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TOX 300 FINAL > MODULE 3 > Flashcards

MODULE 3 Flashcards

1
Q

developmental toxicology

A

adverse effects of xenobiotics that occur conception to puberty

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2
Q

teratogenesis

A

adverse effects of xenobiotics that occur between conception and birth

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3
Q

% factors

A

Known genetic factors 25%:
Known environmental factors 10-15%:
Unknown multifactorial cause 60%:

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4
Q

early development

A

lower sensitivity to teratogen exposure

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5
Q

organogenesis

A

Highly sensitive developmental stage, Day 21-56 in humans

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6
Q

fetal period

A

histogenesis (early organs differentiation) and functional maturation of organs and tissues, significant growth occurs during fetal period and reduced growth is common effect

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7
Q

sexual differentiation

A

bipotential gonads in early embryonic development
mullerian duct –> female
wolfian duct–> males

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8
Q

neoplasia

A

new growth

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9
Q

neoplasm

A

the lesion resulting from the neoplasia

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10
Q

benign

A

lesions characterized by expansive growth

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11
Q

malignant

A

lesions demonstrating invasive growth

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12
Q

tumor

A

lesion characterized by swelling or increase in size

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13
Q

cancer

A

malignant neoplasm

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14
Q

carincogen

A

a physical or chemical agent that cause or induce neoplasia

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15
Q

genotoxic

A

carcinogens that interact with DNA resulting in mutation
covalent binding to DNA

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16
Q

Nongenotoxic

A

carcinogens that modify gene expression but do not damage DNA

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17
Q

cocarcinogens

A

increase the effect of carcinogen. Ex. ethanol induces CYP2E1

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18
Q

solid state carcinogens

A

Group 1 carcinogens
ex. abestos, silica

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19
Q

complete carcinogens

A

xenobiotic mixtures that consist of chemicals that are involved in all 3 stages of cancer
ex. tobacco smoke, ethanol (synergistic effect together)

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20
Q

ultimate carcinogens

A

epoxides

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21
Q

groups of carcinogens

A

Group 1: agent is carcinogenic to humans
Group 2A: agent is probably carcinogenic to humans
Group 2B: agent is possibly carcinogenic to humans
Group 3: agent is not classifiable as to carcinogencity to humans
Group 4: agent is probably not carcinogenic to humans

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22
Q

Step 1: initiation

A

if cell with altered DNA undergoes mitosis, the mutation is retained and the cell is intiated

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23
Q

Step 2: promotion

A

intiated tumor cell –> proliferate in presence of promoters
reversible
promotors: toxicants, hormones, calories, ethanol

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24
Q

Step 3: progression

A

conversion from benign to malignant tumor
irreversible

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25
Q

proto-oncogenes

A

normally code for proteins associated with cell proliferation, mutation of proto-oncogene results in permanent activation and/or over-expression of gene products

26
Q

neoplasia occurs

A

when proto-onogenes are converted to onxogenes

27
Q

Proto-oncogenes and tumor suppressor genes

A

implicated in large number of human cancers
P53 tumor suppressor gene: mutated in about half of all humans’ cancers

28
Q

genotoxic characteristics

A

Mutagenic
Can be complete carcinogens
Tumorigencity is dose responsive
No theoretical threshold

29
Q

nongenotoxic characterisitics

A

Nonmutagenic
Threshold, reversible
Tumorigencity is dose responsive
May function at tumor promotion stage
No direct DNA damage
Species, strain tissue specificity

30
Q

Why is the liver susceptible to toxicity arising from xenobiotic exposure

A

1st pass effect
enterohepatic cycling
bioactivation
xenobiotic binding proteins
increased CYP enzymes (qualitative and quantitive)
high blood flow
altered energy homeostasis
active transport

31
Q

Steatosis

A

reversible effect
ex. ethanol

32
Q

necrosis

A

focal or massive
ex. acetaminophen

33
Q

chloestasis

A

yellowish tinge in skin and eyes
ex. ethanol, certain metals, steroids

34
Q

cirrhosis

A

extensive fibrosis throughout the liver
ex. chronic ethanol consumption

35
Q

major functions of kidney

A

excretion of metabolic wastes
regulation of extracellular fluid volume
electrolyte homeostasis
acid-base balance
blood pressure regulation
metabolizes vitamin D to active form

36
Q

Nephorotoxicants

A

Proximal convoluted tubule

37
Q

sources of lung damage

A

Oxidative stress
Gases and vapors
Particles and aerosols (size is most important)

38
Q

acute effects (lung)

A

can be reversible or irreversible
Airway reactivity: bronchial smooth muscle is target cell type
Pulmonary edema: fluid accumulation in lung, reduces 02/Co2 exchange

39
Q

chronic effects (lung)

A

usually irreversible
Fibrosis: lungs get smaller and stiffer
Emphysema: lungs get larger and more stretchy, due to breakdown of lung elastin
Asthma:
Neoplasia: lung cancer (tobacco smoke, metallic ducts and fumes, asbestos, radon gas)

40
Q

dose-response relationships

A

Compare drug potencies and efficacies and to determine drug safety
To determine toxicity thresholds of xenobiotics

41
Q

Graded dose-response relationships

A

Show responses of individuals and are continuous responses
Y is usually percent response
Provides information about the intensity of response over a dose range
Compare potency and efficacy

42
Q

Quantal dose-response relationships

A

Show population responses and are all or none responses
Y is usually percent of individuals responding
Provides information about the number of individuals exhibiting a specified effect over a dose range
Used mainly to determine xenobiotic safety

43
Q

LD50

A

LD50: median lethal dose of dose causing death in 50% of population

44
Q

potency

A

the further left the more potent

45
Q

efficacy

A

the higher up the more efficient

46
Q

two main principles of animal toxicity tests

A

are applicable to humans
need to use higher doses to ensure that the response will occur frequently enough to be detected

47
Q

categories of toxicity tests

A

Acute lethality: 96 hour LD50
Skin and eye irritations tests:
Subacute toxicity tests: 14 day
Subchronic toxicity tests: Usually 90 days, two species, determine toxicity threshold
Chronic toxicity tests: 6 months to 2 years duration, Mainly used for carcinogenicity testing

48
Q

mutagenicity test

A

Ames Test
Somatic cell mutation: major concern is carcinogenesis
Germinal cell mutation: major concern is DNA damage

49
Q

biomarker

A

Measurable molecular, cellular, histological, physiological or
behavioural responses that provide evidence of either
exposure to, or effects of, toxicants

50
Q

biomarker examples

A

biomarkers of cancer risk (prostate-specific antigen
(PSA), breast cancer susceptibility protein (BRCA)
biomarkers of organ damage (ALT, AST, GGT, etc)
serum cholinesterase activity, CYP enzyme induction,
vitellogenin in male oviparous (yolk-bearing) vertebrates

51
Q

What makes a good biomarker

A

Sensitive
Specific to a specific class of toxicants
Easy to measure
Reproducible and reliable
Inexpensive
Non-invasive
Mechanistically-based
Time for response to occur following exposure
Permanence of response
Applicable to field studies; ideally validated in field

52
Q

bioindicator species

A

sentinel species
bioindicator species are also “early warning systems” for
human health risk

53
Q

What makes a good bioindicator species

A

Size: sufficiently large to allow adequate tissue/blood samples
Longevity: sufficiently long-lived to provide data over prolonged period and be able to accumulate toxicants
Availability: the organism should be abundant
Indigenous species are preferred since they are natural inhabitants of the area of concern
Sensitivity
Residency: ideally should be a year-round resident
Distribution: A broad geographical and ecological distribution is ideal so that comparisons can be made amongst regions
Type of contamination: aquatic vs. terrestrial vs. atmospheric

54
Q

Safety factor

A

100 (10x10)

55
Q

ADI

A

acceptable daily intake
an estimate of the amount of a chemical that can be ingested daily over a lifetime without appreciable health risk
food additives, pesticides and drugs

56
Q

TDI

A

tolerable daily intake
xenobiotics with no reason to be in food

57
Q

NOAEL

A

No-Observed-Adverse-Effect-Levels

58
Q

LOAEL

A

lowest observed adverse effect level

59
Q

Risk assessment

A

hazard identification
dose-response assessment
exposure assessment
risk characterization

60
Q

Risk

A

the probability of an adverse outcome

TOX 300 FINAL (4 decks)

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