Final exam select topics-plant and animal tox Flashcards
what are the 2 delayed onset muschroom toxins
amatoxins and orellanine
what are the 3 rapid onset muschroom toxins
ibotenic acid, muscimol, muscarine
what is the structure of amatoxins
octapeptides
are amatoxins head stable
yes
what is the mechanism of amatoxins (general)
inhibits protein synthesis
what are the 4 stages of amatoxins
- latent no symptoms (24h)
- GI
- apparently recooperation
- hepative failure, encephalopathy, renal failure
what is a way to help prevent further absorption of amatoxins
charcoal
what is the role of charcoal
prevent further amatoxins absorption
what does silibinin do
prevents toxin uptake by hepatocyte
what compound prevents toxin uptake in liver for amatoxins
silibinin
how do amatoxins accumulate in hepatocytes
non specific transporters
how does amatoxins cause centrilobar necrosis
disrupting P450 synthesis (so toxins can damage hepatocytes)
how is amatoxins dealt with in kidneys
filtered by glomerulus and reabsorbed in the tubules - causes acute tubular necrosis
which 3 locations are most hit by amatoxins and why
GIT liver and tubules because they need to constantly synthesize new proteins
what specifically does amatoxins target to cause mechanism
RNA pol 2 (very potent and specific)
how does amatoxins stop RNA pol 2
binds to bridge helix so it prevents polymerase from moving along DNA strand (it goes muchhhhhhhhhhh slower)
how do amatoxins reduce affinity for nucleotide triphosphates
it doesnt
what are the 2 phases for orellanine
pre renal (thirst, more urination and headache) renal (anuria)
where in the body is orellanine toxic to (what does it cause)
tubular epithelium - interstitial nephritis, edema, blood cell infiltration
what does orellanine cause the production of
orthosemiquinine anion radical and ROS + GSH deplretion
what is the mechanism of coprinus spp
inhibits aldehyde dehydrogenase irreversibally
is coprinus spp heat stable
yes
what happens with alcohol and coprinus spp consumption
acetaldehyde build up so feel sick
what is the mechanism of amanita muscaria
mAChR agonist
is amanita muscaria heat stable
yes
what is antivenin
antibody to spider bite
what is the main venim in spiders that can hurt us
alpha-latrotoxin
what does alpha-latrotoxin cause
massive NT release (DA, NA, GABA, glu) and maybe reuptake block
what is the mechanism of alpha-latrotoxin
binds to synaptic terminal proteins (neurexins and latrophilins) to cause NT release
what is the role of latrophillins
when it binds to alpha-latrotoxin, evoked Ca+ independent NT release
how does alpha-latrotoxin cause Ca+ independent NT release
when it binds to latrophillins
how does alpha-latrotoxin cause Ca+ dependent NT release
it can spontaneously insert itself into artificial lipid bilayers to form a cation selective channel (Ca++)
what kind of “mer” does alpha-latrotoxin form
tetramer
what does initial snail sting cause
mild local pain progresses into muscle paralysis
what happens later with snail sting
eyelid droop, blurred vision, speech difficulty, dyspnea, resp arrest, uncounscious
what are the 2 main types of venom in conotoxins
non-disulfide and disulfide rich peptides
what is the diff with non-disulfide and disulfide rich peptides for conotoxins
more SH makes them more rigid
what are 2 main types of targets with conotoxins
NT receptors, ion channels
what are the three types of cabals
lightning strike cabal, motor cabal and nirvana cabal
what is the mechanism of lightning strike cabal
inhibiting VG(Na)C from closing and blocking K+ channels - MASSIVE DEPOL
what is the results from inhibiting VG(Na)C from closing and blocking K+ channels (lightning strike cabal)
massive depol, repetitive firing, receptor desensitization
how many types of toxins are at least needed in the lightning strike cabal
2 because 1 that inhibits VGSC inactivation and one that blocks VGKC
what does motor cabal lead to
peptides distributed to circulatory system to inhibit NT transmission
does the motor or lightning strike cabal work faster
lighting oviB
what is the mechanism of motor cabal
block nAChR and presynaptive NT release via VGCC inhibition (block NT release and receptors)
what is the nirvana cabal
makes victims relaxed and sedated
what is the mechanism of nirvana cabal
NDMA glu R inhibition and Ca++ analgesia
what are 4 kinds of peptides that is in snake venom
neurotoxins, coagulants, hemorrhagins and hemolytics
what is crotamine
polypeptide myotoxin from rattlesnakes which induces hind limb paralysis
what is the mechanism of crotamine
blocks K+
how does crotamine enter the cell
via clathirin endocytosis
where does crotamine go when it enters the cell
ends up in lysosomes, nucleus in rapidly dividing cells
how does crotamine cause necrosis
burst lysosome with hydrolytic enzymes (there is also caspase 3 release)
