Final exam select topics-neurotox Flashcards
neuropathy
irreversible death, apoptosis, necrosis (only some myelin left, no axon)
axonopathy + where repaired
repaired in PNS not CNS, change in cell body too
myelinopathy + where repaired
some repaired in PNS not CNS, slows conduction
nissl substance
clusters of ribosomal complex
what disease foes trimethyltin chloride make
limbic-cerebellar syndrome (neuropathy)
what is a main way that trimethyltin chloride causes limbic-cerebellar syndrome (neuropathy)
stannins
what are stannins + where are they
proteins associated with ER and mito
where are high levels of stannins
limbic cerebellar areas, hippo amyg
what do stannins contain
cytoplasmic metal binding domain
how does trimethyltin chloride affect stannins
they bind, causes Ca++ flux then initiates apoptosis
what does rayon and CS2 cause (simple)
axonopathy
what does CS2 do generally
modified proteins
who does CS2 cause irreversible damage to
amino groups (draw it out)
who does CS2 cause reversible damage to
sulfhydryl groups (draw it out)
what are 2 CS2 markers
valine-lysine and lysine-lysine thiourea
where does lysine-lysine thiourea happen
globin
where does valine-lysine thiourea happen
spectrin
what reaction happens to form acrylamide (what 2 things join)
asparagines and reducing sugars (Maillard reaction)
how is acrylamide metabolized + what into
CYP2E1 into glycidamide
what is the deal with glycidamide
its a much stronger electrophile than acrylamide (can modify proteins, DNA)
what happens to glycidamide
it is converted into glyceramide (non toxic) or detoxed by GSH
so what are the 2 compounds in order that acrylamide can become
glycidamide then glyceramide
what are the steps to make acrylamide (think maillard, 4 steps)
- asparagine and reducing sugar join
- water loss to make Schiff base
- amadori rearrangement to make amadori compound
- amadori loses CO2 to make acrylamide
what is the main acrylamide toxicity (1 main thing)
forms adducts with proteins, esp with SH groups
