tox test 2 Flashcards
cancer
2nd most common death in the u.s men-prostate,lung,colorectal women-breast,lung,colorectal cancer death rate is lower and survival rate higher sir Percivall Pott (chimney sweeps)
IARC (international agency for research on cancer)
identifies carcinogens into five groups
tumor
solid mass of cancer cells
benign tumor
not potentially lethal
malignant
potentially spread and kill
Staging
looking at a biopsy to see how advanced and how much (put into a 1-4 category T1-T4)
Gleason scale
1-10(12) the lower the better they compare normal cancer to biopsy
carcinogenesis
process which cancer develops
mutational theory
most accepted theory in three phases
- initiation
- promotion
- progression
initiation
damage to DNA random or induced
transformed into neoplastic cell
promotion
further cellular changes leading to a tumour (monoclonal)
can involve promoters to stimulate cell division
progression
tumour becomes malignant
metastasis
carcinogens
agent/factor that causes cancer
genetic carcinogen
have damage to DNA (chemical/virus/radiation insert into DNA)
epigenetic carcinogens
some place other than DNA (normally affecting proteins)
procarcinogens
some carcinogens must be activated before they are carcinogenic
Alkylation of DNA bases
covalent bond formed between base and alkyl group(added)
base pairing becomes impaired and mistakes happen during replication by DNA polymerase
Dioxin
- DIrty dozen
- binds to cytosolic receptor protein; complex moves to the nucleus, binds to a DNA receptor binding site induces transcription of the gene for arylhydrocarbon hydroxylase (AH) and other genes)
Methyltransferase enzymes
repair damage DNA by removing methyl groups from Guanine
Nucleotide excision repair systems
- endonucleases
- open DNA strand to allow removal of the damages or mispaired base.
polymerase
insert correct base
Ligase
reseals the strand
Mismatch repair
-everyone has mismatches
recognizes and corrects incorrectly paired bases
Ames test
tests for mutagenicity (uses bacteria to test if chemical can cause mutations in DNA)
not every mutagen is a carcinogen
threshold model
a small dose can be beneficial
dose that begins to show effect
non-threshold model
based on biological responses at high radiation doses and dose rates
testes
sperm formation begins at puberty
tight junctions (blood testis barrier)
between adjacent sertoli cells of the SI tubules
- provides limited protection
- testes have P450 activity making it stuff more lethal
sperm production
can be inhibited, lower sperm counts, or be deformed
SI epithelium
can be injured or destroyed
Affects energy in Sertoli cells
ex. Phthalates, m-DNB, DNT
Heavy metals
Pb (lead) and Cd (cadmium) cause infertility, chromosome damage, testicular necrosis
ethanol
delays testicular development
damage to oocytes
anthineoplastics agents, heavy metals, PAH’s, radiation, tobacco, pesticides, chlorinated hydrocarbons, aromatic solvents
theo colborn
“our stolen future” (1996)
Enviromental estrogens
low concentration in the environment
endocrine disruptor
chemical that mimics or disrupts hormone
anabolic steroids
decrease male fertility