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Toxicology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Endpoint

A

death, biochemical physiological

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2
Q

Results

A

LC50, LD50, EC50, ED50, NOAEC, NOAED, LOAEC, LOAED

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3
Q

Selective toxicity ratio

SER

A

Medial lethal dose or concentraion for species A / meidal lethal dose or concentration for species B

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4
Q

ERA : Factors defined as

A 
Formulation of the chemical
Rate of dosing
Feeding regimen
Temperature
Humidity 
State od health of animals
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5
Q

Standard toxicity testing

A

Give a measure of toxicity under closely defined sets of operating conditions

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6
Q

Addivity

A

Combination of two or more chemicals is the sum of the expected individuals response

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7
Q

Antagonism

A

Exposure to one chemical results in a reduction in the effect of the other chemical

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8
Q

Potentiation

A

Exposure to one chemical results in the other chemical producing an effect greater than if given alone

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9
Q

Synergism

A

Exposure to one chemical causes a dramatic increase in the effect of another chemical

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10
Q

Testing earthworms

A

OECD guideline - standard testing

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11
Q

Vertebrates

A

Mammals

  • Standard testing measuring LD50
  • Different dosing method (injection)
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12
Q

Testing with auatic organism

A
  • Direct uptake from water (gills)
  • Food
  • Sediments
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13
Q

Maintaining a constant concentration of chemicals in water

A
  • Static
  • Semi static
  • Continous flow
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14
Q

Risk quotient ratio

A

PEC/PNEC
predicted enviromental concentration / predicted enviromental no effect concentration

Risk ratio above 1 : Potential risk
Risk ration below 1 : Low risk

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15
Q

Alternative methodes

A
  • Using live vertebrates
  • Using cellular systems , in vitro systems
  • Predictive models
  • Fields studies
  • Microcosms and mesocosms studies
  • Modeling works
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16
Q

Protective biochemical responses

A
  • Induction of monooxygenase enzymes => metabolites
  • Induction of MT, metallothionein - binding proteins
  • Response that correct damage after it has occured
    • Induction of stress protein
    • DNA repair
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17
Q

Molecular mechanism of toxicity

A

3 reasons

  • Develop drugs or antidotes
  • Lead to the dev of biomarkers
  • Helps for extrapolation across taxa
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18
Q

Relationship between the dose and the extend of effecs of chemicals

A
  • At low levet of exposure : May not produce measurable interactions - compounds does not reach the site of action
  • At higher level of exposure: Protective mechanism may reduce the amount of chemical that reaches the active site.
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19
Q

Reserve capacity

A

Intribition of brain acetylcholesterase must exceed 50 %

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20
Q

No minimum safe level

A

Single molecule interaction can initiate toxic mechanism

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21
Q

Examples of molecular mechanism of toxicity

A
  • Pesticide dimilin, inhibits the synthesis of chitin
  • Organophosphorous insecticides, affect the nervous system
  • Dinitroorthocresol, mitochondria membrane
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22
Q

Genotoxicity compounds

A

Cacinogenic compounds that can causes damage on DNA

Production of mutant cells => potentially tumor cells

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23
Q

DNA adduct formation

A

Covalent binding of the pollutant with DNA

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24
Q

General about genotoxicity

A
  • Good biomarkers of exposure
  • Enzymatic metabolism
  • Formation of reactive matabolism bind to DNA
  • The original compound being relatively stable and not reactive
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25
Q

Neurotoxicity

A

Nervous system af vertebrates + invertebrates can be affected by chemicals

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26
Q

Natural neurotoxicity

A
  • Botulinium toxic

- Natural insecticides as nicotine and pyrethin

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27
Q

Antroprgenic compounds

A
  • Organochlorine insecticides
  • Organophosphorous insecticides
  • Carbamates
  • Pyrethoid insecticides
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28
Q

GABA receptor

A

Chlorinated cyclodiene insectice or their metabolites

Is a “calming” neurotransmitter that reduces neuronal excitability
Act as antagonist - reduce flow of Cl

29
Q

Mitochondria poisons

A
  • Found in all eukaryotes
  • Electron transport chain- electrochemical gradient
  • Speciel transport of H+ and ATP (production of energy)
30
Q

Enviromental estrogen

A

Can mimiric estrogen by binging to the extrogen receptor
Stimulate the transciption activity of estrogen

Known estrogen: Oganochlorine insecticides and tributyl tin

Biomarker:

  • induction of vitellogenin
  • Enzymatic of aromatase disruptied
31
Q

Effects at the organ level in animals

- Pollutants compartmetalized in particular organs

A
  • Thyroid gland for radioactive isotopes

- Liver and kidneys for Cd

32
Q

Effects at the whole organism level

1) Neurophysiological effects
2) Effects on behavior
3) Effects on reproduction

A

1) Chemicals interacting with the nervous system : Organophosphorus insecticides, organochlorine insecticides, carbamate, pyrethoids
2) Foraging behavior / Failure to avoid predation

3) TBT on molluscs
DDE-induced eggshell thining in raptors and fish
eating birds
Various disruptors of the endocrine system

33
Q

Energy cost od physiological

A

Scope for growth = Energy intake - total metabolic losses.

34
Q

Trade off

A

Between the loss of production and the mortality

35
Q

Hepatotoxicity

A

Liver

36
Q

General abour the liver

A
  • Largest organ in the body
  • Exposed to significant concentrations of chemicals which can results in liver disfunction, cell injury or organ failure
37
Q

Position in circulatory system

A
  • Encounters: Nutrient, vitamins, metal, drugs, enviromental toxicants, waste of bacteria products
  • Main organ metabolizing chemicals
38
Q

Enterohepatic circulation

A

Circulation of drugs or other substances from the liver to the bile
- Transport by portal vein
-Absorption from stomach
-Absorption from instestines
Some xenobiotics may be “recycled” many times before they are finally excreted in the feces
Many lipophilic xenobiotics undergo this proces carrying repeated liver damage

39
Q

Types of liver injury

A
  • Fatty liver (steatosis)
  • Cell necrosis
  • Cholestasis
  • Cirrhosis
  • Carcinogenesis
40
Q

Fatty liver

A
  • Increase in the hepatic lipid content
  • Due to diabetes
  • Different mechanism that increase the accumulation of lipid in the liver
41
Q

Cell necrosis

A

-Cell swelling, leakage, nuclear distergation, influx on inflammatory cells
-Can be massive
-Not always anitical
Example: Tylenol, carbon tetrachlorid, beryllium

42
Q

Cholestasis

A

-Decrease volume of bile formed or impaired secretion of specific solutes into biles
-Usually drug-induced
Example: Anabolic steroids, ethanol, paraquat, methylene dianiline

43
Q

Cirrhosis

A
  • Chronic liver injury
    -Accumulation of collagen fibers => formation of fibrotic tissue => Cirrhosis
  • Alcohol consumption or metal with chronic exposure
    Example: Carbon tetrachloride, ethanol with poor diet, reduced vitamine and protein
  • Not reversible
44
Q

Carcinogenesis

A
  • Many chemicals are capable of producing tumors in the liver
  • Hepatocytes
    -Cholangiocarcinorma: Bile duct cell
    Example : Carbon tetrachloirde, vinyl chloride, Aflatoxin B1
45
Q

Toxicant -induced injury

A
  • Ethanol (biotransformation, genetic polymorphism

- Acetaminophen (do not mix with alcohol)

46
Q

Evaluation of liver injury using blood test

A
  • Acess to functional capability of the liver or capability to extract and metabolize foreign compounds from the blood
  • Acess whether there are abnormally high levels in the blood of intracellular hepatic proteins: Endence of liver cell destruction
47
Q

Stategic location of the liver

A

Between intestial tract and the rest of the body facilitates its maintenance of metabolic hemostasis in the body

48
Q

Hepatocytes

A

Rich supply of phase 1 enzyme that often convert xenobiotics to reactive electrophilic metabolites and of phase 2 enzymes that add a polar group to a molecule and thereby enhence its removal from the body

49
Q

Balance between phase 1 enzyme and phase 2 enzyme

A

Determine whether a reactive metabolite will initiate liver cell injury or be safety detoxified

50
Q

Nephrotoxicity

A

Kidneys

51
Q

General about kidneys

A

Two bean shaped organs
Recieve blood flow from the hearth
Contains 1 to 2 millions nephrons

52
Q

Morphology and functions for kidneys

A
  • Reciece its blood supply from a single artery that orginates in the aorta
  • Circulate into a single vein that connect with the inferior vena cava
53
Q

3 main anatomical areas

A
  • Renal cortex (90 % blood flow)
  • Renal medulla (6-10 % blood flow)
  • Renal papilla (1-2% blood flow)

When a bloodborne toxicant is delivered to the kidney a high percentage of the material will be delivered to the cortex

54
Q

Nephron

A

Functional unit of the kidney
3 mechanism - Glomerular filtration
- Tubular reabsorption
- Tubular secretion

55
Q

Kidney injury

A
  • Acute kidney injury
    • Abrupt decline in glomerular filtration
    • Result in azotemia
    • Eleviation in serum creatinine
    • Anuric renal failure
  • Chronic kidney injury
    • Chronic tubolointerstitial fibrosis
    • Papillary necrosis
  • Adaptation to injury
56
Q

Susceptibility to the kidney to toxic injury

A
  • Drugs and chemicals in the systemic circulation are delivered to the kidneys in relative high amount
  • Process to form urine: concentrate potential toxicants in the tubular fluid, therefore exposing toxicants to tubular cells
  • Consequently, a nontoxic concentration of a chemical in the plasma may reach toxic concentrations in the kidney
57
Q

Specific nephrotoxicants

A
  • Metal (cause renal cellular injury)
  • Hg (transfer Hg2+ into the cell of proximal tubular
  • Cd
58
Q

Halogenated hydrocarbons

A
  • Chloroform

- Bromobenzene

59
Q

Therapeutic agents

A
  • Acetaminophen
  • Nonsteroidal anti-inflammatory drugs
  • Cis platin
60
Q

Non-invasive assesment of renal functions

A
  • Blood and serum analysis
  • Glomerular filtration rate (creatinine and inulin)
  • Indirect markers of glomerular filtration rate (blood urea nitrogen and serum creatinine)
61
Q

Xenobiotics in kidneys

A

Will be delivered to the kidney in relatively high amounts

62
Q

Bioaccumulation

A

BCF = concentraion of the chemical in the organism / concentration in the ambient enviroment

63
Q

Bioavailability

A

Fraction of ingested metal absorbed into the systemic circulation

64
Q

Bioaccessibility

A

Fraction of total metal that dissolve in the stomach and is available for absorption during transit through the small intestine

65
Q

Measure bioaccessibility

A
  • Studying metal speciation in digestive fluid
  • In vitro gastric model
  • Culturing gut cells
66
Q

Metalbolism

A

lipophilic xenobiotics -> (phase 1) -> Metabolite -> (phase 2) -> Conjugate
Increasing in polarity ->

67
Q

Zero order kinetics

A
  • Concern aspirin and ethanol
  • The rate of elimination is constant
  • The half-life is not constant
68
Q

First order kinetics

A
  • Concern most drugs
  • The rate of elimination is not constant
  • The half-life is constant
69
Q

Equation for first order kinetic

A

Ct = C0e^(-kt)

t½ = 0.693/k

Toxicology (3 decks)

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