Final exam select topics-plant and animal tox

Question 1

what are the 2 delayed onset muschroom toxins

Answer 1

amatoxins and orellanine

Question 2

what are the 3 rapid onset muschroom toxins

Answer 2

ibotenic acid, muscimol, muscarine

Question 3

what is the structure of amatoxins

Answer 3

octapeptides

Question 4

are amatoxins head stable

Answer 4

yes

Question 5

what is the mechanism of amatoxins (general)

Answer 5

inhibits protein synthesis

Question 6

what are the 4 stages of amatoxins

Answer 6

• latent no symptoms (24h)
• GI
• apparently recooperation
• hepative failure, encephalopathy, renal failure

Question 7

what is a way to help prevent further absorption of amatoxins

Answer 7

charcoal

Question 8

what is the role of charcoal

Answer 8

prevent further amatoxins absorption

Question 9

what does silibinin do

Answer 9

prevents toxin uptake by hepatocyte

Question 10

what compound prevents toxin uptake in liver for amatoxins

Answer 10

silibinin

Question 11

how do amatoxins accumulate in hepatocytes

Answer 11

non specific transporters

Question 12

how does amatoxins cause centrilobar necrosis

Answer 12

disrupting P450 synthesis (so toxins can damage hepatocytes)

Question 13

how is amatoxins dealt with in kidneys

Answer 13

filtered by glomerulus and reabsorbed in the tubules - causes acute tubular necrosis

Question 14

which 3 locations are most hit by amatoxins and why

Answer 14

GIT liver and tubules because they need to constantly synthesize new proteins

Question 15

what specifically does amatoxins target to cause mechanism

Answer 15

RNA pol 2 (very potent and specific)

Question 16

how does amatoxins stop RNA pol 2

Answer 16

binds to bridge helix so it prevents polymerase from moving along DNA strand (it goes muchhhhhhhhhhh slower)

Question 17

how do amatoxins reduce affinity for nucleotide triphosphates

Answer 17

it doesnt

Question 18

what are the 2 phases for orellanine

Answer 18

pre renal (thirst, more urination and headache)
renal (anuria)

Question 19

where in the body is orellanine toxic to (what does it cause)

Answer 19

tubular epithelium - interstitial nephritis, edema, blood cell infiltration

Question 20

what does orellanine cause the production of

Answer 20

orthosemiquinine anion radical and ROS + GSH deplretion

Question 21

what is the mechanism of coprinus spp

Answer 21

inhibits aldehyde dehydrogenase irreversibally

Question 22

is coprinus spp heat stable

Answer 22

yes

Question 23

what happens with alcohol and coprinus spp consumption

Answer 23

acetaldehyde build up so feel sick

Question 24

what is the mechanism of amanita muscaria

Answer 24

mAChR agonist

Question 25

is amanita muscaria heat stable

Answer 25

yes

Question 26

what is antivenin

Answer 26

antibody to spider bite

Question 27

what is the main venim in spiders that can hurt us

Answer 27

alpha-latrotoxin

Question 28

what does alpha-latrotoxin cause

Answer 28

massive NT release (DA, NA, GABA, glu) and maybe reuptake block

Question 29

what is the mechanism of alpha-latrotoxin

Answer 29

binds to synaptic terminal proteins (neurexins and latrophilins) to cause NT release

Question 30

what is the role of latrophillins

Answer 30

when it binds to alpha-latrotoxin, evoked Ca+ independent NT release

Question 31

how does alpha-latrotoxin cause Ca+ independent NT release

Answer 31

when it binds to latrophillins

Question 32

how does alpha-latrotoxin cause Ca+ dependent NT release

Answer 32

it can spontaneously insert itself into artificial lipid bilayers to form a cation selective channel (Ca++)

Question 33

what kind of "mer" does alpha-latrotoxin form

Answer 33

tetramer

Question 34

what does initial snail sting cause

Answer 34

mild local pain progresses into muscle paralysis

Question 35

what happens later with snail sting

Answer 35

eyelid droop, blurred vision, speech difficulty, dyspnea, resp arrest, uncounscious

Question 36

what are the 2 main types of venom in conotoxins

Answer 36

non-disulfide and disulfide rich peptides

Question 37

what is the diff with non-disulfide and disulfide rich peptides for conotoxins

Answer 37

more SH makes them more rigid

Question 38

what are 2 main types of targets with conotoxins

Answer 38

NT receptors, ion channels

Question 39

what are the three types of cabals

Answer 39

lightning strike cabal, motor cabal and nirvana cabal

Question 40

what is the mechanism of lightning strike cabal

Answer 40

inhibiting VG(Na)C from closing and blocking K+ channels - MASSIVE DEPOL

Question 41

what is the results from inhibiting VG(Na)C from closing and blocking K+ channels (lightning strike cabal)

Answer 41

massive depol, repetitive firing, receptor desensitization

Question 42

how many types of toxins are at least needed in the lightning strike cabal

Answer 42

2 because 1 that inhibits VGSC inactivation and one that blocks VGKC

Question 43

what does motor cabal lead to

Answer 43

peptides distributed to circulatory system to inhibit NT transmission

Question 44

does the motor or lightning strike cabal work faster

Answer 44

lighting oviB

Question 45

what is the mechanism of motor cabal

Answer 45

block nAChR and presynaptive NT release via VGCC inhibition (block NT release and receptors)

Question 46

what is the nirvana cabal

Answer 46

makes victims relaxed and sedated

Question 47

what is the mechanism of nirvana cabal

Answer 47

NDMA glu R inhibition and Ca++ analgesia

Question 48

what are 4 kinds of peptides that is in snake venom

Answer 48

neurotoxins, coagulants, hemorrhagins and hemolytics

Question 49

what is crotamine

Answer 49

polypeptide myotoxin from rattlesnakes which induces hind limb paralysis

Question 50

what is the mechanism of crotamine

Answer 50

blocks K+

Question 51

how does crotamine enter the cell

Answer 51

via clathirin endocytosis

Question 52

where does crotamine go when it enters the cell

Answer 52

ends up in lysosomes, nucleus in rapidly dividing cells

Question 53

how does crotamine cause necrosis

Answer 53

burst lysosome with hydrolytic enzymes (there is also caspase 3 release)