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Cell Biology > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

Epigenetics (def)

A

DNA expression w/o change in DNA structure caused by external/environmental factors
-can be heritable
-allows for differing cell types (w/ same DNA)

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2
Q

Diethylstilbestrol

A

Potent estrogen drug
Given for miscarriage prevention
= modified child epigenome & reproductive abnormalities

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3
Q

DNA methylation

A

gene silencing
methyl groups added to histone tails

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4
Q

DNA methylation process

A

CpG methylation (cytosine-phosphate-guanine)
Methyltransferase adds methyl group = 5-methylcytosine
RNA polymerase cannot bind = gene silencing
HDACs recruited –> chromatin condenses! (heterchromatin)

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5
Q

Histone modifications

A

Methylation
Acetylation
Phosphorylation

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6
Q

Histone tail structure

A

amino acids | positively charged
Modified histones –> neutralized charge

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7
Q

Histone Methylation

A

Increase or decrease transcription (depend on number and what is methylated- multiple histone tails can be methylated)
-Arginine (R) & Lysine (K)

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8
Q

Methylation Process

A

histone methyltransferase adds methyl groups
= increase or decrease gene transcription

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9
Q

Acetylation

A

promotes transcription
neutralizes DNA charge
loosens DNA (euchromatin)

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10
Q

Acetylation Process

A

HATs (histone acetyltransferases) remove methyl and adds acetyl groups = change proteins produced

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11
Q

Phosphorylation

A

decrease transcription (condense DNA=heterchromatin)
Can be phosphorylated- Serine | Threonine | Tyrosine

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12
Q

Phosphorylation Process

A

phosphate groups added by kinases/phosphatases

Aurora B: condenses chromatin (heterochromatin)
Protein kinase: de-condense (euchromatin)

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13
Q

What epigenetics is cancer associated with?

A

unmethylated cytosines | acetylated histones
High oncogene expression
deacetylated histones | methylated cytosines
Low tumor suppressor genes

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14
Q

Oncogene (def)

A

overactive/expressed mutated gene form
cancer accelerator

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15
Q

Proto-oncogenes

A

normal gene involved with cell growth

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16
Q

Oncogene example

A

Ras point mutation

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17
Q

Tumor Suppressor Genes (def)

A

slow cell growth | assist in DNA repair
cancer decelerator

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18
Q

Tumor Suppressor Gene Example (which leads to cancer)

A

P53 protein stops cell cycle
cells replicate w/ mutated DNA = cancer
Caused by heat, radiation, chemicals

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19
Q

Tumor Cell Lines (def)

A

Tumor cells will grow in petri dish, unlike normal cell which die

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20
Q

HDAC inhibitors

A

cancer treatment
drug which kills cancer cell lines
effect in Mast Cell Tumor

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21
Q

RNAi (def)

A

RNA interference
inhibits specific mRNA which decreases protein expression
Types: siRNA | shRNA | miRNA

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22
Q

siRNA (def)

A

small interference RNA
silences protein

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23
Q

siRNA structure

A

double-stranded | 20-25 nucleotides | exogenous | degrades quickly

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24
Q

siRNA process

A

AGO protein complex peels passenger (sense) strand –> becomes RISC
RISC breaks up mRNA = silencing
in cytosol

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25
Q

What RNAi silences FVR (feline herpesvirus 1) & how?

A

siRNA
targets viral protein D required for FVR replication = silencing

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26
Q

shRNA (def)

A

short hairpin RNA
central section of RNA “folds over”

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27
Q

shRNA structure

A

1 stranded and folds to 2 stranded RNA
exogenous | long-lasting

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28
Q

shRNA process

A

Dicer chops “hairpin” part = silence mRNA
constantly reproduced so long-lasting
in cytosol

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29
Q

Ago

A

Argonaut
Protein complex used in silencing process of siRNA to peel off passenger (sense) strand

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30
Q

RISC

A

RNA-induced silencing complex
breaks up mRNA for silencing in siRNA

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31
Q

Explain shRNA in cattle / texel sheep

A

Myostatin inhibits muscle growth in cattle
Mutation of myostatin (shRNA) = big muscles!

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32
Q

miRNA (def)

A

micro-RNA
targets several mRNAs for silencing

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33
Q

miRNA structure

A

target several mRNAs
endogenous | long RNA precursors (pri-miRNA)

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34
Q

miRNA process

A

made in nucleus –> transported to cytosol
pri-miRNA –> pre-miRNA by Drosha
Dicer chops off hairpin
mRNA degraded either by cleaving or suppressing during translation = silencing

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35
Q

Common diseases with miRNA

A

cancer
neurodegenerative
cardiovascular
viral infections

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36
Q

Explain miRNA’s role in Canine Mammary Cancer

A

miRNA-21 decreases tumor suppressors
miRNA-15a decreases oncogenes
=cancer

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37
Q

Pros/Cons of using RNAi for therapeutic purposes

A

Pros: more specificity than chemical drugs
Cons: price | delivery

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38
Q

Antagomirs

A

inhibit miRNAs that are causing issues (ie cancer)

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39
Q

3 Types of Antagomirs

A

Inhibitors
Sponges
Masks

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40
Q

Inhibitor (Antagomir type)

A

floods cells with passenger strands to take up the guide strands so miRNA cannot bind

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41
Q

Sponges (Antagomir type)

A

synthetic RNA used as “decoy” to soak up complexes (miRNA cannot cause effect)

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42
Q

Masks (Antagomir type)

A

Bind to target sequence on mRNA but w/o Arg
Act like “receptor-blocker” so miRNA cannot bind

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43
Q

Gene Therapy (def)

A

introduces new genes to restore or add gene expression

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44
Q

What disease is a good candidate for gene therapy and why?

A

Neuronal Ceroid Lipofuscinosis
only single nucleotide deletion

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45
Q

Forms/Modes of Gene Therapy

A

Direct
Cell-Based

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46
Q

Direct (form of gene therapy)

A

Inject DNA that encodes for a protein

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47
Q

Cell-Based aka indirect (form of gene therapy)

A

inject DNA into petri dish cells, then patient
use cells from same patient to prevent immune response

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48
Q

Types of Gene Therapy

A

Somatic gene therapy
Germline gene therapy

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49
Q

Somatic Gene Therapy

A

DNA transferred to patient only
no effect on progeny

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50
Q

Germline Gene Therapy

A

DNA transferred to eggs/sperm
passed to progeny (permanent)

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51
Q

Gene Therapy Process

A

Cut & open plasmid
insert DNA and make protein

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52
Q

3 considerations for effectiveness of gene therapy

A

Packing/delivery to cell
Sufficient protein expression
Tissue specificity

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53
Q

Delivery Methods for Gene Therapy

A

Direct injection
Viruses
Nanoparticles

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54
Q

Viruses (for gene delivery) types

A

Adenovirus
Adeno-associated virus
Lentivirus

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55
Q

Why are viruses used for gene delivery in gene therapy?

A

can be produced for a lifetime if integrated into host DNA (via reverse transcriptase)

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56
Q

Pros/Cons Adenovirus in gene therapy delivery

A

Pros: good at getting into cell
Cons: short efficacy | immune response | no cell specificity

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57
Q

Pros/Cons Adeno-associated viruses in gene therapy delivery

A

Pros: long-lasting | cell specificity
Cons: small | limited gene delivery | possible mutation

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58
Q

Pros/Cons Lentiviruses for gene therapy delivery

A

Pros: last lifetime | cell-specificity | low immune response
Cons: could interrupt functional gene | from HIV

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59
Q

Nanoparticles (gene delivery type)

A

synthetic particles (lipids, polymers, metals) that encase DNA for delivery

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60
Q

Pros/Cons of Nanoparticles for gene delivery

A

Pros: easy to make | no risk of infection | low immune response | no size limit
Cons: not efficient in transport | no cell specificity

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61
Q

2 ways to achieve tissue specificity

A

tissue-specific promoter
directed delivery to target cells
peptides engineered on surface only
recognized by certain cell types

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62
Q

Totipotent stem cell

A

can make any cell

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63
Q

Pluripotent stem cell

A

can make any cell except zygotes

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64
Q

Multipotent stem cell

A

can make several cell types within lineage (ex: multiple WBC types)

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65
Q

Unipotent stem cell

A

can only make one cell type

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66
Q

Embryonic stem cells

A

pluripotent (generate many cell types)
formed from “inner mass”
embryo gets destroyed
can lead to uncontrolled tumor/growth

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67
Q

Adult stem cells

A

multipotent or unipotent
derived from patient (no immune response)
less chance for tumor growth

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68
Q

iPCS

A

induced pluripotent cells
normal cell made into pluripotent stem cells
no immune rejection
over-expresses oncogenes (possible cancer)

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69
Q

Allogeneic stem cells

A

from different individual but same species

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70
Q

Syngeneic stem cells

A

from different identical individual (twin)

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71
Q

Autologous stem cells

A

from same individual

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72
Q

Genetic Engineering (def)

A

exogenous DNA or mod of genome that transmits to progeny

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73
Q

Types of Genetic Engineering

A

Transgenic
Knockout
Knock-in

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74
Q

Transgenic (genetic engineering)

A

foreign DNA added to genome

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75
Q

Transgenic gene process

A

-Make transgene (generic or cell specific promoter)
-Inject into egg (male pronucleus of fertilized ovum)
-Insert transgene into genome (random)

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76
Q

Transgenic pros/cons

A

Pros: easy | quick | fine-tuning
Cons: random insertion so possible mutation | overexpression

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77
Q

Knock-out (genetic engineering)

A

suppress/delete endogenous gene
gene cannot express

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78
Q

Knock-out Process

A

-make targeting construct
-introduce embryonic stem cells
-integrate into genome
-inject ES cells into blastocysts for implanting into pseudo-preg female

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79
Q

Knock-in (genetic engineering)

A

mutations added into endogenous gene

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80
Q

CRISPR/Cas9 technology

A

gene-editing in embryonic stem cells
single guide RNA directs nuclease into specific gene site which activates gene and cuts out DNA

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81
Q

Knock-in Process

A

swap normal piece DNA with mutation

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82
Q

Knock-in & Knock-out pros/cons

A

Pros: no random insertion | fine-tuning
Cons: long | expensive | embryonic lethality | protein w/ false genotype possible

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83
Q

Purposes of Genetic Engineering

A

research
food production
therapeutics
disease prevention

84
Q

Why are mice used for genetic engineering?

A

well-defined genetics
easy to isolate and maintain ES cells & ova
short gestation period

85
Q

Knock-out Pigs

A

generated virus-resistant pigs (PRRSV disease)
Knocked out SIGLEC1 gene for virus binding

86
Q

Transgenic Salmon

A

express growth hormone transgene
larger growth in short time
possible problem with wild release

87
Q

Transgenic Goats

A

antithrombin used for human clotting disease
transgenic goats produce antithrombin
promoter switched on in mammary tissue
secreted in goat milk

88
Q

Transgenic Cattle

A

Lysostaphin is protein that protects cow from mastitis
cows = mastitis-resistant

89
Q

Rabbit Hemorrhagic Disease (symptoms & cause)

A

Viral disease (RHDV2-rabbit hemorrhagic disease virus-2)
lethargy | decreased appetite | hypothermia | down platelets | heart issues | protein/heme in UA
Death in 24 hours
Necropsy: discolored liver | hemorrhage | pericardial effusion

90
Q

Virus characteristics

A

MUST have host for replication
Acellular (NOT cells/organisms)
Replicate by assembly

91
Q

Latent virus

A

viral genome in host but inactive (not replicating)

92
Q

Productive virus

A

active viral genome replication

93
Q

Capsid (def & function)

A

protein coat of viruses
function: protect genome

94
Q

Capsid shapes

A

icosahedral or helical

95
Q

Viral envelope

A

membrane layer
Not in all viruses
made from host cell’s plasma membrane (so it can evade immune system)

96
Q

Types of viral structures & example viruses

A

Naked Icosahedral (adeno)
Naked Helical (tobacco mosaic-non animal)
Enveloped Icosahedral (lentivirus, flavivirus)
Enveloped Helical (rhadbo, corona)
Complex (poxviruses, bacteriophage)

97
Q

Viral genome

A

RNA or DNA
required for viral life cycle and making new viruses
relies on host cell for translation, metabolism, membrane synthesis

98
Q

Monopartite genome

A

linear genome of virus

99
Q

Segmented genome

A

multi-molecular parts of viral genome
reassortment & variants possible

100
Q

Parts of a Virus

A

Capsid
Envelope
Genome
Protein

101
Q

Nonstructural protein

A

protein “inside” portion of virus
produced early-on
importance: genome

102
Q

Structural protein

A

protein “outside” portion of virus
produced later on
importance: structure (capsid)

103
Q

Steps of Virus Life Cycle

A

Attachment
Entry
Uncoating
Replication
Transcription
Translation
Assembly
Release

104
Q

Attachment phase of virus

A

virus binds to host cell receptors
mediated by glycoproteins (on capsid/envelope)

105
Q

Entry phase of virus

A

virus enters host
2 entry mechanisms:
Endocytosis (no capsid)
Membrane fusion (w capsid) viral contents into
cell, capsid fuses at membrane surface

106
Q

Uncoating phase of virus

A

capsid removed
necessary for viral replication

107
Q

Replication phase of virus (DNA/RNA virus)

A

via assembly
DNA viruses- in nucleus | own DNA polymerase or host cells
RNA viruses- in cytosol | own RNA polymerase

108
Q

Replication process of virus exceptions

A

Retroviruses (cDNA in cytosol | “intermediate” DNA in nucleus)
Poxviruses (DNA replication in cytosol via factories)

109
Q

Transcription phase of virus

A

must produce sense mRNA (+mRNA) for host cell machinery to translate all viruses

110
Q

Translation phase of virus

A

fully dependent on host cell
makes single polypeptide that’s cleaved

111
Q

Assembly phase of virus

A

occurs at replication site (nucleus or cytosol)
self-assembly

112
Q

Types of viral assembly

A

spontaneous (simple)
directed (complex)

113
Q

Release phase of virus types

A

Lytic –> kills cell
Non-lytic –> does not kill cell

114
Q

Lytic release

A

non-enveloped viruses rupture plasma membrane and kill cell
fast process

115
Q

Non-lytic release

A

enveloped viruses “bud off” membrane (no killing of cell)
slow process

116
Q

Antiviral therapies

A

Vaccines
Drugs

117
Q

Vaccine as antiviral therapy types & examples

A

inactivated virus (rabies, WNV)
live, attenuated virus (canine adenovirus)
DNA plasmids (WNV, feline leuk)
mRNA (SARS-CoV2, zika)
recombinant capsid proteins (hepatitis, papilloma)

118
Q

Drugs as antiviral therapy & example

A

target viral DNA replication
example: acyclovir | tenofovir (inhibit reverse transcriptase)

119
Q

4 Classifications of Parasites

A

-Arthropods (diptera-flies, mosq; mites, ticks)
-Protozoa (apicomplexans-cytaux & crypto; flagellates)
-Platyhelminths (cestodes-tapeworm; trematode-fluke)
-Nematodes (strongylida-hooks, rhabditia, spiruids)

120
Q

Cryptosporidium

A

protozoan parasite (Cryptosporidium parvum)
affects all mammals + humans!
zoonotic disease

121
Q

Crypto symptoms/transmission

A

S: rapid/acute D+ | long asymptomatic period
T: feces | waterborne

122
Q

Cryptosporidium (life cycle)

A

Oocyst encases sporozoites
Embed in GI lining
Transmitted via oocysts in feces

123
Q

Oocyst

A

hard shell casing | infectious agent of parasites

124
Q

Cryptosporidium (cell uptake)

A

Micronemes & Rhoptries move to cell surface & interact with epithelial host cell surface
Get into cell via actin remodeling
Feeder organelle transfers nutrients from host

125
Q

Micronemes & Rhoptries

A

receptor-like proteins in Crypto that interact with host cell epithelial membrane
Induce actin remodeling for cell uptake

126
Q

Actin Remodeling

A

host cell actin forms stress fibers which bring parasite into host cell

127
Q

Feeder organelle

A

allows for nutrient transfer from host to parasite via cpABC transporters (in crypto)

128
Q

cpABC transporters

A

part of host cell that takes in nucleotides from parasite which allows for its replication
allows for feeder organelle to form (for parasite nutrition from host)

129
Q

Cryptosporidium D+ process

A

parasite causes decrease in absorption (microvilli) of intestines
Intestines retain and add water

130
Q

Treatment for Cryptosporidium

A

none specifically approved
Current: nitazoxanide (antiprotozoal in cattle)
Potential: lectins- block parasite anchoring
cpABC inhibitors- starve parasite

131
Q

Cytauxzoon (symptoms & transmission)

A

Apicomplexan protozoan (Cytauxzoon felis)
ONLY affects cats
S: fever | anemia | icterus | enlarged organs | high mortality (60%)

132
Q

Cytauxzoon transmission

A

T: lone star tick (amblyomma americanum)

133
Q

Cytauxzoon disease mechanisms

A

Initial stage: macrophage infection = clog vessels
Progression: RBC infected = transmission by tick blood meal

134
Q

Cytaux life cycle

A

-Sporozoites –> enlarged macrophage
-Enter RBC –> transmission (tick blood meal)

135
Q

Cytaux cell uptake

A

“Zippering” on host cell
Enter via phagocytosis (evade immune system)
Proteins released into cell for replication

136
Q

Cytauxzoon Treatment

A

Only tick prevention

137
Q

Prion Disease

A

Zoonotic disease caused by misfolded prion protein
PrPc (normal) –> PrPsc (abnormal)

138
Q

Prion Disease examples

A

Scrapie (sheep/goat)
Chronic Wasting Disease (cervids)
Bovine Spongiform (cattle)
TSE (non-human primates)

139
Q

Prion Disease transmission

A

feed, soil, brains

140
Q

Prion Disease resistant/sensitive to…

A

R: heat | pressure | UV
S: proteinase K | denaturants (urea)

141
Q

Prion Disease uptake

A

passed to dendritic cells
transferred to enteric nerves (GI)
brought to CNS

142
Q

PrPc

A

Normal/endogenous prion form
a cell surface protein

143
Q

PrPc structure

A

3 alpha helices
anchored to plasma membrane by GPI (phospholipid)

144
Q

PrPc function

A
  1. copper regulation (prevents buildup)
  2. control of axon/neurite outgrowth (prevents overgrowth)
145
Q

PrPsc structure

A

B-sheet
Aggregate B-sheet to create insoluble protein fibril
Fibrils build up in brain = prion disease

146
Q

Steps for Prion Disease

A
  1. Conversion (PrPc –> PrPsc)
  2. Seeding
  3. Propagation
  4. Toxicity
147
Q

Types of Prion Conversion

A

Spontaneous
Nucleation
Template/Assisted

148
Q

Spontaneous prion conversion

A

PrPc mutates = PrPsc
by genetic mutation (but unfavorable)

149
Q

Nucleation prion conversion

A

PrPsc binds to PrPc = convert to abnormal

150
Q

Template/Assisted prion conversion

A

PrPc unfolds and PrPsc mutates it during unfolded state

151
Q

Seeding (prion disease)

A

PrPsc aggregate into seeds
Create fibrils which build-up in brain
Seeds spread to other neurons

152
Q

Propagation (prion disease)

A

PrPsc seeds spread to other cells in brain

153
Q

Toxicity (prion disease)

A

Cell internalizes PrPsc and tries to digest
Unfolded proteins build-up in ER
ER stress = massive Ca2+ into cell –> death

154
Q

Potential Treatment of prion disease

A

-target prion protein (antibodies reduce PrPc so PrPsc cannot develop)
-inhibit PrPsc toxicity (prevent aggregation or reduce ER stress)

155
Q

Tetanus Toxin

A

potent bacterial toxin
horses greatly affected
caused by Clostridium tetani which attacks NMJ

156
Q

Clostridium tetani

A

gram-positive | anaerobic bacteria
causes tetanus toxin

157
Q

Tetanus Toxin forms

A

Vegetative (infectious | rod-shaped)
Spore (long-lasting)

158
Q

Tetanus Toxin symptoms

A

stiffness | difficulty swallowing | muscle spasms (lock-jaw)

159
Q

Tetanus Toxin transmission

A

soil, feces

160
Q

Structure of Tetanus Toxin

A

Light chain + Heavy chain

161
Q

Light Chain of Tetanus Toxin

A

Protease | “business end”

162
Q

Heavy Chain of Tetanus Toxin

A

for neuron binding & transports light chain

163
Q

Infection Process of Tetanus Toxin

A
  1. Transported from Ach neuron (excitatory) –> GABA neuron (inhibitory)
  2. Toxin endosome acidified
  3. Heavy chain of toxin forms pore
  4. Light chain released into cytosol
  5. Light chain digests SNARE proteins
  6. cleaving of SNARE prevents GABA
  7. Constant Ach release = constant contraction
164
Q

SNARE Protein

A

Ca2+ driven protein required for binding/fusion of vesicles for NT release

165
Q

V-SNARES

A

proteins on vesicles with NT
required for NT release

166
Q

T-SNARES

A

proteins on plasma membrane
required for NT release

167
Q

Tetanus Toxin Treatment

A

Current: vaccine
immediate anti-toxin administration
High-dose antibiotic + clean wound
Potential: antibodies (tetanus–>botox)
lectins
inhibitors of light chain

168
Q

Anthrax Toxin

A

bacterial toxin
cause: Bacillus anthracis
affects all mammals, mostly ruminants

169
Q

Bacillus anthracis

A

gram-positive bacteria | causes anthrax toxin

170
Q

Anthrax Toxin Forms

A
  1. Vegetative (rods | fragile)
  2. Spore (ovoid | requires O2 | last for years)
171
Q

Routes of Anthrax Infection

A

Cutaneous- skin abrasions (survivable)
Gastrointestinal- ingest food/soil (fatal)
Oropharyngeal- breathing in

172
Q

Forms of Anthrax

A

Peracute
Acute
Subacute

173
Q

Peracute

A

Anthrax form = Sudden death
Mainly ruminants
Symptoms: tremor | neck edema/asphyxiation | bloody discharge

174
Q

Acute

A

Anthrax form | rapid onset (days)
Symptoms: tremor | neck edema/asphyxiation | bloody discharge

175
Q

Subacute

A

Anthrax form | chronic (days to weeks)
Symptoms: gradual neck edema | anorexia | V+/D+ | GI necrosis

176
Q

Anthrax Toxicity proteins involved

A

Protective Agent (PA) - carrier to get factors into cell
Lethal Factor (LF)
Edemic Factor (EF)

177
Q

ANTXR1 & 2

A

endogenous receptors that bind anthrax toxin

178
Q

Mechanism of Anthrax Toxin

A

cell brings in toxin
pore in cell by increasing acidity = release EF & LF
EF converts ATP to cAMP = cell “leaky” = edema
LF cleaves MAPKK (survival protein) = cell death

179
Q

MAPKK

A

survival protein in cell that inhibits apoptosis in normal cell
cleaved by lethal factor in anthrax

180
Q

Anthrax Toxin treatments

A

Current: antibiotics | vaccine
Potential: anti-PA antibodies | EF inhibitors | “decoy” proteins bind to PA | anthrax receptor antagonists

181
Q

Gossypol

A

toxic agent in cottonseed

182
Q

What apoptotic pathway is stimulated by gossypol?

A

intrinsic apoptotic pathway –> cell death

183
Q

Extrinsic Apoptosis Pathway

A

receptor-mediated
cell folds in on itself
uses caspase for cell death

184
Q

Caspase

A

enzyme that allows for cell death in extrinsic apoptosis pathway

185
Q

Intrinsic Apoptosis Pathway

A

use mitochondria in roundabout way to lead to cell death (used by gossypol to make cottonseed toxic)

186
Q

Intrinsic Apoptosis Pathway mechanism

A

ischemia | UV | hypoxia activate Bax
Mitochondria release CytC
CytC binds to Capase = cell death
non-toxic cell inhibits pathway via Bcl2

187
Q

Bax

A

hole/pore created in outer mitochondrial membrane created by ischemia, UV, hypoxia in intrinsic apoptotic pathway

188
Q

CytC

A

used in mitochondria for ETC
released during intrinsic apoptosis pathway = binds to caspase for cell death

189
Q

Bcl2

A

inhibits intrinsic pathway so no cell death occurs in cell w/o toxin

190
Q

Yew (Taxus)

A

plant toxin; toxic to all animals, monogastrics especially

191
Q

Yew (Taxus) toxic agent

A

Taxine-A & Taxine-B

192
Q

Taxine-A & Taxine-B

A

taxine alkaloids (lots of benzene)
active (no metabolism needed)
cardiotoxic (affect heart)

193
Q

Yew toxicity mechanism

A

affect AP conduction
block Na+ & Ca2+ channels
PR, QRS, ST phases elevated (on ECG)
= arrythmias (decrease cardiac function)

194
Q

Perilla mint (Perilla frutescens)

A

invasive plant toxin | affects LA (mostly cattle)
insensitive in pigs/dogs
Need to be metabolized for toxicity

195
Q

Perilla mint toxic agent

A

Perilla ketone

196
Q

Perilla mint toxicity mechanism

A

P450 enzymes convert perilla ketone to toxic form
PK activates TRP Ca2+ channel
Ca2+ into cell = contraction of endothelial/epithelial cells
–> pores between cells = fluid in lungs

197
Q

TRP

A

transient receptor potential channels
NSCC

198
Q

P450 enzymes

A

convert perilla ketone –> toxic form

199
Q

Pigweed (Amaranthus species)

A

invasive | toxic in LA | non-toxic in SA
plant toxin

200
Q

Symptoms of pigweed toxin

A

weakness | ataxia | recumbency | symptoms are a few days | usually fatal

201
Q

Pigweed Toxic Agent

A

oxalates

202
Q

Pigweed toxicity mechanism

A

oxalates bind to Ca2+ in blood = crystal formation –> renal failure

203
Q

Gossypol as therapy

A

anti-cancer agent
cancer increases Bcl2
gossypol decreases Bcl2 = cell death

204
Q

Name 2 plant toxins used as chemotherapeutics

A

Taxol (paclitaxel)
Vincristine

205
Q

Which plant toxin is used for heart failure? How does it help?

A

digoxin
increases cardiac contractility

206
Q

Which plant toxin is used as an anti-diabetic agent?

A

Curcumin

Cell Biology (6 decks)

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