specific adult stem cells -> mutations & epigenetic changes cause tissue-specific tumors.
in utero stem cells -> childhood and adult cancer

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29
Q

where can we find BPA?

A

air, soil, water, prepared foods (most largely found synthetic chemical in production)

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30
Q

what receptors does BPA bind to?

A

activates ERalpha and beta and mERs.
antagonist to androgen receptors ARs.

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31
Q

what happens to BPA in the liver? give example?

A

it gets transformed through oxidation into metabolites that have worst physiological impact. ex: can affect ERalpha binding affinity

32
Q

what can degrade BPA?

A

some bacteria, fungi or algae

33
Q

how does BPA affect GR (glucocorticoid R)?

A

no effect/we don’t know

34
Q

what is TDI?

A

tolerable daily intake (but effects below TDI can still have significant effects)

35
Q

why can’t we use toxicological risk assessment in endocrinology? what do we call this?

A

because high doses don’t always have the same effects as low doses. it’s not linear (non-monotonic dose response effect)

36
Q

what epigenetic changes can BPA cause?

A

methylation pattern (hypomethylation), abundance of non-coding RNAs (long and miRNAs)

37
Q

what cancers is early exposure to BPA linked to?

A

prostate, breast, hepatic cancer

38
Q

how can DNA hypomethylation after BPA exposure be limited?

A

maternal diet supplemented with methyl donors like folic acid and genistein

39
Q

what is transgenerational transmission?

A

epigenetic mutations caused by BPA and EDC exposure can cause epigenetic mutations for like 3 generations

40
Q

effects of BPA on brain development

A

neurogenesis, neuronal migration, gilogenesis, synaptogenesis, apoptosis

41
Q

the 4 highlighted reported effects of low dose BPA

A

obesity in adults after in utero exposure
reversal in brain sexual dimorphism
changes in formation of synapses in the brain
changes in behavior

42
Q

why are organotin used in anti-fouling paints?

A

antifugal properties

43
Q

what are organotin’s potential adverse effects on animal and human health?

A
  • promotion of reproductive dysfunction
  • endocrine function disruption (Ex hypothalamo-pituitary axis)
  • alteration of hormone synthesis and direct damage to endocrine glands
  • alteration of bioavailability and hormone receptors in target cells
44
Q

where do human get organotin from?

A

bioaccumulation in fishes!

45
Q

how do EDCs affect thyroid gland?

A

cause hypothyroidism

46
Q

in what 5 ways can EDCs affect hormones?

A

synthesis, secretion, transport, binding action, elimination

47
Q

how do pesticides usually affect insect?

A

they upset larval development by disrupting hormonal activity

48
Q

how are EDCs effects transmitted through generations?

A

mother uterus -> fetus germline cells -> germline cells used for F2 production -> F3 has no direct EDC exposure

49
Q

how do EDCs increase metabolic disease?

A

interference with glucose function, insulin function, induce non-alcoholic fatty liver, act as obesogens

50
Q

how can EDCs affect pancreas?

A

pancreas: loss of beta-cells (produce insulin) which leads to diabetes (involved in metabolic disorder)

51
Q

how do obesogens lead to cardiovascular diseases?

A

increase obesity -> insulin resistance, glucose intolerance, dyslipidemia -> T2 DM -> CVD

52
Q

how do diabetogens lead to cardiovascular diseases?

A

hypoinsulinemia, glucose intolerance, insulin resistance, fatty liver, dyslipidemia -> T2 DM -> CDV

53
Q

BPA falls into what categories of EDCs?

A

obesogens, diabetogens, cardiovascular disruptors

54
Q

name a few obesogenic compounds

A

phtalates, phenolic ompounds, organotin, dioxins, pesticides, flame retardants

55
Q

how does the immune system in the liver affect metabolic disorders?

A

kupffer cells;
hepatic macrophages;
proinflammatory cytokine production;
insulin resistance

56
Q

what hormonal receptors is associated with inflammation signaling?

A

ER alpha

57
Q

which inflammatory compound’s activation is undesirable because it leads to apoptosis?

A

caspase-1. especially bad in hepatocytes

58
Q

how are EDCs and immune system linked to metabolic syndrome?

A

inflammation. EDCs can induce pro-inflammatory response in all organs

59
Q

what happens to fishes who swim in water contaminated by synthetic estrogen?

A

there are way more females than males

60
Q

how sensitive to EDCs are kisspeptin receptors?

A

highly sensitive to early life estrogen exposure! can cause dysfunction in adulthood

61
Q

what does EDCs affecting kisspeptin neurons cause?

A

affect progesterone peak at the beginning of pregnancy

62
Q

how does EDC exposure turns fetus to female instead of male?

A

dysruption in anti-muller hormone production by sertoli cell (usually suppresse female mullerian duct cells)

63
Q

what is cryptorchidism? how can it be caused?

A

when testis don’t descend.
can be caused by EDCs causing decreased Leydig cell function.

64
Q

what is testicular dysgenesis syndrome?

A

bunch of problems with testis like cryptorchidism, hypogonadism, reduced semen quality, testicular cancer, hypospadias

65
Q

what is EDC’s effect on leydig cells?

A

cryptorchidism, hypospadias, short AGD, hypogonadism

66
Q

at what 3 levels do EDCs affect sperm quality?

A
  • leydig cell steroidogenesis
  • t production in sertoli cells
  • sperm maturation
  • sertoli cells differentiation
67
Q

6 ways how EDCs reduce male fertility

A
  1. sperm motility/morphology
  2. sperm concentration/count
  3. DNA integrity
  4. steroid action
  5. time to pregnancy
  6. miscarriage
68
Q

in what steroidogenesis processes can EDCs interfere with?

A
  • mineralocorticoids: aldosterone
  • glucocorticoid: cortisol
  • sex hormones: estradiol (can affect every step of the process)
69
Q

what is DES?

A

synthetic estradiol homolog used to be used for stabilizing pregnancies

70
Q

what are DES effects?

A

low dose enhances estrogen response, high dose dampens it

71
Q

what is therapeutic width?

A

dose at which a substance has positive medical effect instead (not toxic)

72
Q

give examples of EDCs effect on the ovary?

A
  • apoptotic oocyte
  • flattened granulosa cells
73
Q

what cancers can be caused by EDCs?

A

hormone-dependent cancers (breast, prostate, testicular) in OFFSPRING

74
Q

what hormone has many very similarly structured EDCs?

A

thyroid (also steroid) (just lacks a hydroxy group)

75
Q

what are EDCs effect on thyroid gland?

A

hypothyroidism; interferes with production of hormone

76
Q

when does thyroid EDA start forming when exposed to EDCs?

A

very early: in infants

77
Q

what can happen to adrenal glands when exposed to EDCs?

A

hypertrophy of adrenal cortex

ANAT322 (10 decks)

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