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NUTR*3210 > UNIT 10: MICRONUTRIENTS II; Vit E, Selenium, Vit C > Flashcards

UNIT 10: MICRONUTRIENTS II; Vit E, Selenium, Vit C Flashcards

1
Q

Oxidants act as ____ agents and Anti-oxidants act as ____ agents.

A

Oxidizing agents.

Reducing agents.

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2
Q

NAD is derived from ___ while FAD is derived from ___.

A

NAD - vitB niacin

FAD - vitB riboflavin

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3
Q

How are ROS formed?

A

O2 instead of ideally accepting 4e- to form H2O,

O2 accepts 1 or 2 e- to form –> ROS

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4
Q

What is a radical?

A

an unpaired e- in an orbital

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5
Q

Rank the order of reactivity of ROS and formation.

A

O2 (chain of donating e-)

  • mitochondrial leakage –>
  • superoxide anion radical (modest reactive)
  • -> via superoxide dismutase (SOD)
  • hydrogen peroxide (modest reactive)
  • -> via reduced iron or copper (e- donors)
  • hydroxyl radial (most reactive)
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6
Q

What are some biological roles of ROS?

A
  • T3/T4 synthesis (H2O2 needed to attach iodide)
  • arachidonic acid –> eicosanoids
  • immune function (macrophage generates to kill)
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7
Q

What are the 2 types of oxidant defense systems?

A
  • non-enzymatic

- enzymatic defense

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8
Q

Vitamin E and Vitamin C work as a part of which oxidant defense system?

A

non-enzymatic defense

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9
Q

Zinc, copper, manganese, selenium work as a part of which oxidant defense system?

A

enzymatic defense

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10
Q

What is the overall role of vitE in oxidant defense?

A

protect against lipid damage by hydroxyl radical

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11
Q

What is the overall role of of vitC in oxidant defense?

A

regenerate E to improve GSH:GSSG ratio

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12
Q

What is the overall role of copper, zinc, manganese in oxidant defense?

A

help superoxide dismutase (SOD) convert superoxide anione to hydrogen peroxide

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13
Q

What is the overall role of selenium in oxidant defense?

A

required for glutathione peroxidase

- converts hydrogen peroxide H2O2 –> water

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14
Q

What is vitamin E?

A

fat soluble vitamin

- mostly plants, less in animal tissues

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15
Q

How does vitamin E act as an antioxidant?

A
  • it donates e- to reduce damaging oxidant molecules

- it is the chain breaking antioxidant

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16
Q

What is the first line of oxidant defense?

A

glutathione (GSH) peroxidase

  • selenium required
  • converts H2O2 –> H2O
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17
Q

What is the second line of oxidant defense?

A

vitamin E

- chain breaking anti-oxidant

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18
Q

What is the only active/natural form of vitamin E? Dietary recommendations (RDA) for this form only.

A

RRR-a-tocopherol

R = natural configuration of methyl

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19
Q

What is the difference in structure of tocopherol and tocotrienol?

A

tocopherol - saturated

tocotrienol - unsaturated (-ene)

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20
Q

What is TTP?

A

Tocopherol Transfer Protein

  • incorporates tocopherol as a required form of vitE into VLDL to send to extrahepatic tissues
  • does not recognize tocotrienols - therefore not part of RDA
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21
Q

What is the chain breaking antioxidant defense?

A
  • role of vitamin E

- breaks the chain of lipid peroxidation initiated by hydroxyl radical

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22
Q

How is the superoxide anion radical formed?

A

O2 –> superoxide anion radical

- leakage of e- from ETC

23
Q

How is H2O2 formed?

A

superoxide anion radical –> H2O2

- superoxide dismutase

24
Q

How is hydroxyl radical fomed?

A

H2O2 –> OH . (hydroxyl radical)

- reduced by iron or copper

25
What are the reactions involved in lipid peroxidation?
- hydroxyl radical (OH . ) attacks PUFA = PUFA free radical (short lived) - PUFA free radical + O2 = PUFA peroxyradical - vitamin E breaks PUFA peroxyradical before it attacks another PUFA - -> forms PUFA hydroperoxide
26
What happens to PUFA hydroperoxide?
product of vitE breaking down PUFA peroxyradical - degrade to short aldehyde or - degraded by fatty acid peroxidase enzyme to reduce to fatty acid alcohols
27
What is the third line of antioxidant defense?
Fatty acid peroxidase enzyme - uses selenium and glutathione (GSH) as electron donor - converts PUFA hydroperoxide --> fatty acid alcohols
28
How is the vitE radical metabolized?
- vitE radical that formed from PUFA peroxy --> PUFA hydroperoxide - vitE radical is regenerated by vitamin C --> active vitE - vitE dimerizes to be excreted in the feces in bile - vit E is incoroporated to quinone and excreted in urine
29
What causes vitE deficiency?
not diet! - mutation in TPP (TPP moves vitE to be incorporated to VLDL to extrahepatic tissues) - gall bladder removed/impaired pancreatic damage - premature infants who are exposed to too much O2 (ROS)
30
What are effects of vitE toxicity?
- one of the least toxic vitamins but damage can cause muscle weakness, fatigue, GI distress - increases in hemorrhagic CVD
31
What is selenium?
a micromineral | - soil selenium is incorporated into cysteine and methionine via plant foods
32
What are 3 forms of selenium in the diet?
- selenocysteine - selenomethionine - selenite (inorganic)
33
What is the role of selenium in oxidant defense?
Selenoprotein enzymes: - GSH peroxidase - Fatty acid peroxidase
34
Glutathione GSH substrate is a _____ agent. It ____ __ electrons.
- Reducing agent - donates one e- - therefore, 2 GSH are required for 2 e- transfers
35
Both GSH peroxidase (1) and FA peroxidase (3rd line of defense) require selenium as the form of..
active selenocysteine
36
GSH peroxidase uses 2GSH molecules, donates 2 e- to convert ____ to ____. FA peroxidase uses 2GSH molecules, donates 2e- to convert ____ to ____.
GSH peroxidase: H2O2 ---> H2O FA peroxidase FAOOH = PUFA hydroperoxide --> FAOH = PUFA alcohol
37
GSH is converted to ____ during (GSH/FA) peroxidase activity
GSSG - ratio of GSSG increases as peroxide activity increases
38
How is GSH regenerated?
2 e- donated from NADPH to 2 GSSG --> 2GSH
39
How is NADPH regenerated?
HMPS - hexose monophosphate shunt (it also makes ribose sugars for DNA/RNA)
40
What is the engine that drives oxidant defense?
HMPS | - chronic upregulation of HMPS genes
41
What is a healthy ratio of GSH:GSSG?
90% GSH 10% GSSG too much GSSG = indicator of oxidative stress
42
What is Keshan's disease?
deficiency in selenium | - Keshan county in China - low selenium diet
43
What is vitamin C?
water soluble vitamin | = ascorbic acid
44
Vitamin C is synthesized in the small intestine of humans. True/False
False. Humans cannot synthesize vitamin C. - due to lack of gulonolactone oxidase - converts glucose/galactose --> ascorbic acid
45
What is the role of vitamin C?
oxidant defense | - electron donor to vitamin E radical --> reduced vitamin
46
Vitamin C deficiency changes ____ GSH:GSSG.
increase in GSSG and decrease in GSH
47
Vitamin C is also required for ____ reactions, and _____ modfication
- hydroxylation reaction (indirectly) | - post-translational modification of pro-collagen
48
Vitamin C is essential for the formation of _____
collagen
49
Explain how procallagen is post-translationally modified.
- procollagen goes under post-translational modification | - hydroxyl groups are added to proline via prolyl hydroxlase
50
Prolines account for 30% of amino acids in procollagen. Prolines are modified -->
hydroxyproline via prolyl hydroxylase
51
How is vitamin C involved in procollagen modfications?
- Prolyl hydroxylas has reduced iron in centre - when proline is hydroxylated to hydroxproline, iron centre is oxidized to Fe3+ - VitaminC/ascorbic acid, donates an e- to reduce Fe3+ to Fe2+ - prolyl hydroxylase Fe2+ is now active
52
How does vitC treat colds?
- reduce oxidized products from WBC viral infections and decrease inflammation
53
What are symptoms of vitC deficiency?
- impaired collagen synthesis (teeth, hair loss, wound healing, bleeding gums) - low absorption of iron in small intestine
54
What are indicators of vitamin C toxicty?
- diarrhea (osmotic effects) - kidney stones (urine excreation of oxalate and urate) - rebound scurvy infants with vitC-supplementing mothers

NUTR*3210 (15 decks)

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