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PMCOL 303 > respiratory toxicity > Flashcards

respiratory toxicity Flashcards

1
Q

what are 5 main cell types in the respiratory system

A

ciliated cells, goblet cells, clara cells, Type 1 and 2 alveolar cells

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2
Q

what do goblet cells do

A

produce mucous

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3
Q

what do clara cells do

A

have P450 enzymes, act to regenerate other cells, secrete surfactant and mucus

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4
Q

what is the structure/location of clara cells like

A

the major non-ciliated bronchiolar cells of terminal bornchioles

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5
Q

what is another name for Type 1 and 2 alveolar cells

A

pneumocytes

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6
Q

what are type 1 alveolar cells, structure location

A

cover a large surface area, very thin

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7
Q

why do you want type 1 alveolar cells to be very thin

A

for efficient gas exchange

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8
Q

what do type 2 alveolar cells do

A

secretes surfactant, they are like stem cells where they can convert into type 1

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9
Q

which type of alveolar cells make surfactant

A

2

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10
Q

which type of alveolar cells make are like stem cells

A

2

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11
Q

what is the point of surfactant

A

reduce surface tension, prevents surfaces from sticking together

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12
Q

what is the alveolar wall/septum

A

the interstitial space between adjacent alveolus and capillaries, consist of the alveolar epithelium and capillary endothelium.

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13
Q

generally, what do lung toxicants do

A

decrease the efficiency of lung function by impairing gas exchange

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14
Q

how can oxidative stress occur with lung toxicants

A

from the inhaled toxicants and phagocytic cells

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15
Q

what kind of phagocytic cells cause oxidative stress and what are the effects

A

the ones associated with inflammation (neutrophils, monocytes, macrophages), causing cell injury and cell death

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16
Q

what can the immune response do to the lungs

A

can trigger the relase of bronchoconstrictors like leukotrienes and histamine

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17
Q

what 2 things about the toxicants determine the site of toxicity within the long

A

water solubility and size

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18
Q

what happens physically in acute response to toxicants in airway

A

bronchoconstriction, decreased airflow, mucous secretion

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19
Q

what is bronchoconstriction

A

reflex contraction of bronchial smooth muscle

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20
Q

why do you increase mucous secretion with acute response to toxicants in airway

A

because you are trying to trap the irritant

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21
Q

what 2 molecular pathways determine the acute response to toxicants in airway

A

the parasympathetic system and the tachykinin receptors

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22
Q

what does the tachykinin receptors do in the acute response to toxicants in airway

A

TACT1 and 2 on smooth muscle mediate constriction, TACR2 mediate muscle secretion

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23
Q

what does the parasympathetic system do in the acute response to toxicants in airway

A

ACh binds to M3, increases cGMP, activates PLC, increases Ca++, increase smooth muscle contraction

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24
Q

what does TACR1 do

A

mediates smooth muscle contraction

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25
Q

what does TACR2 do

A

mediates smooth muscle contraction and mucous secretion

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26
Q

which receptors does ACh bind to with acute response

A

M3

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27
Q

what are 4 chronic responses to irritants in the conducting airways

A

asthma, fibrosis, COPD, cancer

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28
Q

what is asthma

A

increased airway sensitivity to bronchoconstriction, (ultrasensitive) causing attacks and shortness of breath

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29
Q

what is fibrosis

A

epithelial cell damage, collagen excess, tissues become non functional

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30
Q

what does COPD stand for

A

chronic obstructive pulmonary disease

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31
Q

what is COPD

A

progressive, non reversible airflow obstruction

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32
Q

where does ozone come from

A

mostly photochemical smog

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33
Q

what reaction makes ozone

A

NO2 + UV –> O* NO*
then
O* + O2 –> O3

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34
Q

what does ozone react with and where and what does it cause

A

polyunsaturated fatty acids (PUFAs) in the airways and propagates lipid radicals

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35
Q

what is the first product of ozone and PUFA

A

trioxolane

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36
Q

what is a breakdown product of tioxolane with no water present

A

criegee ozonides

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37
Q

what do criegee ozonides do

A

penetrate deeply into lung tissue and damage lipids

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38
Q

how/when is criegee ozonides formed

A

when one of the lipid reactive aldehydes from ozone breaks down/ transforms without water

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39
Q

what is a breakdown product of tioxolane with water present

A

reactive aldehydes and H2O2

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40
Q

how/when is reactive aldehydes and H2O2 formed

A

when one of the lipid reactive aldehydes from ozone breaks down/ transforms with water

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41
Q

is the reactive aldehydes and H2O2 or criegee ozonides pathway favored and why

A

reactive aldehydes and H2O2 because lungs have an aqueous environment, so that reaction is favored

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42
Q

what does trioxolane do

A

damage lungs

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43
Q

what 2 general things does ozone exposure cause

A

structural damage and promotes inflammation

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44
Q

what and WHERE kind of physical damage happens with ozone

A

The septum between alveoli break down, lose elasticity

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45
Q

what is the deal with nrf2 in the lungs with ozone

A

it is first upregulated, but 3-6weeks later, it is lost

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46
Q

what happens with ozone exposure initially

A

lung epithelial cells upregulate the electrophile response pathway (NRF2)

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47
Q

what happens with ozone exposure 3-6 weeks in

A

loses ability to do electrophile response pathway (NRF2)

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48
Q

why do you lose ability to do electrophile response pathway (NRF2) after time

A

carbonylation and damage to proteins that regulates expression of Nrf2 genes

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49
Q

which part of the cell gets high levels of nrf2 at first

A

nucleus

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50
Q

what is the deal with ozone and nrf2 (general)

A

initially activates nrf2 pathway but then inhibits it

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51
Q

what are 2 types of damage that ozone promotes

A

epithelial apoptosis and collagen deposition

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52
Q

where does collagen deposition happen with ozone

A

submucosal

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53
Q

what structure changes with collagen deposition in ozone

A

alteration of alveolar structure

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54
Q

how is ozone a powerful oxidant

A

via H2O2 and aldehyde formation

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55
Q

what does ozone do to TNFalpha + what does it cause

A

increases its expression which leads to inflammation

56
Q

what does ozone do to inflammatory agents

A

increases the amount of them so there is increased inflammatory response in immune cells

57
Q

what does ozone do to nitrogen species + how (explain)

A

increases iNOS which increases NO and peroxynitrite production

58
Q

what is iNOS

A

inducible nitric oxide synthase

59
Q

what does iNOS lead to

A

more NO and more peoxynitrite production

60
Q

which cells are lost with ozone and how

A

epithelial cells along most of respiratory tract via apoptosis and necrosis

61
Q

what is the water solubility of ozone like

A

lower water solubility

62
Q

where is the greatest dose per unit of surface area occur for ozone

A

in deep regions of the lungs (alveolar zone)

63
Q

where does foamy pink discharge occur + why

A

upper airway (like epiglottis), capillaries bleeding out

64
Q

which sulfur oxide is the most important

A

SO2

65
Q

what are 4 sources of SO2

A

coal combustion, paper mills, metal refineries, burning foam rubber

66
Q

what does SO2 look like

A

colorless gas

67
Q

what does SO2 smell like

A

pungent, like just struck match

68
Q

what is the water solubility of SO2 like

A

very water soluble

69
Q

what is SO2 to lungs at normal levels

A

upper respiratory system irritant

70
Q

what is SO2 to lungs at high levels

A

DNA damage, potential carcinogen - cancer

71
Q

what is the mechanism of SO2 and oxidative stress

A

unclear but likely free radical generation like SO3*

72
Q

what is the deal with SO3*

A

it is a free radical that can be further oxidized to produce the hydroxyl radical OH*

73
Q

what can SO3* induced OH* formation cause

A

lipid peroxidation and protein carbonyl formation

74
Q

what happens to bax with increasing SO2

A

increasing (pro apoptotic)

75
Q

what happens to bcl-2 with increasing SO2

A

decreasing (anti apoptotic)

76
Q

what happens to p53 with increasing SO2

A

increasing (pro apoptotic)

77
Q

what happens to caspase-3 with increasing SO2

A

increasing (pro apoptotic)

78
Q

what are the 3 main anti apoptotic things we measure for SO2 damage

A

bax, p53, caspase-3

79
Q

what is the main pro apoptotic things we measure for SO2 damage

A

bcl-2

80
Q

what is asbestos

A

a group of silicate minerals with fibrous form

81
Q

what was the use for asbestos

A

heat insulation, fire barrier

82
Q

what does the health hazard of asbestos relate to

A

fiber shape, length and surface properties

83
Q

what are the 2 types of asbestos

A

serpentine and amphiboles

84
Q

what is serpentine asbestos

A

longer, curved

85
Q

what is amphibole asbestos

A

short, straight, spikey

86
Q

which form of asbestos is more damaging

A

amphibole

87
Q

which form of asbestos is short, straight, spikey

A

amphibole

88
Q

which form of asbestos is longer, curved

A

serpentine

89
Q

what is asbestosis

A

a form of pulmonary fibrosis, many collagen nodules and presence of asbestos fibres with or without a coat of protein coating

90
Q

what kind of asbestos exposed people get lung cancer

A

miners and smokers

91
Q

what is malignant mesothelioma

A

a rare cancer in the pleural mesothelium

92
Q

what is the pleural mesothelium

A

the protective lining of the lungs

93
Q

is malignant mesothelioma related to smoking

A

no

94
Q

what is the carcinogenicity of amphiboles like compared to chrysotile/serpentine

A

2 fold more

95
Q

what are 3 ways that asbestos induced ROS production

A
  • asbestos had iron on surface
  • macrophage activation
  • mitochondria and immune ROS
96
Q

explain asbestos fibre surface reactivity and ROS production

A

diff types of asbestos have diff iron levels on their surface which contributes to ROS production via the fenton reaction

97
Q

explain asbestos activation of alveolar macrophages

A

they attempt to engulf fibres and release ROS

98
Q

explain asbestos with mito and immune making ROS

A

mitochondria in lung epithelial cells and immune cells start to generate and release ROS

99
Q

how do they prove that asbestos can do fenton reactions

A

they produce OH in presence of H2O2 and reducing agent

100
Q

what are 2 examples of iron chelators

A

EDTA and DES

101
Q

what happens if you add EDTA and DES into a reaction

A

they prevent radical formation

102
Q

what can asbestos do to DNA + what does this cause

A

DNA damage, leading to p53 expression

103
Q

what happens to p53 with asbestos

A

increase expression

104
Q

what is a way to prevent increased p53 by asbestos and why

A

give the alveolar cells phytic acid which is an iron chelator

105
Q

what does phytic acid do

A

iron chelator

106
Q

what does it mean that phytic acid reduces p53

A

it implies that iron on the surface of asbestos participates in ROS which initiates apoptosis

107
Q

what do macrophages do to asbestos

A

attack them by invading and try to phagocytose them

108
Q

what happens if the asbestos fibre cannot be swallowed by the macrophages

A

it traps the macrophages in the alveoli

109
Q

what is frustrated phagocytosis and why does it happen

A

if it is too big to engulf, phagocytes will isntead released ROS RNS and other inflammatory signals

110
Q

what happens once frustrated phagocytes release their inflammatory signals

A

stimulates collagen deposition in the airways

111
Q

what are 3 main results of asbestos and immune cells

A

inflammation, fibrosis and cancer

112
Q

what plays a large role in mitochondrial ROS production in response to asbestos (1 main type)

A

alveolar macrophages

113
Q

what are 3 cell types that play a role in mitochondrial ROS production in response to asbestos

A

lung epithelial and mesothelial cells

114
Q

what is the mechanism of ROS and asbestos

A

unclear, likely mitochondria and macrophages

115
Q

which components of the cell may be part of ROS and asbestos + how did they know

A

they made mitochondrial ETC non function - reduced ROS production in response to asbestos

116
Q

what is a way to reduce asbestosis

A

block H2O2 production

117
Q

what needs to happen for mitochondrial ROS production to occur

A

hints of asbestos fibers need to be internalized for mitochondrial ROS production to occur

118
Q

what 2 responses does asbestos initiate

A

macrophage and epithelial cell response

119
Q

what 4 things does asbestos induced macrophage and epithelial cell response cause

A

ROS RNS cytokine and growth factor production and release

120
Q

what is an example of a cytokine released by macrophage and epithelial cell response

A

TNF alpha

121
Q

what is TNF alpha

A

tumor necrosis factor alpha, inflammatory cytokine

122
Q

what does TNF alpha cause

A

NFKB translocation to nucleus (more inflammation and anti apoptosis)

123
Q

what does NFKB translocation to nucleus cause

A

increase transcription of inflammatory and anti apoptotic genes like bcl2

124
Q

what 2 things does TGF beta do

A

makes more collagen and prevents it from being broken down

125
Q

where does TGF beta act

A

autocrine paracrine function (same cell and local area)

126
Q

what do alveolar macrophages release with early asbestos exposure

A

TNF alpha

127
Q

what do alveolar macrophages release with late asbestos exposure

A

TNF beta

128
Q

what is the formula for crystalline silica

A

SiO2

129
Q

what causes silicosis

A

inhalation of crystalline silica, often quartz

130
Q

what kind of disorder is silicosis

A

chronic, progressive and fibrotic disorder of the lung

131
Q

when does fibrosis develop with silicosis

A

following an initial inflammatory process

132
Q

what do macrophages do with silicosis

A

ingest silica into phagosomes, cant digest, frustrated phagocytosis again

133
Q

what does frustrated phagocytosis in silicosis look like

A

burst of inflammatory cytokine release which kills macrophages, releasing the silica and starting the cycle again

134
Q

how does collagen synthesis happen in silicosis

A

alveolar macrophages release growth factors that induce fibroblast proliferation and collagen synthesis

135
Q

how does cardiorespiratory failure happen in silicosis

A

silicotic nodules develop throughout the lung

136
Q

where does silica come from

A

mining, masonry, sand blasting

PMCOL 303 (25 decks)

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