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60 Cards in this Set

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backtracking methodology
PCM--> gel electrophoresis
biomarkers
indicators of molecular/cellular events in biological systems

allow us to examine relationship btw environmental hazards and human health effects

exposure(internal/effective dose)
early effect(non-diseased biological response)
susceptibility(diff among individuals)
prognosis(predict disease outcome)
why do we need biomarkers?
detect effects long before disease

don't need big pop

mechanistic info can be obtained
biomarkers of exposure
monitor internal/effective doses received by person exposed to toxic chemical

measurement of chem, metabolites or rxn products to a target molecule
biomarkers of early effect
measure biological/biochemical changes in target cells/tissues
biological response markers
point mutations, cytogenetics(chromo damage)
biomarkers of susceptibility
indicators of genetic or acquired factors, existing before/independently of exposure
metabolomics
study of all metabolites that are present at any one moment in biofluid of org
biomarker tech
single cell sequencing to detect chromosome abs
exposure to benzene
petroleum refineries, factories, gasoline, automobile exhaust, diesel fuel, cigarette smoke
effect of benzene
<1ppm is associated w/ decreased WBCs, granulocytes, lymphocytes, b cells, platelets
causes of PBBs
nervous, immune systems liver, kidneys, thyroid gland disease in animals
Structure of PBBs, PCBs, PBDE
209 theoretically possible congeners
Routes of exposure for flame retardant chemicals
inhale/ingest
esp fish
breast milk
Neurodeveopmental outcomes of flame retardants
decreased memory, learning

hyperactivity
endocrine disruption from flame retardants
alter brain development of young children

decreased thyroid hormone levels

hyperthyroidism
reproductive system effects from flame retardants
delayed puberty, abnormal gonadal development, decreased sperm counts, abnormal sperm function
non-cancer effects of benzene
hematotoxicity
neurotoxicity
immunotoxicity
reproductive toxicity
developmental toxicity
IARC classification
1. Carcinogenic
2A. probably carcinogenic
2B. possibly carcnigenic
3. not classifiable
4. probably no carcinogenic
genomics
genome sequence allows for study of human genetic variation
transcriptomics
studies gene expression by measuring RNA levels from all genes
proteomics
studies all proteins that are expressed using mass spectrometry
metabonomics
metabolites in body fluids studied by NMR and pattern recognition technology
cDNA MicroArrays
based on analysis of RNA extracted from targeted cells
acute poisoning of arsenic
nausea/vomit
diarrhea
hemolysis
shock
death
chronic exposure of arsenic
vascular disease
skin lesions
cancer
diabetes
lung disease
reproductive effects
cognitive effects in children
effects chronic arsenic ingestion
skin cancer
bladder cancer
lung cancer-only agent linked to lung cancer following ingestion
neoplasm
heritably altered, relatively autonomous growth-can be benign or malignant
phases of cancer
initiation(mutation)
promotion
progression
steps in chem carcinogenesis
precarcinogen
activated
initiation
promotion
progression
metastatic cancer
p53
tumor supressor
promotion
must be prolonged
proliferation of initiated cells
no further changes in dna

caused by abnormal responses to hormones

caused by continuous exposures to hormones that induce toxic stress
progression
metastasis

further mutations in genes that control body's defenses to tumor cells/development of new blood vessels for tumor

promoted cells now sensitive to weak mutagens
dietary carcinogens
PAA-fried meats
PAH-broiled, smoked meat, oil
Aflatoxins-peanuts, corn
nitroamines
pyrolizidines
safrole
hydrazines
anticarcinogens
citrus oils
polyphenols
DIM
lycopene
allysulfides
isoflavones
hormesis
exposure to low dose of agent that is toxic at higher doses induces beneficial effect

ex: ischemic precondition, phytochemicals
Nrf2
regulates NADPH synthesis, drug excretion DNA repair
opiates
morphine-->diacetylmorphine-->heroin
black tar heroin
impure
produced in Mexico
western US
cocaine
initially feel sick
stimulant
binding/inactivating dopamine transporters, blocks dopamine re-uptake. increased dopamine levels activate dopamine receptors
Marijuana
hallucinogen, depressant
increase heart rate, decrease blood pressure

stimulates appetite

active ingredient delta-9-THC
natural ligand for THC receptor
anandamide-pain sensations, memory regulation, food intake, immune system
heavy cannabis users exhibit what behavior?
psychosis=delusions, hallucinations
heroin
mimics natural endorphins

in brain heroin is converted to morphine which binds to opioid receptors-->increased dopamine
reward area of the brain
nucleus accumbens increased activity by increased dopamine transmission
paracelsus
described clinical manifestations of Arsenic/Mercury poisoning
toxic substances control act was passed by who?
EPA
critical components of a dose
duration of exposure
G-E interactions
berylium induced lung disease/HLA-DPB1

smoking+NAT2

organophosphate tox+ PON

benzene hematotoxicity+ NQO1
cDNA microarrays
analysis of RNA extracted from target cells

made from RNA using RT

ID changes in pattern of gene expression associated w/ specific exposure
2ppm
2000mcg/L
if dose exceeds threshold dose
unsafe
Woburn childhood leukemia
Trichloroetheylene
not source of TCE
automobile exhaust
TCE
2A
exposure: dry cleaning, water, metal degreasing
not arsenic exposure
shoe/glue factories
population mixing
changes patter of infection in children
PhIP
produced by cooking fatty red meat

must be activated by body's detox enzymes to form adducts w/ DNA
benzene in air
1ppm
who is likely to get affected by benzene exposure the most
person w/ MPO and NQO1 polymorphism