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NUTR 4510- Food, Tox, Nutrition > Physiology of Xenobiotic Metabolism and Scientific Studies > Flashcards

Physiology of Xenobiotic Metabolism and Scientific Studies Flashcards

1
Q

What are the three interactions between toxicology and nutrition?

A
  1. Food as a source of xenobiotic exposure
  2. Effect of nutritional status on xenobiotic metabolism
  3. effect of xenobiotic exposure on nutritional status
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2
Q

describe a nutritional xenobiotic

A

overconsumption of macronutrients and micronutrients, food additives

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3
Q

describe a microbiological xenobiotic

A

salmonella, botulinum

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4
Q

describe an environmental xenobiotic

A

persistent organic pollutants, mercury, dioxins

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5
Q

describe food contamination xenobiotic

A

synthetic pesticides

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6
Q

describe food processing xenobiotic

A

polyaromatic hydrocarbons, nitrosamines

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7
Q

describe a plant xenobiotic

A

phytochemical, natural pesticides

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8
Q

describe an example of an effect of nutritional status on xenobiotic metabolism

A

sulfer amino acid deficiency and acetaminophen metabolism

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9
Q

describe an example of an effect of xenobiotic exposure on nutritional status

A

alcohol consumption and vitamin A deficiency

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10
Q

Explain excess protein intake in relation to renal dysfunction

A
  • excess protein intake a day is anything over 100g a day
  • metabolic acidosis which results in increased urinary excretion of nitrogen and calcium
  • decreased urinary pH and decreased reabsorption of calcium in the kidney
  • increases bone resprption to maintain blood calcium levels and as a result increases the risk of bone fractures
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11
Q

explain excess intake of total calories and obesity

A
  • habitual over-nutrition in the form of calories over time can result in obesity
  • increased risk of co-morbidies (t2d, CVD, cancer)
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12
Q

What is botulism

A

a serious illness caused by the botulinum toxin

- the toxin causes paralysis that starts in the face and can spread to limbs

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13
Q

describe food borne botulism

A

harmful bacteria thrive and produce the toxin in environments with little oxygen (ie home-canned food)

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14
Q

describe wound botulism

A

if these bacteria get into a cut, they can cause a dangerous infection that produces the toxin

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15
Q

describe infant botulism

A

this is the most common form of botulism

- begins after the bacterial spores grown in baby intestinal tract

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16
Q

describe DDT

A
  • insecticide used to reduce malaria risk
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17
Q

why is DDT less effective

A

many species of mosquitoes ave developed resistance

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18
Q

why is DDT harmful

A
  • accumulates up the food chain,
  • fat soluble
  • toxic to humans
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19
Q

describe the human toxicity of DDT

A
  • liver damage including liver cancer
  • nervous system damage
  • congenital disabilities
  • reproductive dusfunction
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20
Q

What are PCBs

A

polychlorinated biphenyls

- organic chlorine compounds

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21
Q

Are PCBs resistant? How so?

A

they are extremely perisistent

- last for many years because they do not break down on their own and they are hard to destroy

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22
Q

where do PCBs originate?

A
  • ingredients in many industrial materials

- used to make coolants and lubricants for electrical equipment

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23
Q

What is TCDD?

A

Dioxin
POP
herbicide
agent orange

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24
Q

How does TCDD/Dioxin work?

A
  • binds to the aryl hydrocarbon receptor and functions as a transcription factor
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25
Q

properties of dioxin

A
  • carcinogenic
  • teratogen
  • low water solubility
  • fat soluble
  • half life of 7-8 years
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26
Q

what causes chloracne

A

dioxin/tcdd

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27
Q

What does PAH stand for

A

poly aromatic hydrocarbons

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28
Q

what are PAHs

A
  • class of carbon and hydrogen containing molecules
  • non polar
  • lipophilic
  • result from incomplete combustion of organic materials
  • also produced on charred foods
  • carcinogen
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29
Q

what is the food processing xenobiotic that is created by charring food, typically meats

A

PAH

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30
Q

how are PAHs created

A

incomplete combustion of organic materials (coal, cigs)

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31
Q

what is an example of a PAH

A

benzo-a-pyrene

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32
Q

what was the consequence of PAH exposure within the industrial revolution

A

scrotal cancer

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33
Q

what is HCA

A

heterocyclic amines

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34
Q

how are HCAs formed

A

formed when amino acids, sugars and crating or creatinine react at high temperatures during the cooking of meats

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35
Q

describe the structure of HCS

A

5 or 6 carbon ring with nitrogen

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36
Q

what is an example of an HCA

A

PhIP

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37
Q

What is nitrosamines

A

a food processing xenobiotic

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38
Q

how are nitrosamines produced

A

produced from nitrites (used to cure meats) and secondary amines)

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39
Q

if a food source likely has nitrosamines, what will it also contain

A

sodium nitrite

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40
Q

without metabolism and excretion, where do lipophilic xenobiotics go in the body

A

they will accumulate in lipid rich regions or tissues of the body (brain, adipose tissue)

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41
Q

what risk increases when lipophilic xenobiotics accumulate in the body

A

risk of toxicities and adverse effecrs

  • neurotoxicity
  • cancer
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42
Q

how do you get rid of lipophilic xenobiotics so they dont accumulate

A

have to metabolize the xenobiotic to convert them from a lipophilic parent compound to a water soluble metabolite that can be excreted in the urine

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43
Q

where does nutrient rich blood from the GIT mix with oxygenated blood

A

in the liver in the sinusoids

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44
Q

everything leaving the liver goes where?

A

hepatic vein

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45
Q

where do large lipophilic xenobiotics go from the liver

A

they go to the lymph in a chylomicron along with large dietary lipids

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46
Q

describe blood flow from liver sinusoids to heart

A
  1. sinusoids
  2. central vein
  3. hepatic vein
  4. inferior vena cava
  5. heart
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47
Q

where does phase 1 and 2 reactions happen

A

in the hepatocytes

48
Q

describe hepatocyte contact with sinusoid and bile canaliculi

A
  • each hepatocyte is in contact with both the sinusoid and the bile canaliculi
  • this permits the movement of xenobiotic or xenobiotic metabolites across the hepatocyte cell membrane (they can move between the sinusoids, hepatocyte and bile canaliculi)
49
Q

what organ produces bile

A

liver hepatocytes produce bile which contains bile acids

50
Q

what is the purpose of bile acids

A

bile acids aid in lipid digestion by acting as a detergent or emulsifier

51
Q

what is the polarity of bile

A

bile is amphipathic (water and lipid soluble)

52
Q

how do lipophilic xenobiotics bind with bile acids

A

bile has the ability to bind or trap lipophilic xenobiotics and transport them to the small intestine in the enterohepatic circulation
- lipophilic xenobiotics bind with bile acids in the hepatocyte and enter into the bile canaliculus which connects to the bile duct

53
Q

how are lipophilic X Brough to the liver via the HPV

A

lipophilic xenobiotics can be bound to bile salts/ acids in the intestine which brings them in to the liver Bia the HPV

54
Q

what happens to xenobiotics when the reach the liver depends on two things:

A
  1. liver expression of the phase 1 enzyme (CYPs): will impact how much phase 1 reaction is possible and how many reactive intermediates are produced
  2. liver expression of phase 2 enzymes and conjugating agents: determine how much phase 2 reaction is possible
55
Q

describe the ideal speed for phase 1/2 reactions

A
  • ideally phase 1 reactions happen slowly and controlled so that phase 2 reactions can keep pace with phase 1 reactions for reduced risk of DNA damage
  • ideally phase 2 reactions will happen fast
56
Q

Once lipophilic xenobiotics reach the liver, what happens if liver hepatocytes do nothing?

A

xenobiotic will leave the liver and phase1.2 reactions can happen outside the liver in another tissue

57
Q

once lipophilic xenobiotics reach the liver, what happens if phase 1 reaction only happens

A

the reactive intermediate (xenobiotic metabolite) will leave the liver and either:

  1. damage DNA in another tissue
  2. phase 2 reaction will occur in another tissue and the product will be excreted
58
Q

once lipophilic xenobiotics reach the liver, what happens if both phase 1 and 2 reactions happen

A

the water soluble xenobiotic metabolites leave the liver to the kidney and then are excreted in the urine

59
Q

once lipophilic xenobiotics reach the liver, what happens if the xenobiotic is bound to bile acids

A

the lipophilic xenobiotic will be trapped in the enterohepatic circulation

60
Q

where does the blood from GIT go

A

all of the blood from the GIT goes directly to the liver via the HPV

61
Q

what organ gets first chance to metabolize and remove compounds absorbed by GIT

A

the liver gets 1st chance

62
Q

what are extra hepatic tissues

A

tissues that are not the liver

63
Q

generally, what does the liver regulate

A

the liver regulates how much xenobiotic or its metabolites reach the other tissues of the body, and how harmful they are

64
Q

what has implications on how effective pharmaceutical drugs are

A

first pass metabolism by the liver

65
Q

all of the venous blood returning to the heart goes where

A

all of the venous blood returning to the heart then goes to the lung

66
Q

what organ is most vulnerable to xenobiotocs/metabolites that are in venous blood flow

A

the lung

67
Q

what organ has greatest xenobiotic metabolizing capacity

A

the liver has the greatest xenobiotic metabolizing capacity and a great capacity to regenerate when injured

68
Q

when does the liver synthesize bile

A
  • immediately after first pass metabolism

- after xenobiotics or xenobiotic metabolites are delivered to the liver via venous blood flow

69
Q

what are the three natural routes of xenobiotic exposure

A

skin
lung
oral

70
Q

describe action of topical xenobiotic exposure

A

direct action/exposure on skin

71
Q

describe action of inhalation xenobiotic exposure

A

direct action/exposure on lung

72
Q

describe the action of per of xenobiotic exposire

A

direct action/exposure on GIT

73
Q

describe where xenobiotic goes after topical exposure

A
  • encountered on skin
  • x passes into localized capillary bed in skin
  • x travels into Venus blood
  • lung is first major capillary bed that x goes to
  • x is then distributed to all tissues of the body
74
Q

is there first pass metabolism in topical exposure

A

no

75
Q

describe where xenobiotic goes after inhalation exposure

A
  • encountered in lung

- x is evenly distributed to all tissues

76
Q

is there first pass metabolism in lung exposure

A

no

77
Q

describe where xenobiotic goes after per os exposure

A
  • oral, esophageal, and GIT encounter x
  • x must cross both apical and basolateral membrane of the epithelial cell to enter blood or lymph
  • x goes to liver for first pass metabolism
78
Q

what are the 2 possible fates of large lipophilic x in small intestine

A
  1. bind to bile/bile acids so that it enters HPC
    - then goes to liver and is trapped in ECH
  2. incorporated into a chylomicron and circulate in lymph first
    - then through systemic circulation and return to liver in a chylomicron remnant
79
Q

once in the liver what are the two fates of x/x metabolite

A
  1. trapped in EHC

2. X leaves liver via hepatic vein, goes to inferior vena cava, then heart, lung, then body

80
Q

what xenobiotics will accumulate in lipid-rich tissues?

A

PCB, dioxins, mercury

- resist metabolism and have very long half lives

81
Q

when a xenobiotic acumulates in subcutaneous adipose tissue what happens

A

dioxin causes choracne

82
Q

what happens when xenobiotic accumulates in fetal brain

A

neurotoxicity, death

83
Q

what happens when xenobiotic accumulates in adult brain

A

neurotoxicity and cognitive dysfunction

84
Q

what are sinusoids

A

3D structures that allows the oxygen rich and nutrient-/x-rich blood mixes and flows past hepatocoyes for first pass metabolism

85
Q

what stores and releases biel

A

gall bladder

86
Q

why is liver resistant to carcinogenesis

A

low levels of cell division

- when liver is injured it can regenerate its structure via cell division

87
Q

describe topical and inhalation models

A
  • commonly used to mimic those types of natural human exposures
  • well-controlled dose and timing of x
  • no first pass metabolism
88
Q

describe IV/IM injection model

A
  • IV: x enters venous circulation, reaches the lung, then distributes throughout the body
  • IM: x enters muscle, then venous circulation, then lung
  • well controlled dose and timing of x
  • no first pass metabolism
  • not physiologically similar to natural human exposure
89
Q

describe oral xenobiotic model

A
  • x is mixed with food
  • x may unintentionally react with food ingredients
  • dose and timing of x is dependent upon animals food intake
  • vulnerable to first pass metabolism
90
Q

define ad libitum

A

eat as much or as often as desired

91
Q

describe gavage injection

A

ball-ended needle is inserted down esophagus and injects x into stomach

92
Q

describe gavage model

A
  • well controlled dose and timing
  • no food interactions
    no composure to oral/esophageal tissues
  • vulnerable to first pass
93
Q

benefits of in vitro study model

A
  • great control over variables
  • low system complexity
  • follows scientific method, proves casualty
  • often short and least expensive
  • minimal ethical burden
94
Q

negatives of in vitro study

A
  • low system complexity
  • potential lack of human applicability
  • ethical burden
95
Q

benefits of in vivo study

A
  • control over many variables
  • varying system complexity
  • follows scientific method
96
Q

negatives of in vivo study

A
  • less control over variables
  • potential lack of human applicability
  • ethical burden
97
Q

what are knockout mice

A

a genetically modified mouse in which researchers have inactivated or knocked out an existing gene

98
Q

what is an inducible knockout mouse

A

chemical inducing agent exposure will knockout gene of interest
- researchers control when gene is no longer expressed

99
Q

what are reporter mice

A

a gene encoding a fluorescent, bioluminescent proteins or biochemical tag are inserted into the genome
- when gene is expressed and translated into a protein, that protein will be fluorescent and can be detected

100
Q

describe human intervention invivo study

A
  • randomized, double bladed, placebo-controlled human intervention or RCT is described as the gold standard
101
Q

benefits of human intervention study

A
  • control over some variables

- high system complexity

102
Q

negatives of human intervention study

A
  • high system complexity
  • potential lack of human applicability
  • lack of human applicability
  • ethical burden
  • long duration and expensive, or short and misleading and still expensive
103
Q

benefits of surveys- observational studies

A
  • applicable to human health

- limited ethical burden

104
Q

negatives of surveys- observational studies

A
  • limited control over variables beyond study design
  • no control of behaviour
  • no randomization
  • no intervention
  • does not prove causality, only association
105
Q

what is a case-control/retrospective survey

A
  • 2 populations at the start; diseased and healthy
  • effective for low incidence and long latency diseases
  • effective for capturing life-long behaviours
106
Q

benefit of case-control/ retrospective survey

A

shorter and less expensive than cohort

107
Q

negative of case-control/retrospective survey

A
  • real of exposure information introduces error and bias
  • control group may not be optimally matched to case group
  • case and control groups may not be representative of general population
108
Q

what is a cohort/prospective survey

A
  • one population at the start, all healthy

- effective for high incidence and short latency diseased

109
Q

benefit of cohort/prospective survey

A
  • less real error/ bias

- control group optimally matched to diseased group

110
Q

negative of cohort/prospective survey

A
  • selection of starting population may be biased
  • larger sample size needed, more expensive
    may not accumulate disease outcomes of interest
111
Q

what is an odds ratio and relative risk/risk ratio

A

estimates of the strength of association between an exposure and an outcome

112
Q

what is the interpretation of a OR or RR of 1

A

no statistical significant difference in the risk of the outcome between the exposed and unexposed groups

113
Q

what is the interpretation of a OR or RR of 0.5

A

one group is at half risk of the outcome as the other group

114
Q

what is the interpretation of OR or RR of 0.7

A

one group has a 30% decreased risk of the outcome

115
Q

what is the interpretation of OR or RR fo 1.7

A

one group has a 70% increased risk of the outcome, or 1.7-fold risk

116
Q

if the confidence interval contains 1:

A

there is no statistically significant difference in the risk of the outcome between the exposed and unexposed groups

117
Q

p- value of <0.05

A

less than 5% chance of false positive result, meaning researchers are 95% confident in the stated outcome

NUTR 4510- Food, Tox, Nutrition (5 decks)

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