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CVD > Polyphenols 1 > Flashcards

Polyphenols 1 Flashcards

1
Q

What does >12 years education do to your life expectancy?

A

+ 5 years

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2
Q

What does being overweight do?

A
  • 4 months
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3
Q

What does being obese do?

A
  • 4 years
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4
Q

What does smoking do?

A
  • 7 years
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5
Q

What does increasing fruit and veg consumption from 1 to 5 portions/day do?

A

+1 year

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6
Q

What happens with age?

A

There is an increased risk of chronic disease

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7
Q

What is hugely linked to chronic disease?

A

oxidative stress

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8
Q

What can cause oxidative stress?

A

Living and breathing
Environment
UV exposure
Diet e.g high sugars, high fat

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9
Q

What does oxidative stress lead to in general?

A

Chronic

Inflammation and perturbed metabolism

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10
Q

What does Chronic

Inflammation and perturbed metabolism lead to?

A

Cancer
Cardiovascular
Diabetes
Accelerated ageing

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11
Q

What is oxidative stress?

A

imbalance between the production of free radicals/reactive oxygen species (ROS) and the neutralization of ROS before damage is caused, or subsequent repair of damage

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12
Q

What is a free radical?

A

any chemical species (atom, molecule or ion), capable of independent existence, with 1 or more unpaired electrons

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13
Q

What are ROS molecules like?

A

highly unstable molecules created normally in vivo and also due to external risk factors

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14
Q

What are important radicals?

A

Quantitatively most important: superoxide radical (O2•-)

Other important radicals: hydroxyl radical (OH• ) and nitric oxide (NO•)

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15
Q

How is oxidative stress and chronic disease linked?

A

Progression of several chronic diseases linked to oxidative stress in vivo e.g.
Oxidation of LDL –> plaque formation in blood vessels

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16
Q

What is the rate of living hypothesis?

A

the higher the metabolic rate of an organism, the greater the production of reactive oxygen species (ROS) and hence the shorter the life span.

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17
Q

What goes against the rate of living hypothesis?

A

Birds live longer than predicted by their metabolic rates.
At a given metabolic rate, mitochondria from birds produce fewer ROS so ROS production rather then metabolic rate provides the strongest correlation with overall longevity.

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18
Q

What are endogenous sources of oxidative stress?

A 
Mitochondria 
Peroxisomes 
Lipoxygenases 
NADPH oxidase 
Cytochrome P450
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19
Q

What are exogenous sources of oxidative stress?

A

Ultraviolet light

Ionizing radiation Chemotherapeutics Inflammatory cytokines Environmental toxins

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20
Q

What are antioxidant defences that counteracts and regulates overall ROS levels to maintain physiological homeostasis?

A

Enzymatic systems (CAT, SOD, GPx)
Non-enzymatic systems (Glutathione,
Vitamins (A,C and E))

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21
Q

What does too little ROS in body cause?

A

Impaired physiological function

  • Decreased proliferative response
  • Defective host defences
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22
Q

What does the right level of ROS cause?

A

Homeostasis, normal growth and metabolism

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23
Q

What does too much ROS in body cause?

A

Impaired physiological function

  • random damage to proteins, lipids and DNA
  • may also constitute a stress signal that activates specific redox-sensitive signalling pathways
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24
Q

What happens in lipid peroxidation?

A
  • free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage.
  • commonly affects polyunsaturated fatty acids, they contain multiple double bonds that possess especially reactive hydrogen atoms.
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25
Q

What is step 1 of lipid peroxidation?

A

Initiation: fatty acid radical is produced. Common initiators in living cells are reactive oxygen species (ROS), such as OH· and HOO·, which combines with a hydrogen atom to make water and a fatty acid radical.

Unsaturated lipid + -OH –> lipid radical (H2O removed)

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26
Q

What is step 2 of lipid peroxidation?

A

Propagation: fatty acid radical is not a very stable molecule, so it reacts readily with molecular oxygen, creating a peroxyl-fatty acid radical. This radical is also an unstable species that reacts with another free fatty acid, producing a different fatty acid radical and a lipid peroxide, cycle continues

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27
Q

What can this propagation cause?

A

chains of destruction damaging DNA, proteins, lipids etc.

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28
Q

What is step 3 of lipid peroxidation?

A

Termination: occurs when a radical meets another radical (needs high conc of radical species) or an antioxidant e.g. vitamin C

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29
Q

Why are ROS produced?

A

On purpose: cell proliferation & signalling (H202) or during inflammation
Accidentally: superoxide radical through electron leakage in mitochondria

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30
Q

Who came up with the Free Radical Theory of Ageing?

A

in 1956 by Denham Harman

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31
Q

What does evidence suggest regarding obesity and oxidative stress?

A

Obesity induces oxidative stress

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32
Q

How do oxidative stress levels increase in obesity?

A

Increasing oxidative stress levels with increasing BMI (linked to TBARS, F2-isoprostanes, oxLDL levels) and lower antioxidant capacity and plasma antioxidant levels

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33
Q

What does the excessive accumulation of fat lead to?

A

enhanced production of ROS in adipocytes and systemic tissues

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34
Q

What else is ROS positively correlated with (other than obesity)?

A

incidence of neuronal degeneration, cardiovascular events, diabetes mellitus and cancer

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35
Q

What is the antioxidant hypothesis?

A

Concept that “antioxidants” could cure cancer, CVD or diabetes mellitus

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36
Q

What does epidemiology suggest regarding the antioxidant hypothesis?

A

associations between high consumption of fruit and vegetables (=high in antioxidants) and lower incidence of certain “oxidative stress” related diseases

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37
Q

What is an example of an application of this?

A

“5 a day” campaign in UK since 2002 – based on WHO advice to consume 400g Fruit & Veg per day

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38
Q

Oxidation is essential to get energy from fats, but what is the problem?

A

The functioning of mitochondrial protein can cause superoxides that cause damage/oxidative stress
BUT can be removed by endogenous defences

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39
Q

What is the problem with endogenous defences?

A

May be insufficient

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40
Q

What is a solution to insufficient endogenous defences?

A

Exogenous antioxidant defences from the diet – e.g. vitamin E, C

Increase endogenous defences (boost our own defences)

Inhibit oxidative processes such as superoxide generating metabolic enzymes

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41
Q

How do polyphenols work in the body?

A

Although polyphenols are chemical antioxidants, they do not act by direct chemical antioxidant mechanisms in the body

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42
Q

What does the evidence between diet and CVD disease risk show? (Hu and Willett, 2002)

A

Fruits and some vegetables and WG high in polyphenols

Causes reduced risk

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43
Q

What is important in the definition of antioxidants?

A

Compounds (polyphenols, vitamin C, E, carotenoids) and food preservatives such as BHT are antioxidants in vitro

  • Inhibition of lipid rancidity
  • All “antioxidant” assays not involving cells or organisms
  • Chemical property to scavenge radicals etc.
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44
Q

What are examples of in vitro antioxidant assays?

A 
Superoxide scavenging 
Hydrogen peroxide scavenging 
Hydroxyl radical scavenging 
Metal ion-dependent hydroxyl radical scavenging 
Peroxyl radical scavenging 
Lipid-soluble peroxyl radicals 
ORAC, TEAC, TRAP
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45
Q

What is not an antioxidant?

A

Concept of an antioxidant has been refined especially based on in vivo experiments

Chemical antioxidant assays such as TRAP, TEAC, ORAC etc. are NOT indicative of a biological condition

Rather they are content, rather than functional assays

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46
Q

What is an example of these content rather than functional assays?

A

Vitamin C – water soluble essential antioxidant
Vitamin E – fat soluble essential antioxidant
Polyphenols – good antioxidants, generally healthy
BHT – excellent antioxidant, some mild toxicity
a-Amanitin – antioxidant but deadly mushroom toxin

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47
Q

What does the current more complex view look at?

A
  • how much is absorbed into the body
  • specific molecular actions which are affected in the body, resulting in a change of a biomarker and disease risk
  • Chemical antioxidant assays on foods give information on content of polyphenols and other redox active compounds but NOT health benefit
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48
Q

How can antioxidant activity of plasma by measured?

A

by the TEAC assay e.g. vitamin C 3%

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49
Q

What did EFSA publish on cocoa flavanols and maintenance of normal endothelium-dependent vasodilation?

A

200 mg of cocoa flavanols should be consumed daily.
This amount could be provided by 2.5 g of high-flavanol cocoa powder or 10 g of high-flavanol dark chocolate, both of which can be consumed in the context of a balanced diet.
The target population is the general population.
*evidence from 5 published and 1 unpublished randomised controlled trials in healthy subjects

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50
Q

How can phytochemical, phytonutrients be categorised?

A

Phenolics (e.g. ferric acid, caffein acid)
Polyphenols
Glucosinolates (sulforaphane)

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51
Q

Where are chlorogenic acids found?

A

In coffee

An ester of quinic acid and caffeic acid (linked in 3 different positions via ester bond)

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52
Q

What is the major form of chlorogenic acid in coffee?

A

5-caffeoylquinic acid (5-CQA)

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53
Q

What strongly affects amount of chlorogenic acid in the diet?

A

coffee consumption
None: 10-100mg chologenic acid in diet
Heavy: 500-2000

54
Q

What can polyphenols be separated into?

A

Phenolics
ellagic acid/ellagitannins
Flavonoids
Isoflavones (genistein, daidzein)

55
Q

What can flavonoids be separated into?

A

Flavonols (e.g. quercetin)
Flavanols
Anthocyanins
Flavanones (e.g. hesperidin)

56
Q

What is high in quercetin?

A

onions (present as glycosides)

57
Q

How are many flavonoids found in foods?

A

As glycosides

58
Q

Describe hesperidin?

A

Hesperidin is a flavanone rhamnoglucoside that is present in Citrus fruits and juices especially oranges.
(a-L-rhamnose + b-D-glucose
+ hesperetin)

59
Q

What do anthocyanins give in food?

A

Dramatic colour

60
Q

What has high anthocyanin content?

A

chokeberry, red grapes

61
Q

What can flavanols be separated into?

A

Catechins

Pro(antho)cyanidins

62
Q

What are examples of catechin?

A 
Catechin
epicatechin
epigallocatechin
epigallocatechin gallate
epicatechin gallate
63
Q

Top three foods based on phenol content?

A

Dark choc, blackberry, high bush blueberry

64
Q

How can we measure polyphenols?

A

Measurement of polyphenols is by HPLC linked to UV an/or mass spectrometry detection

65
Q

What is the polyphenol % in tea?

A

30%
Mostly catechins
In green tea mostly EGCG

66
Q

What is the difference between green and black tea?

A

Green tea has no colour and catechin
After short fermentation

Oolong tea is orange-yellow and has theaflavins
After full fermentation

Black tea is red-amber and has thearubigins

67
Q

What are catechin quantities in leaves?

A

Green tea dry leaves 12514mg/100g

Black tea dry
3316mg/100g

68
Q

What happens when 2 to 5 of the catechins join?

A

they are called dimers; and when two to five are linked they are called proanthocyanidins

69
Q

What is the role of polyphenols in the plant?

A 
Protection from UV light
Wound healing
Protection against stress
Anti-fungal 
Anti-bacterial
Anti-insect
70
Q

What does boiling do to quercetin?

A

Boiling does not change the level of quercetin glucosides in onion, but some is leached into the cooking water.

71
Q

What does storage do?

A

On storage, some quercetin-4’-monoglucoside is lost whereas quercetin-3,4’-diglucoside increases. There is almost no free quercetin.

72
Q

What does frying do?

A

There is a 20-25% loss in quercetin (Q) conjugates after frying for 15 min.

73
Q

What does autolysis (destruction of own cells) result in?

A

conversion of Q-3,4’-diglucoside to Q-4’-glucoside and to free Q, over a period of 24 h.

74
Q

What does microwaving broccoli do?

A

15 min hardly affects the amount or nature of flavonol glycosides.

75
Q

What is cocoa high in?

A

Cocoa is high in epicatechin, but processing affects the content dramatically

76
Q

What are transit times in the body?

A 
Stomach: 10 min (saline) to 
4 h (lipid portion of large meal)

Small intestine: 3-4 h

Large intestine: 48-96 h

77
Q

Where does most absorption occur?

A

in the small intestine

78
Q

How is the mechanism of absorption examined?

A

Cultured human intestinal Caco-2 cells as a model to examine the mechanism of absorption

79
Q

How does food absorption work in general?

A

Only a fraction of a food component is absorbed

Only a certain percentage (0-100%) of a compound is absorbed –> metabolized (0-100%) –> and finally available to certain organs of the human body

Some is released into colon (faeces), some through intestine (some goes back to colon) then some into bloodstream and liver

80
Q

How can bioavailability of flavonoids be determined?

A

Oral faecal balance

Post prandial test

Chronic consumption

81
Q

Oral faecal balance

A

BV = intake – faecal content

Gut degradation means that flavonoids appear “100%” absorbed
Ileostomists (no colon) more useful for small intestinal absorption
Most useful for minerals

82
Q

Post prandial test

A

BV = Area Under Curve after oral
consumption of one
dose

Best for comparison between
treatments
Subject is his own control

83
Q

Chronic consumption

A

BV = amount in urine (e.g. over 24 h)

Closer to consumer situation
Steady state, and can indicate
absorption over a long period of time
Gives a MINIMUM amount or percentage absorbed
Different flavonoids behave differently – so can only compare for the same flavonoid

84
Q

What does Cmax mean in bioavailability?

A

max concentration it reaches, indicates the max conc in the plasma

85
Q

What does AUC mean?

A

Area under curve

- indicates how much has gone into plasma

86
Q

What must be considered in bioavailability?

A

Effect of

  • dose
  • matrix
  • chemical attachments
  • chemical structure
  • hydrophobicity
87
Q

What is cmax for flavonoids in humans normalised to?

A

50mg dose

assuming xmax increases linearly with dose e.g. with 50mg dose of isoflavones cmax=2um then 100mg rose would give 4um

88
Q

What is 50mg dose of hesperidin?

A

0.5um cmax

89
Q

What can be said about quercetin glucoside?

A

Bioavailability almost as high as isoflavones

90
Q

What can be said about Rutin (other form of quercetin)?

A

much less bioavailable

  • it is very similar to the glucoside
  • has an extra rhamnose attached so less easily absorbed
91
Q

What can be said about flavanol bioavailability?

A

EC + ECGC = medium levels, EGC = much more bioavailable

92
Q

What can be said about • Anthocyanidins + proanthocyanidin dimers?

A

poorly absorbed

93
Q

How can we derive the Half life of the polyphenols?

A

from the pharmacokinetic curve

94
Q

What can be said about polyphenols in body?

A

Unlike vitamins/minerals which are used in the body, they aren’t stored in the body – only spend certain amount of time in blood

95
Q

What does half life indicate?

A

Time spent in body

96
Q

What can be said about cmax and half life?

A

There is no correlation

97
Q

What would we predict about effectiveness?

A

Would predict that most effective ones would be ones with highest cmax (best bioavailability) but half life can also affect effectiveness

98
Q

What are the general Half life?

A
  • Isoflavones: 5-7h
  • Flavanones: 2h
  • Flavonols: 17-20h
  • Flavanols: 2-4h
99
Q

How can we find out tmax?

A

From the curve

the time the cmax occurs

100
Q

What does tmax effect?

A

Where the compound is absorbed (under 4 hours is stomach and SI - mostly SI)

101
Q

Where are isoflavones, flavanones and rutin absorbed?

A

Colon = higher Tmax

102
Q

Where are Quercetin glucoside + flavanols absorbed?

A

Small intestine = lower Tmax

103
Q

What is rhamnose and glucose attached to?

A

o Hesperidin
o Naringin
o Rutin

104
Q

What does rhamnose and glucose attached to Hesperidin, Naringin and Rutin mean?

A

o All have higher Tmax = abs in colon

105
Q

What occurs with only glucose attached?

A

Lower Tmax = absorption in SI (e.g. quercetin glucoside)

106
Q

What occurs when no sugar is attached e.g. flavanols?

A

Also low Tmax = abs in SI

107
Q

What does this imply?

A

glucose is removed in SI and rhamnose cannot be removed in SI so has to be hydrolysed in the colon

108
Q

What are enterocytes in SI responsible for?

A

deciding if polyphenols move from gut lumen into blood stream

109
Q

What is the arrangement between gut lumen, enterocyte and blood?

A

Gut lumen boarders enterocyte with apical membrane and enterocyte boarders blood with basolateral membrane

110
Q

What occurs in first step in metabolism of lactose or polyphenol with glucose attached?

A

LPH = lactase phlorizin hydrolase
o Hydrolyses lactose
o Remove glucose from polyphenols
o Is on surface of enterocyte, so to be hydrolysed the molecule doesn’t have to enter the cell

111
Q

What is an example of this?

A

quercetin glycoside (3- or 4’-) –> quercetin aglycone

Can now abs by passive diffusion

Membrane is hydrophobic, quercetin aglycone = sufficiently hydrophobic to pass through

112
Q

What is the alternative pathway to this?

A

o Quercetin 4’-glycoside slowly diffuses through membrane
o Cytosolic b-glucosidase can de-glycosylate
o Minor pathway compared to the other

113
Q

What does passive diffusion depend on?

A

flavonoid size, hydrophobicity, cellular gradient

114
Q

What occurs with attached rhamnose?

A

prevents absorption in the small intestine

115
Q

What is an example of this?

A

Rutin (quercetin with glucose + rhamnose)
o is not a substrate for LPH
o Too big to diffuse through membrane
o Even if it did, no enzyme to remove rhamnose
o Gut microflora can produce enzyme to remove rhamnose
o So in colon = hydrolysed + absorbed

116
Q

What is the deciding factor if something is absorbed in SI?

A

brush border enzymes

117
Q

What happens after the initial step of metabolism?

A

A proportion of absorbed polyphenols are conjugated in the enterocyte

118
Q

What happens once quercetin is in enterocyte?

A

• Chemically changed by various enzymes e.g. UGT (glucuronosyl transferase)
–> adds glucuronide group to quercetin
• This changes properties of quercetin –> more H2O soluble –> can’t diffuse through membrane anymore so needs specific protein transporter

119
Q

What happens after this step?

A

Polyphenols are exported back to the lumen or absorbed into the blood depending on the specificity of apical and basolateral transporters

120
Q

What happens if quercetin is changed to 3’-glucuronide?

A

o ABCG2 transporter on apical membrane = specific to this form
o So it is effluxed back out into gut lumen

121
Q

What happens if quercetin is changed to the 2 other forms (3- and 7-glcA)?

A

ABCC1/C3 transporter on basolateral membrane = transport them into blood

122
Q

What is an aglycone?

A

No sugar attached (so can enter enterocyte)

123
Q

What does specificity of enzymes e.g. UGT do?

A

Decides whether it is absorped as different forms require different transporters

124
Q

Why is colonic bacteria important?

A
  • Important for some polyphenols e.g. rutin

* Can remove rhamnose

125
Q

What can colonic bacteria produce?

A

glycosidases, glucuronidases, and sulfatases that can strip flavonoid conjugates of their sugar moieties, glucuronic acids and sulfatases

126
Q

What biological effects we associate with flavonoids are linked to cardio-vascular disease?

A 
Inflammation
Hypertension
Improvement of vascular function
Antiatherogenic
Platelet aggregation  
Proliferation
Cellular and mitochondrial protection  
Modulating blood glucose and blood lipids  
Modulating NO metabolism
127
Q

What does dark chocolate consumption do?

A

Ingestion of dark chocolate (40 g) significantly improves flow mediated dilation (FMD) after two hours.
White chocolate has no effect.
N = 10 in each group.
The increase in FMD lasts for eight hours after the ingestion of dark chocolate.

128
Q

Does green tea affect FMD?

A

consumption of 200mg EGCG as isolated EGCG, green tea extract, or green tea
Only green tea increased FMD

129
Q

What is the relationship between EGCG plasma levels and changes in FMD?

A

EGCG plasma levels not correlating with changes in FMD
HOWEVER
Caffeine correlated with FMD changes

130
Q

Does Orange juice and hesperidin affect CV risk markers?

A
  • Acute trial
  • Baseline and 5h post intake
  • Men with higher risk 320mg hesperidin
  • tested control, OJ, hesperidin supplementation
  • Plasma levels only high after juice intake
  • No effect on vascular markers of both juice and supplement
131
Q

Do berries effect FMD?

A

Double blind randomized controlled crossover trial
N=10
FMD % response up to 8h post consumption

1% increase in FMD - decrease in CVD risk of 10-13%

132
Q

How do polyphenols improve vascular function?

A

Likely involving a number of mechanisms

increase in NO bioavailability as FMD is at least partially NO mediated

Induction of eNOS enzyme to increase NO

Prevention of oxidative damage in endothelial cells by increased Nrf2 signalling

CVD (12 decks)

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