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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
proto-oncogenes
normally code for proteins associated with cell proliferation, mutation of proto-oncogene results in permanent activation and/or over-expression of gene products
26
neoplasia occurs
when proto-onogenes are converted to onxogenes
27
Proto-oncogenes and tumor suppressor genes
implicated in large number of human cancers P53 tumor suppressor gene: mutated in about half of all humans’ cancers
28
genotoxic characteristics
Mutagenic Can be complete carcinogens Tumorigencity is dose responsive No theoretical threshold
29
nongenotoxic characterisitics
Nonmutagenic Threshold, reversible Tumorigencity is dose responsive May function at tumor promotion stage No direct DNA damage Species, strain tissue specificity
30
Why is the liver susceptible to toxicity arising from xenobiotic exposure
1st pass effect enterohepatic cycling bioactivation xenobiotic binding proteins increased CYP enzymes (qualitative and quantitive) high blood flow altered energy homeostasis active transport
31
Steatosis
reversible effect ex. ethanol
32
necrosis
focal or massive ex. acetaminophen
33
chloestasis
yellowish tinge in skin and eyes ex. ethanol, certain metals, steroids
34
cirrhosis
extensive fibrosis throughout the liver ex. chronic ethanol consumption
35
major functions of kidney
excretion of metabolic wastes regulation of extracellular fluid volume electrolyte homeostasis acid-base balance blood pressure regulation metabolizes vitamin D to active form
36
Nephorotoxicants
Proximal convoluted tubule
37
sources of lung damage
Oxidative stress Gases and vapors Particles and aerosols (size is most important)
38
acute effects (lung)
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
chronic effects (lung)
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
dose-response relationships
Compare drug potencies and efficacies and to determine drug safety To determine toxicity thresholds of xenobiotics
41
Graded dose-response relationships
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
Quantal dose-response relationships
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
LD50
LD50: median lethal dose of dose causing death in 50% of population
44
potency
the further left the more potent
45
efficacy
the higher up the more efficient
46
two main principles of animal toxicity tests
are applicable to humans need to use higher doses to ensure that the response will occur frequently enough to be detected
47
categories of toxicity tests
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
mutagenicity test
Ames Test Somatic cell mutation: major concern is carcinogenesis Germinal cell mutation: major concern is DNA damage
49
biomarker
Measurable molecular, cellular, histological, physiological or behavioural responses that provide evidence of either exposure to, or effects of, toxicants
50
biomarker examples
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
What makes a good biomarker
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
bioindicator species
sentinel species bioindicator species are also “early warning systems” for human health risk
53
What makes a good bioindicator species
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
Safety factor
100 (10x10)
55
ADI
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
TDI
tolerable daily intake xenobiotics with no reason to be in food
57
NOAEL
No-Observed-Adverse-Effect-Levels
58
LOAEL
lowest observed adverse effect level
59
Risk assessment
hazard identification dose-response assessment exposure assessment risk characterization
60
Risk
the probability of an adverse outcome

TOX 300 FINAL (4 decks)

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