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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
Q

What are the reactions involved in lipid peroxidation?

A
  • 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
Q

What happens to PUFA hydroperoxide?

A

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
Q

What is the third line of antioxidant defense?

A

Fatty acid peroxidase enzyme

  • uses selenium and glutathione (GSH) as electron donor
  • converts PUFA hydroperoxide –> fatty acid alcohols
28
Q

How is the vitE radical metabolized?

A
  • 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
Q

What causes vitE deficiency?

A

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
Q

What are effects of vitE toxicity?

A
  • one of the least toxic vitamins but damage can cause muscle weakness, fatigue, GI distress
  • increases in hemorrhagic CVD
31
Q

What is selenium?

A

a micromineral

- soil selenium is incorporated into cysteine and methionine via plant foods

32
Q

What are 3 forms of selenium in the diet?

A
  • selenocysteine
  • selenomethionine
  • selenite (inorganic)
33
Q

What is the role of selenium in oxidant defense?

A

Selenoprotein enzymes:

  • GSH peroxidase
  • Fatty acid peroxidase
34
Q

Glutathione GSH substrate is a _____ agent. It ____ __ electrons.

A
  • Reducing agent
  • donates one e-
  • therefore, 2 GSH are required for 2 e- transfers
35
Q

Both GSH peroxidase (1) and FA peroxidase (3rd line of defense) require selenium as the form of..

A

active selenocysteine

36
Q

GSH peroxidase uses 2GSH molecules, donates 2 e- to convert ____ to ____.
FA peroxidase uses 2GSH molecules, donates 2e- to convert ____ to ____.

A

GSH peroxidase:
H2O2 —> H2O

FA peroxidase
FAOOH = PUFA hydroperoxide –> FAOH = PUFA alcohol

37
Q

GSH is converted to ____ during (GSH/FA) peroxidase activity

A

GSSG

  • ratio of GSSG increases as peroxide activity increases
38
Q

How is GSH regenerated?

A

2 e- donated from NADPH to 2 GSSG –> 2GSH

39
Q

How is NADPH regenerated?

A

HMPS
- hexose monophosphate shunt
(it also makes ribose sugars for DNA/RNA)

40
Q

What is the engine that drives oxidant defense?

A

HMPS

- chronic upregulation of HMPS genes

41
Q

What is a healthy ratio of GSH:GSSG?

A

90% GSH
10% GSSG

too much GSSG = indicator of oxidative stress

42
Q

What is Keshan’s disease?

A

deficiency in selenium

- Keshan county in China - low selenium diet

43
Q

What is vitamin C?

A

water soluble vitamin

= ascorbic acid

44
Q

Vitamin C is synthesized in the small intestine of humans. True/False

A

False.
Humans cannot synthesize vitamin C.
- due to lack of gulonolactone oxidase
- converts glucose/galactose –> ascorbic acid

45
Q

What is the role of vitamin C?

A

oxidant defense

- electron donor to vitamin E radical –> reduced vitamin

46
Q

Vitamin C deficiency changes ____ GSH:GSSG.

A

increase in GSSG and decrease in GSH

47
Q

Vitamin C is also required for ____ reactions, and _____ modfication

A
  • hydroxylation reaction (indirectly)

- post-translational modification of pro-collagen

48
Q

Vitamin C is essential for the formation of _____

A

collagen

49
Q

Explain how procallagen is post-translationally modified.

A
  • procollagen goes under post-translational modification

- hydroxyl groups are added to proline via prolyl hydroxlase

50
Q

Prolines account for 30% of amino acids in procollagen. Prolines are modified –>

A

hydroxyproline via prolyl hydroxylase

51
Q

How is vitamin C involved in procollagen modfications?

A
  • 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
Q

How does vitC treat colds?

A
  • reduce oxidized products from WBC viral infections and decrease inflammation
53
Q

What are symptoms of vitC deficiency?

A
  • impaired collagen synthesis (teeth, hair loss, wound healing, bleeding gums)
  • low absorption of iron in small intestine
54
Q

What are indicators of vitamin C toxicty?

A
  • 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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