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60 Cards in this Set
- Front
- Back
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backtracking methodology
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PCM--> gel electrophoresis
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biomarkers
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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) |
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why do we need biomarkers?
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detect effects long before disease
don't need big pop mechanistic info can be obtained |
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biomarkers of exposure
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monitor internal/effective doses received by person exposed to toxic chemical
measurement of chem, metabolites or rxn products to a target molecule |
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biomarkers of early effect
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measure biological/biochemical changes in target cells/tissues
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biological response markers
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point mutations, cytogenetics(chromo damage)
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biomarkers of susceptibility
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indicators of genetic or acquired factors, existing before/independently of exposure
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metabolomics
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study of all metabolites that are present at any one moment in biofluid of org
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biomarker tech
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single cell sequencing to detect chromosome abs
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exposure to benzene
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petroleum refineries, factories, gasoline, automobile exhaust, diesel fuel, cigarette smoke
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effect of benzene
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<1ppm is associated w/ decreased WBCs, granulocytes, lymphocytes, b cells, platelets
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causes of PBBs
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nervous, immune systems liver, kidneys, thyroid gland disease in animals
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Structure of PBBs, PCBs, PBDE
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209 theoretically possible congeners
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Routes of exposure for flame retardant chemicals
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inhale/ingest
esp fish breast milk |
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Neurodeveopmental outcomes of flame retardants
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decreased memory, learning
hyperactivity |
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endocrine disruption from flame retardants
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alter brain development of young children
decreased thyroid hormone levels hyperthyroidism |
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reproductive system effects from flame retardants
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delayed puberty, abnormal gonadal development, decreased sperm counts, abnormal sperm function
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non-cancer effects of benzene
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hematotoxicity
neurotoxicity immunotoxicity reproductive toxicity developmental toxicity |
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IARC classification
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1. Carcinogenic
2A. probably carcinogenic 2B. possibly carcnigenic 3. not classifiable 4. probably no carcinogenic |
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genomics
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genome sequence allows for study of human genetic variation
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transcriptomics
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studies gene expression by measuring RNA levels from all genes
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proteomics
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studies all proteins that are expressed using mass spectrometry
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metabonomics
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metabolites in body fluids studied by NMR and pattern recognition technology
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cDNA MicroArrays
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based on analysis of RNA extracted from targeted cells
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acute poisoning of arsenic
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nausea/vomit
diarrhea hemolysis shock death |
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chronic exposure of arsenic
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vascular disease
skin lesions cancer diabetes lung disease reproductive effects cognitive effects in children |
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effects chronic arsenic ingestion
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skin cancer
bladder cancer lung cancer-only agent linked to lung cancer following ingestion |
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neoplasm
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heritably altered, relatively autonomous growth-can be benign or malignant
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phases of cancer
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initiation(mutation)
promotion progression |
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steps in chem carcinogenesis
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precarcinogen
activated initiation promotion progression metastatic cancer |
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p53
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tumor supressor
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promotion
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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 |
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progression
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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 |
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dietary carcinogens
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PAA-fried meats
PAH-broiled, smoked meat, oil Aflatoxins-peanuts, corn nitroamines pyrolizidines safrole hydrazines |
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anticarcinogens
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citrus oils
polyphenols DIM lycopene allysulfides isoflavones |
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hormesis
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exposure to low dose of agent that is toxic at higher doses induces beneficial effect
ex: ischemic precondition, phytochemicals |
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Nrf2
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regulates NADPH synthesis, drug excretion DNA repair
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opiates
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morphine-->diacetylmorphine-->heroin
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black tar heroin
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impure
produced in Mexico western US |
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cocaine
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initially feel sick
stimulant binding/inactivating dopamine transporters, blocks dopamine re-uptake. increased dopamine levels activate dopamine receptors |
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Marijuana
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hallucinogen, depressant
increase heart rate, decrease blood pressure stimulates appetite active ingredient delta-9-THC |
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natural ligand for THC receptor
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anandamide-pain sensations, memory regulation, food intake, immune system
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heavy cannabis users exhibit what behavior?
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psychosis=delusions, hallucinations
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heroin
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mimics natural endorphins
in brain heroin is converted to morphine which binds to opioid receptors-->increased dopamine |
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reward area of the brain
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nucleus accumbens increased activity by increased dopamine transmission
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paracelsus
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described clinical manifestations of Arsenic/Mercury poisoning
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toxic substances control act was passed by who?
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EPA
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critical components of a dose
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duration of exposure
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G-E interactions
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berylium induced lung disease/HLA-DPB1
smoking+NAT2 organophosphate tox+ PON benzene hematotoxicity+ NQO1 |
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cDNA microarrays
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analysis of RNA extracted from target cells
made from RNA using RT ID changes in pattern of gene expression associated w/ specific exposure |
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2ppm
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2000mcg/L
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if dose exceeds threshold dose
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unsafe
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Woburn childhood leukemia
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Trichloroetheylene
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not source of TCE
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automobile exhaust
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TCE
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2A
exposure: dry cleaning, water, metal degreasing |
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not arsenic exposure
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shoe/glue factories
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population mixing
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changes patter of infection in children
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PhIP
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produced by cooking fatty red meat
must be activated by body's detox enzymes to form adducts w/ DNA |
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benzene in air
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1ppm
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who is likely to get affected by benzene exposure the most
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person w/ MPO and NQO1 polymorphism
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