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Toxicology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Tyrone Hayes

A

Studied the effects of Atrazine on frogs. paper: Hermaphroditic, demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.

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2
Q

Louis Guillette

A

Studied the effects of endocrine disruptors on alligators in Lake Apopka, florida.
High levels of DDT caused skewed sex hormone ratios (low testosterone, high estrogen), and small phallus size in alligators.
a polarizing figure, big communicator. spoke to congress about the fact that if we are seeing this in alligators, then we should be looking at humans. Will people have reduced sperm count and phallus size as well?

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3
Q

What is toxicology and how would your definition expand to encompass environmental toxicology?

A

The study of adverse chemical effects on living organisms. The definition of environmental toxicology would expand to include populations, communities, and ecosystems (adverse effects over the entire biological hierarchy).

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4
Q

List the four processes collectively referred to as chemical disposition

A

Absorption
Distribution
Excretion
Metabolism

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5
Q

Who was Paracelsus and what contribution did he make to the field of toxicology?

A

Paracelsus is considered to be “the father of modern toxicology.” His important contribution was to state that “the dose determines the poison,” meaning that anything can be toxic, it just depends on the dose.

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6
Q

potency vs efficacy

A

see midterm, question 4.

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7
Q

A toxicant has to cross a biological membrane to produce damage. List the different ways in which entry can be achieved.

A 
diffusion
filtration
active transport
secondary active transport
facilitated diffusion
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8
Q

for which sex are reproductive effects of toxic agents more damaging?

A

women. reproductive effects are much more damaging long-term because females are born with a set number of eggs, whereas males replenish sperm.

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9
Q

Dr Theo Colborn

A

studied endocrine disruptors in the great lakes… effects on birds
Her 1988 research on the state of the environment of the Great Lakes revealed that persistent, man-made chemicals were being transferred from top predator females to their offspring and undermining the construction and programming of their youngsters’ organs before they were born.

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10
Q

examples of endocrine disruptors

A

PCB, DDT, atrazine, DES

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11
Q

trenbolone

A

used as a growth promotor for beef production… anabolic steroid, makes cattle produce muscle.
effects on fish: females exhibit characteristics of male fish when exposed. this can have negative effects for the population… decreased number of eggs.

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12
Q

Kidd et al. paper

A

Collapse of a fish population after exposure to a synthetic estrogen.

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13
Q

Atrazine

A

an herbicide. banned in europe, but made by a european company

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14
Q

endocrine disrupting compounds

A

binds to nuclear receptor for a hormone

  • can deactivate receptor : anti-estrogenic
  • can mimic function: estrogenic.
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15
Q

definition of pesticide and 4 types

A

any substance intended for destroying, repelling, or mitigating any pest.

  1. insecticides
  2. fungicides
  3. herbicides
  4. rodenticides
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16
Q

historical background of pesticides

A

1st gen: natural products, ex. tobacco, sulfur
2nd gen: modern synthetic chemicals. ex DDT, dieldrin, aldrin
3rd gen. OP and carbamate insecticides, herbicide 2,4 D
4th gen: gene engineering. either plant secretes own pesticide or plant is made resistant to herbicide (ex, roundup-ready corn and soybeans)

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17
Q

organochlorine pesticides

A

aldrin, dieldrin, DDT, lindane. used extensively in the 40s, 50s, 60s

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18
Q

DDT

A

acts on the central nervous system by interfering with the movement of ions through neuronal membranes, delays the closing of the sodium ion channel and prevents the full opening of the potassium gates.
targets a specific ATPase that controls the rate of sodium, potassium, and calcium fluxes , plays a vital role in neuronal repolarization
Na+ gate leaking/open, causes “DDT jitters”

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19
Q

DDT controversy

A

banned in US in 1972 by Ruckelhaus, administrator of the FDA.
still used in other countries, ex south africa. very low toxicity for humans.
persistent in environment, interference with the inability of birds to mobilize sufficient for stabile egg shell formation

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20
Q

organophosphorous and carbamate compounds

A

used in chemical warfare. increased use since organochlorine compounds banned in the 70s.
degrade rapidly in the environment, less bioaccumulation, less chronic effects. greater potential toxicity for humans. greater potential for insect resistance.
inhibit enzymes like acetylcholinesterase, causing accumulation of acetylcholine

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21
Q

lifestyle choices as cancer causing agents

A

tobacco (30%)
alcohol (3%)
diet (35%)

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22
Q

neoplasia

A

new growth or autonomous growth of tissue

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23
Q

neoplasm

A

the lesion resulting from the neoplasia

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24
Q

benign

A

lesions characterized by expansive growth, frequently exhibiting slow rates of proliferation that do not invade surrounding tissues

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25
Q

malignant

A

lesions demonstrating invasive growth, capable of metastases to other tissues and organs

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26
Q

metastases

A

secondary growths derived from a primary malignant neoplasm

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27
Q

tumor

A

lesion characterized by swelling or increase in size, may or may not be neoplastic

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28
Q

cancer

A

malignant neoplasm

29
Q

carcinogen

A

a physical or chemical agent that causes or induces neoplasia

30
Q

genotoxic

A

carcinogens that interact with DNA resulting in mutation

31
Q

nongenotoxic

A

carcinogens that modify gene expression but do not damage DNA

32
Q

eight hallmarks of cancer

A
  1. sustaining cell proliferation
  2. resisting cell death (apoptosis)
  3. inducing angiogenesis
  4. enabling replicative immortality
  5. activating invasion and metastasis
  6. evading growth suppressors
  7. reprogramming of energy metabolism
  8. evading immune destruction
33
Q

stages of the carcinogenesis process

A
  1. initiation: DNA modification, mutation, genotoxic. nonreversible.
  2. promotion: no direct DNA modification nongenotoxic. expansion of the initiated cell population. increase in proliferation or decrease in apoptosis. reversible.
  3. progression. DNA modification, genotoxic. mutation, chromosome disarrangement. changes from preneoplasia to neoplasia benign/malignant. irreversible.
34
Q

carcinogenic factors associated with lifestyle

A

alcoholic beverage- esophagus, liver, oropharynx, and larynx
aflatoxins- liver
betel chewing- mouth
dietary intake (fat, protein, calories)- breast, colon, endometrium, gallbladder
tobacco smoking- mouth, pharynx, larynx, lung, esophagus, bladder

35
Q

functions of the liver

A

filters nasties, nitrogenous waste destruction, glucose metabolism, break down insulin etc.

36
Q

acetaminophen

A

most common cause of pharmaceutical poisoning/death and acute liver failure

anaglesia: pain reliever
antipyresis: fever reducer

37
Q

absorption, distribution of acetaminophen

A

absorption: rapidly absorbed from the GI tract
distribution: 20% plasma protein bound, may increase to 50% in overdose, can cross placenta

38
Q

metabolism of acetaminophen

A

occurs via several pathways:
sulfation, glucuronidation: phase 1, type II reactive conjugating ligand
2% excreted unchanged in the urine
4% biotransformed by CYP450 MFO system

39
Q

excretion of acetaminophen

A

metabolic products are excreted by the kidneys

minimal excretion into breast milk

40
Q

CYP450 and acetaminophen

A

most is metabolized through glucuronidation and sulfating, but a small amount is transformed via Cytochrome p450 2E1, which forms a reactive intermediate that can lead to toxicity.

41
Q

ethanol

A

amphiphile (has both hydrophobic and hydrophilic characteristics) readily passes through biological membranes.
distributes from the blood into all tissues and fluids in proportion to their relative content of water
90% removed by ethanol oxidation, which occurs in the liver

42
Q

general scheme for alcohol metabolism

A

alcohol-> aldehyde via alcohol dehydrogenase
aldehyde-> aldehyde hydrate-> carboxylic acid
aldehyde dehydrogenase

43
Q

to alleviate effects of alcohol

A

hydrate beforehand
coffee 4 hrs afterwards
vitamin B

44
Q

cortisol

A

stress hormone

45
Q

normal gene activation

A

hormone enters cell, hormone binds to and activates receptor, receptor enters through nuclear pores and activates genes

46
Q

interfering with transcription

A

toxicants acting on ligand-activated transcription factors can interfere with the signal getting to transcription

47
Q

two ways to communicate a signal across distance

A

1) phosphorylation/dephosphorylation

2) put a molecule such as ubiquitin onto a protein that signals the protein for degradation

48
Q

apoptosis

A

cell death that is programmed.. signal for the cell to retire.
reasons:
-kill mutated cells before they replicate
-limit cell growth before it gets out of hand
-defends against cancer

49
Q

phosphorylation and ubiquitin

A

can work together to increase transcription

50
Q

transcription

A

initiated by signal from membrane to nucleus

51
Q

molecules that can affect cellular maintenance

A

calcium levels

ATP (mitochondria)

52
Q

mitochondrial ATP synthase

A

this is an important form of maintenance. there are different ways to interfere, including cyanide.

53
Q

calcium

A

stored in the ER, mitochondria, leave the cell via Na/Ca exchanger, or leave the cell via Ca ATP-ase

54
Q

effects of toxicants on target molecules

A

1) dysfunction
2) destruction
3) neoantigen formation
4) globalized change in environment ex. chlorine has-> general tissue breakdown

55
Q

dysfunction

A

dysfunction of target molecules. some toxicants activate protein target molecules, mimicking endogenous ligands. protein function is impaired when conformation or structure is altered by interaction with the toxicant. toxicants may interfere with the template function of DNA by binding to the DNA and causing nucleotide misfiring during replication.

56
Q

destruction

A

destruction of target molecules. toxicants can alter the primary structure of endogenous molecules by means of cross-linking and fragmentation. several forms of DNA fragmentation are caused by toxicants

57
Q

neoantigen formation

A

when the altered proteins evoke an immune response. T cell mediated immune response

58
Q

toxicant-induced cellular dysregulation

A

cells are regulated by signaling molecules that activate specific cellular receptors linked to signal transuding networks that transmit the signals to the regulatory regions of genes and/or functional proteins. receptor activation may lead to:
1. altered gene expression that increases or decreases the quantity of specific proteins
2.a chemical modification of specific proteins
dysregulation of transcription

59
Q

types of signaling pathways

A
  1. nuclear receptor. “normal gene activation”-> block or activate
  2. phosphorylation/dephosphorylation
  3. ubiquitination..usually signals degradation, interfere with transcription
  4. take advantage of voltage gated ion channels, in a polarized membrane. what we use when we run, jump. fast process, fast signal generators
60
Q

disorders that chemicals inflicting cell death may initiate

A

ATP depletion, sustained rise in intracellular Ca2+

61
Q

interference with cell maintenance

A
  1. ATP generation in the mitochondria- Krebs cycle, oxidative phosphorylation. can interfere, take away O2, ATP synthase, etc
  2. Ca2+ levels- inducing influx into cytoplasm, inhibiting export from cytoplasm. (should be stored in mitochondria)
62
Q

DNA structure

A

wound/supercoiled: double helix-> chromosomes

nucleotides. guanine, cytosine. thymine, adenine.

63
Q

types of DNA variation

A
  • base pair substitutions
  • structural mutations (copy number variation, section deleted, inserted, inverted). largest source of different between species.
64
Q

synonymous

A

does not alter amino acid sequence

65
Q

chemical carcinogenesis

A
  1. initiation
  2. promotion
    after this point, cancer is growing without checks and balances
66
Q

DNA repair types

A
  • mismatch repair: tricky determining which is template and which is new strand. determine by methylated bases.
  • base excision repair
  • nucleotide excision repair
  • non-homologous end joining ( if double strand break)
67
Q

basic timeline of the genome

A

key: rapid progression of DNA research
watson and crick and rosalind franklin: double helix structure(50s)
fred singer: developed methods for sequencing DNA 70s-80s
next gen: pyrosequencing, single molecule sequencing

68
Q

chemical modifications of DNA

A

direct and indirect genotoxic chemical carcinogens covalently modify DNA (adduct formation)

  • almost all DNA damage is reversed by very effective and efficient cellular DNA repair mechanisms
  • cells w unrepairable DNA damage usually undergo apoptosis
  • errors in DNA repair lead to mutations that can result in cancer initiation
  • mutations passed on to daughter cells by mitosis and clonal expansion
  • damage of these types is much easier to repair than base substitution errors

Toxicology (2 decks)

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