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TOX > biomedical toxicology > Flashcards

biomedical toxicology Flashcards

1
Q

define toxicant

A

an agent capable of producing a deleterious response in a biological system

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2
Q

define organism

A

a thing that has target sites, storage depots and metabolic enzymes

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3
Q

what are toxins

A

endogenous agents that interact with proteins, lipids, or nucleic acids in cellular targets

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4
Q

what are adverse effects

A

any change from an organism’s normal state

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5
Q

what does adverse effects depend on

A

depends on the concentration of an active compound at the target site for a sufficient time

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6
Q

define poison

A

a substance that is capable of causing the illness or death of a living organism

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7
Q

what toxic substances are termed as poisons

A

toxic substances not directly of biological origin are termed poisons

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8
Q

what is venom

A

a toxin recreated by an animal for the purpose of causing harm to another

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9
Q

what is mycotoxin

A

a toxin produced by fungi

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10
Q

what is exotoxin

A

a toxin secreted by bacteria

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11
Q

what is pharmacokinetics

A

examines drug absorption, distribution, metabolism, and excretion within an organism

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12
Q

what is pharmacodynamics

A

studies drug interactions with biological receptors

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13
Q

difference between drug and toxicant

A

toxicant has no beneficial impact, while drugs have a therapeutic dose

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14
Q

what is toxicokinetics

A

the study of kinetics of absorption, distribution, metabolism, and excretion of a xenobiotic under the conditions of toxicity evaluation

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15
Q

what is toxicodynamics

A

describes the dynamic interactions of a toxicant with a biological target and its biological effects

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16
Q

what was the Bhopal gas tragedy

A

carbine pesticide plant released methyl isocyanate gas

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17
Q

what does it mean to have lachrymal properties

A

makes you cry

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18
Q

how is toxicity measures

A

toxicity is measured as clinical endpoints which include any disruption to an organisms homeostasis

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19
Q

with acute studies, what is the common endpoint

A

with acute studies, a common endpoint is LD50 (lethal dose 50)

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20
Q

within chronic studies, what are the common endpoints

A

chronic studies are longer in duration and include endpoints such as reproduction, long-term survival, and growth

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21
Q

if the substance that enters circulation is water soluble describe where it goes

A

if it is water soluble, it will stay in circulation

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22
Q

if the substance that enters circulation is lipid soluble, describe where it goes

A

if it is lipid soluble, it will cross the cell membrane

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23
Q

describe hoe mercury vapour interacts with an organism

A

mercury vapour is readily absorbed into the circulatory system

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24
Q

describe the difference between methyl mercury and ethyl mercury

A
  • ethyl mercury is much more toxic than metallic mercury

- ethyl mercury is less toxic than methyl mercury

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25
Q

describe how MeHg-L0cystein conjugate interacts with an organism

A

MeHg-L-cystein conjugate is actively transported across the blood brain barrier, which may be responsible for the high Hg levels found in the brain after exposure

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26
Q

when exposed to MeHg-L-cystein conjugate, where will it be found

A

after exposure, high concentrations will be found in the brain, as it is actively transported across the blood brain barrier

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27
Q

describe the interaction and correlation between MeHg and extracellular glutamate

A

MeHg stimulates extracellular glutamate levels and the over activation of glutamate receptors increases Ca2+ influx into neutrons, therefore leading to the activation of important pathways involved with cell death

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28
Q

what are the six steps in the systematic overview of a toxicant

A
  1. exposure
  2. absorbed
  3. delivered (to target site)
  4. bioactivated
  5. detoxified
  6. excreted
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29
Q

three attributes of target

A
  • reactivity
  • accessibility
  • critical function
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30
Q

which are more reactive- proteins or dna

A

proteins are more reactive than stable dna

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31
Q

describe non covalent binding reactions with target molecules

A
  • reversible
  • lock/key inhibitors
  • membrane receptors
  • enzymes
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32
Q

example of non covalent binding with target molecules

A

dna intercalates (insert within the stacked bases)

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33
Q

describe covalent bonding reactions with target molecules

A
  • irriversible
  • permanently alters target
  • react with nucleophilic enters in dna and proteins
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34
Q

example of covalent binding with target molecules

A
  • electrophilic epoxides

- carbon monoxide

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35
Q

describe the effect of dysfunction of a target molecule

A

alteration of target configuration

-tertiary protein structure or dna template

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36
Q

describe the effect of destruction of a target molecule

A
  • crosslinking of proteins and nucleic acids

- covalent binding of toxicant with targets that are released from cells can sometimes evoke an immune response

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37
Q

what is the toxoconetic process

A 
xenobiotic 
absorption (external membrane barriers) 
distribution (blood plasma to tissues)
metabolism (phase 1 (CP450, 2(increased polarity)
excretion (kidneys' etc)
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38
Q

four routes of absorption are

A

inhalation
direct contact
ingestion
injection

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39
Q

two ways of crossing the biological membrane

A
  • passive diffusion

- active transport

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40
Q

characteristics favouring absorption with inhalation

A
  • large surface area
  • large blood supply
  • phagocytosis and migration
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41
Q

toxicity through the pulmonary route depends on?

A
  • particulate size and volatility
  • ability to diffuse
  • affinity for transporters
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42
Q

what chemical has a very active transport through the skin

A

DMSO

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43
Q

how to increase skin absorption

A
  • hydration
  • solvent effects
  • temperature
  • amount of dermal appendages
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44
Q

how does hydration increase dermal absorption

A

proves an aqueous media and causes cell swelling

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45
Q

how do solvent effects increase dermal absorption

A

can alter lipids in the membrane

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46
Q

how does temperature increase dermal absorption

A

increasing temp increases blood flow

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47
Q

characters favouring absorption within the gastrointestinal tract

A
  • single cell lipodial membrane
  • large surface area
  • high blood and lymph flow
  • variable ph
  • many specialized transport proteins
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48
Q

describe passive uptake

A

passive uptake is the most common way that xenobiotics cross cell membranes and does not require the input of energy

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49
Q

what are the three factors that determine the rate of passive transfer

A
  • differences in concentration
  • polarity
  • size
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50
Q

explain how differences in concentration will determine rare of passive transfer

A

differences in concentration of the substance on opposite sides of the membrane
-substances move from

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51
Q

example of a lachrymal agent

A

methyl isocyanate

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52
Q

what is a lachrymal agent’s property

A

makes u cry

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53
Q

what is the most abundant target molecule in the human body

A

proteins

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54
Q

what types of reactions can occur with target molecules?

A
  • non covalent
  • covalent
  • fragmentation
  • crosslinking
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55
Q

what are the four aspects of toxokinetics

A

absorption, distribution, metabolism, and elimination

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56
Q

which route of absorption probably results in the least toxicity

A

dermal (skin)

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57
Q

which route of absorption results in the greatest toxicity

A

inhalation

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58
Q

which factor does not influence rate of distribution

  • blood flow
  • physiochemical properties
  • protein binding
  • passive diffusion or active transport
  • none of the above
A

none of the above

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59
Q

what factors influence rate of distribution

A
  • blood flow
  • physiochemical properties of the chemical
  • protein binding
  • passive diffusion or active transport
60
Q

what are the three barriers to distribution within the body

A
  • blood brain barrier
  • blood placenta
  • bood testis
61
Q

what is blood testis

A

type of cell barrier

62
Q

how does methyl mercury pass through blood brain barrier

A

by reacting with cytosine and utilizing the methionine transporter

63
Q

what are the two major routes of excretion

A

kidney (urine), and liver (bile)

64
Q

phase 2 metabolites are generally excreted well through what

A

phase 2 metabolites are generally excreted well through the bile

65
Q

epinephrine acts as a

  • agonist
  • antagonist
  • hormone
  • suicide substrate
A

epinephrine acts as a hormone

66
Q

endocrine disruptors can not interfere with hormone:

  • production
  • transport
  • metabolism
  • elimination
  • synthesis
A

endocrine disruptors can not interfere with hormone synthesis

67
Q

which of the following can not act as an anti-estrogen

  • THC
  • DDT
  • PCB
  • estradiol
A

estradiol acts as an anti-estrogen agent

68
Q

How many pounds of BPA is used/year in consumer products

A

6 billion pounds of BPA are used each year

69
Q

what are the possible edicts of BPA

A
  • increase prostate weight
  • decline in testosterone
  • changes to genital tract
70
Q

what does TCDD cause

A

chloracne
oxidative stress
endocrine disruption
cancer by compounds activated by cyp450

71
Q

why does 50% occupancy of Hb by CO result in death, while 50% occupancy due to low oxygen does not?

A

Co interferes with oxygen unloading by increasing the Hb affinity for oxygen

72
Q

why is the lethal dose of HCN lower than potassium cyanide

A

HCN is a neutral compound with greater membrane permeability

73
Q

how many over-the-counter products contain Tylenol

A

600

74
Q

how many people die in the US/year from Tylenol

A

500

75
Q

what is Tylenol toxicity caused by

A

bioactivation into NAPQI that reacts covalently with liver proteins

76
Q

why is it not a good idea to mix Tylenol and alcohol

A
  • alcohol depletes GSH

- Alcohol can induce CYP450 to cause Tylenol bioactivation

77
Q

what diseases are a result of protein oxidation

A
  • diabetes
  • muscular dystrophy
  • alzheimers
78
Q

what structural change causes the B-form DNA duplex to produce the A-form duplex

A

change in deoxyribose “sugar pucker “

79
Q

what is the final step in chemical carcinogenesis

A

metastasis

80
Q

what are the steps, in order of chemical carcinogenesis

A

initiation
bioactivation
proliferation
metastasis

81
Q

how many compounds are establishes carcinogens

A

100s

82
Q

PAHs are historically thought to cause:

A

scrotal cancer (like the boys from marry Poppins)

83
Q

which region of PAHs is most reactive towards electrophiles

A

K-region

84
Q

the activated compound thought to produce DNA adducts by BP is called

A

BPDE

85
Q

why is a simple arena oxide unreactive towards DNA

A

it undergoes rapid isomerization into a stable phenol, making it unable to react

86
Q

Where are aromatic amines present

A
  • tobacco smoke
  • exhaust
  • organic dyes
87
Q

where are aromatic amines NOT present

A

pesticides

88
Q

The dna reactive intermediate for an aromatic amine is called

A

nitrenium ion

89
Q

what do polycyclic planar structures cause

A

cancer

90
Q

which N-linked c8-aryl-dG adduct lacks mutagenicity

A

An-dG

91
Q

describe AAF-dG on mutagenic outcome

A

highly mutagenic

92
Q

describe AF-dG on mutagenic outcome

A

highly mutagenic

93
Q

describe ABP-dG on mutagenicity

A

weakly mutagenic

94
Q

describe An-dG on mutagenicity

A

lacks mutagenicity

95
Q

what is the major oxidative DNA base lesion called

A

8oxoG

96
Q

06-methylguanine DNA methyltranferase is an example of?

  • glycosylase
  • BER enzyme
  • direct reversal repair enzyme
  • NER enzyme
A

06-methylguanine DNA methyltransferase is an example of a direct reversal repair enzyme

97
Q

Why is BER (base excision repair) convergent

A

it is a family of repair enzymes where they all produce the same abasic site

98
Q

why is NER (nucleotide excision repair) highly promiscuous

A

because it removes a wide range of DNA damage

99
Q

what is the first enzyme employed in NER

A

DNA exonuclease

100
Q

what diseases are a result of defective dna repair

A
  • ataxia telangiectasia
  • blooms syndrom
  • xerderma pigmentosum
101
Q

what are the products of acetylcholine hydrolysis by cholinesterases

A

choline and acetic acid

102
Q

what is the purpose of acetylcholine hydrolysis by cholinesterase’s

A

it permits the termination of impulse

103
Q

how many amino acids are in the 3-finger protein “fasciculin” within venom

A

61

104
Q

what is the mechanism of action of fasciculin

A

blocks acetylcholine binding to acetylcholinesterase

105
Q

how many amino acid residues are in cobra toxin

A

71

106
Q

the mechanism of action for cobra toxin:

A

blocks aceytlcholine binding to its receptor

107
Q

what is venom milking used for

A

antibodies against the toxin within the venom

108
Q

of nerve agents, which one I the least volatile

  • sarin
  • soman
  • tabum
  • VX
A

VX is the least volatile

109
Q

of nerve agents, which one has the lowest LD50 from dermal exposure

A

VX

110
Q

of nerve agents, which one has the shortest aging time

A

soman

111
Q

what is the mechanism of action for man-made nerve agents

A

blocks acetylcholine from undergoing hydrolysis by the esterase

112
Q

what are the routes of failed excretion

A

1-lipid soluble: bioaccumulation
2- reabsorbed kidney or GIT
3-binding:bioaccumulate (ie lead)

113
Q

T or F

metabolism only reduces toxicity of chemicals

A

false- it can increase or decrease toxicity

114
Q

what is an agonist

A

mimics a hormone in binding productively to a receptor

115
Q

what is an antagonist

A

mimics a hormone in binding non-pruductively

116
Q

what do endocrine disruptors do

A

mimics naturally occurring hormones by blocking the way natural hormone and their receptors are made or controlled

117
Q

what are the three mechanisms of endocrine disruptors

A

1-binding and activating the estrogen receptor (acting like an estrogen)
2-exogenous estrogens can bind to the estrogen receptor but the affinity is usually only a fraction of the binding affinity of estradiol
3- binding but not activating the estrogen receptor (acting an an anti-estrogen

118
Q

describe BPA estrogenicity

A

BPA. closely mimics the structure and function of hormone estradiol with the ability to bind to and activate the same estrogen receptor as the natural hormone

119
Q

when is Bisphenol s (BPS) used

A

used where the legal prohibition on BPA allows products containing BPS to be labelled BPA free - although it also had endocrine disrupting properties

120
Q

what is TCCD

A

tetrachlorodibenzo-p-dioxin

-is a contaminant in the herbicide Agent Orange and was shown to produce birth defects in rodents

121
Q

what are the mechanisms of action for dioxins

A
  • dioxins are taken up through the cell membrane passively
  • recognized to be receptor-mediated toxicants
  • exerts effects through interactions with a specific intracellular protein (aHr)
  • functions as a hormone- initiating a cascade of events that is dependent upon the environment of each cell
122
Q

what is AhR

A

its a liugans-activated nuclear transcription factor

123
Q

what does AhR do

A

mediated xenobiotic signalling to enhance the expression of target genes, including p450s

124
Q

what happens when TCDD binds to AhR

A

the complex interacts with genes that promote RNA polymerase to make mRNA to facilitate protein production

125
Q

what are the adverse effects of TCDD

A

-chloracne- an inflammatory condition
-promotion of cancer by other activated compounds
-oxidative stress m
=endocrine disruption

126
Q

how much hemoglobin does a heathy human have

A

15g/L

127
Q

what does cyanice do

A

blocks the use of oxygen

128
Q

how does cyanide block the use of oxygen

A

-binds to cytochrome oxidase and inhibits the last step of the ETC
-then no ATP can be created
= respiratory arrest and death

129
Q

what accounts for 95% of acetaminophen metabolism

A

glucuronidation and salvation

130
Q

what is acetaldehyde

A

reactive electrophile that reacts directly with GSH

131
Q

grapefruit juice inhibits p450 which would do what

A

decrease the production of NADPQIU

132
Q

how much of protein in an 80 year old human is oxidized

A

20-50%

133
Q

what are tutor suppressors

A

normally function to prevent cell growth/ division

134
Q

what are oncogenes

A

normally promote cell growth

135
Q

what are the steps in chemical carcinogenesis

A

1- biotransformation

  • initiation
  • fixation
  • gene expression
  • growth/poliferation
  • progression
  • metastasis
136
Q

what is B-epigenestics

A

increase the likelihood of tumour development

137
Q

what do PAHs need to show toxicity

A

bioactivation by p450

138
Q

what is the most abundant carcinogen in car exhaust

A

benzo[a]pyrene

139
Q

T or F

mutated DNA is damaged

A

false- its just different

140
Q

describe direct reversal mechanisms

A

altered dna bases chemically covered back to the standard structures w/o the removal from the DH

141
Q

describe base excision repair

A

bases are attached to backbone - and are removed by hydrolysis of the glycosidic bond
-convergent and specific

142
Q

describe nucleotide excision repair

A

recognize and remove the damaged portion of a dna strand

-highly promiscuous

143
Q

what is global genome repair

A

mechanism for dealing with stalled replication forks

144
Q

what is transcription couples repair

A

mechanism for dealing with stalled transcription complexes

145
Q

what does global genome repair protect genome against

A

against mutations and ensures that cell replication can be completed

146
Q

what does transition couples repair protect

A

protects actively transcribed genes where lesions on the transcribed strands would become traffic jams

TOX (4 decks)

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