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PHAR 303 (toxicology) > Neurotoxicology > Flashcards

Neurotoxicology Flashcards

final exam

1
Q

major poison in hemlock

A

coniine

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2
Q

mechanism/effect of coniine

A
  • first stimulates then blocks nicotinic receptors
  • so, leads to bradycardia (slowing of heart rate), ascending paralysis (b/c blocking nicotinic in periphery), coma (extension to paralysis, but everywhere), and death.
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3
Q

many plant poisons are a variant of _____

A

nicotine

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4
Q

most toxins found in living creatures are __________

A

neurotoxins

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5
Q

why where neurotoxins developed in living creatures (e.g. plants)?

A
  1. self-protection: other organisms don’t eat them since recognized as toxic
  2. attack mechanism: neurotoxins can paralyze/harm others, allowing the plant to consume it.
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6
Q

top 6 hazardous substances

A
  1. arsenic
  2. lead
  3. mercury
  4. vinyl chloride
  5. polychlorinated bisphenols
  6. benzene
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7
Q

what are advantages and disadvantages of animal/rat studies for neurotoxicology?

A

advantage: can help assess developmental/behavioral neurotoxicity, harder to do in vitro
disadvantage: difficult to extrapolate from for more subtle neurotoxic effects (e.g. mood and intellect)

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8
Q

major advantage of using human induced pluripotent cells (iPSCs)

A
  • can be induced to differentiate into any type of neuron, so can analyze how different neural cells types will react with the neurotoxin.
  • can also observe synapse formation process, which can give insight on neurodevelopmental toxicity.
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9
Q

what do nerve growth assays tell us?

A

help visualize the effect of a toxin on neuron growth

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10
Q

what do automated testing systems help us do?

A

identify neurotoxins based on neuronal growth

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11
Q

Acute vs chronic toxicity testing (showing causation)

A

acute: easier to establish and show causation – can be studies in rat models
chronic: harder to establish causation since looking at subtle things over a long period of time – rats can be used, but imaging in people is preferred since there aren’t any confounding factors.

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12
Q

what are whole animal endpoints that can be studied?

A
  • cognitive function (memory, learning, confusion)
  • motor function (weakness, convulsion, paralysis)
  • sensory function (vision, hearing, touch, balance)
  • mood and personality
  • general effects (loss of appetite, overall fatigue)
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13
Q

what is a major difficult when studying whole animal enpoints?

A

neural plasticity and extra neurons may mask the toxicity for years (so hard to properly identify risks in epidemiology studies)

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14
Q

what other non-whole organism endpoints can be used to study neurotoxicity?

A
  • structure of the neuron
  • dendritic branching
  • specific structures in the brain
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15
Q

what different pathologies of the neuron can be seen?

A

neuropath, axonopathy, myelopathy, transmission

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16
Q

neuropathy

A

the entire neuron is destroyed and cannot be replaced (loss of the cell body is final)

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17
Q

axonopathy

A

only the axon is injured; peripheral Schwann cells can mediate axonal growth

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18
Q

myelopathy

A

only the myelin is injured; if the axon is still intact, the sheath can grow back

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19
Q

transmission neuron pathology

A

blocking the transmission (from blocking of Na channels, so Na-induced depolarization is stopped); with time, repairs can take place

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20
Q

how is dendritic branching affected in various pathologies?

A

decreased

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21
Q

branches of the nervous system

A
  • peripheral nervous system (PNS)
  • autonomic nervous system (ANS)
  • central nervous system (CNS) – brain and spinal cord
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22
Q

how is the CNS protected?

A
  • brain: by BBB, skull, meninges
  • spinal cord: vertebrae
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23
Q

properties of the BBB and how toxicants can affect it/interact with it

A
  • has tight junction between endothelial cells
  • capillary has foot processes of the astrocytes surrounding it, adding transportation control
  • toxicants can either interfere with the permeability or can make use of transportation pathways to get in.
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24
Q

role of the CSF

A

cushions the CNS from harsh impacts

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25
Q

role of the cerebrospinal fluid barrier

A

protect against various toxins from getting into the CNS

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26
Q

what is the CSF/what is it made up of?

A

made by choroid plexus, which has a barrier, of ventricles, flows through the brain and is drained by arachnoid villi (and returned to venous side of circulation)

27
Q

cells of the nervous system

A
  • neurons
  • small blood vessels
  • astrocytes
  • glial cells: microglia and oligodendrocytes
  • endothelial cells
28
Q

role of astrocytes

A

housekeeping and nurturing cells – control the microenvironment around the neuron

29
Q

role of glial cells (generally)

A
  • maintenance of the structure of the nervous system
30
Q

role of microglia

A
  • patrol the neuronal environment for foreign substances (like phagocytes)
  • have pattern recognition receptors, which can recognize many PAMPs
  • release free radicals and trigger inflammation
31
Q

role of oligodendrocytes

A

mediate production of myelin (can myelinate several different CNS axons)

32
Q

role of endothelial cells in the NS

A

keep foreign substances out of the brain

33
Q

effect/mechanism of carbon monoxide

A

interferes with aerobic metabolism:
- blocks ability of Hb to transport oxygen
- brain cannot supply itself with enough energy, leading to cell death
- neuronal cells die very quickly due to high energy demand

34
Q

effect/mechanism of manganese

A

interferes with protein folding:
- cause protein misfolding
- other effects such as receptor dysfunction and inflammation

35
Q

what is MPTP

A

a by-product of attempts to synthesize a psychoactive opioid compound

36
Q

effect/mechanism of MPTP

A

interferes with intermediate metabolism:
- taken up by astrocytes, where MAOs in the cell convert it to MPP+
- MPP+ taken up by dopamine transporters (especially in substantia nigra)
- can interact with and destroy mitochondria
- ATP production stopped so leads to neuronal death

37
Q

where does tetrodotoxin come from?

A

pufferfish

38
Q

tetrodotoxin effect/mechanism

A

alter electrical transmission along the cell membrane:
- block voltage-gated sodium channels
- blocks propagation of AP
- leads to paralysis and death

39
Q

sodium channel blockers (toxins)

A
  • tetrodotoxin (pufferfish)
  • conotoxin (cone shell)
  • scorpion venom
  • batrachotoxin (poison dart frogs + insects)
40
Q

effect/mechanism of vinca alkaloids

A

interfere with axonal transport:
- prevent tubulin formation by binding tubulin monomers
- prevent microtubule formation, blocking effective axonal transport

41
Q

where was hexachlorophene found?

A

disinfectants in hospitals (not anymore)

42
Q

effect/mechanism of hexachlorophene

A

damage to myelin sheath:
- cause demyelination and myelin edema via damage to Schwann cells and oligodendrocytes
- slows transmission of AP, but can also harm health axon

43
Q

where was hexane found?

A

used as solvent in glue (children would breath it in to get high)

44
Q

effect of hexane

A

a diketone metabolite in hexane disrupts the crosslinks in the axonal cytoskeleton, causing axonopathy (in periphery first then goes central)

45
Q

where can arsenic be found/how was it used?

A
  • can be found naturally in ground and water
  • was used to treat wood, so was found in playgrounds.
46
Q

effect of arsenic

A

induce peripheral neuropathy, so symptoms follow a stocking-glove pattern since start at outer extremities before leading to death

47
Q

where is methanol found

A

part of rubbing alcohol and commonly used as a chemical solvent

48
Q

effect of methanol

A
  • converted by ADH to formaldehyde then to formic acid by ALDH
  • formic acid can damage nervous system (cerebral cortex, cerebellum, retina (blindness))
49
Q

what to do when someone ingests methanol? why?

A

give ethanol since will compete for site on ADH and ALDH so will reduce amount of metabolite

50
Q

ways that toxins can interfere with synaptic transmission (pre and postsynaptic)

A

presynaptic:
- direct: increase or decrease transmitter release
- indirect: synaptic modulation
postsynaptic:
- prevent neurotransmitter inactivation or reuptake
- act as direct agonist or antagonist for postsynaptic receptors

51
Q

discarded plastics degrade into ______ and ________

A

microplastics (<5um) and nano-plastics (<1um)

52
Q

characteristic of microplastics

A

bioaccumulate

53
Q

microplastic source and route of exposure

A
  • in air (inhalation)
  • in food (ingestion)
  • can be absorbed dermally
54
Q

what is the Trojan-horse effect in the context of microplastics?

A

can mask the presence of other contaminants/pathogens, permitting them access into different organs they normally could not access

55
Q

effects of microplastics (on brain)

A
  • can mask pathogen/contaminants that can cause neuroinflammation or can modulate brain activity that can lead to behavior changes
  • modify gut microbiome; can affect gut-brain axis
56
Q

process of toxic algae bloom

A

bloom periodically:
- in between blooms, algae cysts settle on ocean floor
- when blooming, algae rise to surface, multiplying and releasing their toxin
- then they settle to ocean floor

57
Q

where does domoic acid come from

A

produced by pseudo-nitzschia, a marine algae

58
Q

property of domoic acid

A

heat-stable and can bioaccumulate

59
Q

effect/mechanism of domoic acid

A
  • act on excitatory pre- and postsynaptic glutamate receptors (Kainate glutamate receptors) – is structurally similar to glutamic acid
  • prolongs opening of the sodium channel – more frequent opening of calcium channel, so more neurotransmitter release
  • can lead to seizures and neuronal death
60
Q

what are some regulation to protect humans and the environment against domoic acid?

A

human:
- international safety level
- monitoring programs in seafood and waters
no environmental regulation, and still a big issue for wildlife
- in California, perform gastric lavage to sea lions to protect them

61
Q

what are some proposed reasons for the domoic acid crisis?

A
  • higher level of international transport (some think that transported water bring algae to areas they didn’t thrive before0
  • climate change (change in temperature permit them to grow in new places)
62
Q

effect of okadaic acid (produced by algae)

A

diarrhetic shellfish poisoning

63
Q

effect of saxitoxin (produced by algae)

A

block sodium channels, cause paralytic shellfish poisoning

64
Q

effect of brevetoxin (produced by algae)

A

activate sodium channels, causing neurotoxicity in shellfish

PHAR 303 (toxicology) (14 decks)

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