NUTR 302 > Vitamin E > Flashcards

Vitamin E Flashcards

(46 cards)

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1
Q

What is the general term for the vitamin E isoforms?

A

Tocochromanols
* General term for structurally similar compounds which exhibit the activity of RRR-α-tocopherol
* Covers 8 different compounds Just by small changes to structure

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2
Q

Classification of the vitamin E isoforms

A
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3
Q

What is the active isoform of vitamin E?

A

𝝰-tocopherol

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4
Q

General structure of Tocopherols and tocotrienols

A

The structure has 2 parts
* head group with methyl substitutions at R1, R2 and R3 which can change the structure
* phytate chain (FA chain) which has double bonds for the tocotrienols but not for tocopherols

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5
Q

What impacts natural vitamin E activity?

A
  • position of methyl group
  • Addition of double bonds
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6
Q

Structure and Activity of Naturally- Occurring forms of Vitamin E

A
  • additions of double bonds reduces vitamin E activity
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7
Q

Synthetic Forms of α-Tocopherol

A
  • Esterified at the phenolic hydroxyl group
  • 3 chiral centres → mixed isomers
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8
Q

why is synthetic 𝝰-tocopherol esterified?

A

Increases stability of a supplement
* Ester usually gets cleaved off during digestion to liberate the active form of a-tocopherol

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9
Q

Difference between natural and synthetic 𝝰-tocopherol

A

the natural has biologically set chiral centres but the synthetic form may be mixed and this can reduce activity

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10
Q

What is the biological activity of Vit E affected by for natural and synthetic?

A
  1. The presence of double bonds in the phytyl tail
  2. The location of methyl groups on the phenolic ring
  3. Configuration of the 3 chiral centres (synthetic only)
  4. Esterification of the phenolic ring (although hydrolyzed in digestive tract)
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11
Q

Tocochromanol Absorption

A

VitE isoforms are non-polar molecules that are incorporated into micelles in the gut and enter enterocyte via passive diffusion where they are incorporated into the middle of Chylomicrons and secreted into lymph.
* ~50% of dietary tocochromanols are absorbed
* remaining excreted in feces
* Esterases cleave synthetic forms to free tocopherol

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12
Q

General lipid absorption

A
  1. fat globule is emulsified by bile salts and forms micelles (containing vitE)
  2. passive diffusion of micelle into enterocyte
  3. packaged into TG rich CM
  4. secreted into lymph
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13
Q

Tocochromanol Transport

A
  • VitE is transported in CM and most is delivered to liver in CMr.
  • α-tocopherol transfer protein (α-TTP) preferentially binds 𝝰-toco and can transfer it between membranes
  • Repackaged into VLDL for delivery to other tissues
  • Some may also be transferred to HDL via ABCA1 (ATP-binding cassette protein A1)
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14
Q

Intracellular metabolism of tocochromanol in the hepatocyte (what happens when vitE reaches the liver?)

A

Essentially the metabolic processes in the hepatocyte concentrate the 𝝰-tocopherol form.
* CMr come back to liver
* Uptake is receptor mediated endocytosis
* During intake, aTTP preferentially recognizes 𝝰-toco and transfers it into different membranes (bile, VLDL, HDL)
* Other isoforms are broken down by ER and mito to soluble forms and are excreted

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15
Q

How are Tocochromanols excreted?

A

Efficiently metabolized for excretion (Does not exceed >2-3 x [plasma]) the VitE breakdown converts it from lipid soluble to aqueous soluble which can then be excreted via tocopherol-ω- oxidation

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16
Q

Tocochromanol Breakdown

A

Breakdown chain and make it smaller and excretion can occur through bile or through urine
* Initiated by CYP-4F2
* truncation of the phytyl side chain to 2’-carboxyethylhydroxychromanol metabolites (CEHC’s)
* Conjugated to glucuronic acid/sulfates for urinary (or biliary) excretion

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17
Q

How are tissues enriched with 𝝰-tocopherol?

A

α-TTP -preferentially binds α-tocopherol repackaging it while CYP-4F2 has lowest affinity for 𝝰-toco so other isoforms are broken down/ excreted.

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18
Q

Vitamin E storage

A

Intracellularly, vitamin E is stored in membranes but nosingle storage organ for vitamin E
* 90% of vitamin E is stored in white adipose tissue – very immobile pool and cannot adequately supply vitamin E to circulation in times of need
* Vitamin E in liver and RBC is readily available to be redistributed to places where needed

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19
Q

Where do free radicals target in disease?

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A
  • PUFAs
  • DNA + RNA
  • Proteins
20
Q

What does vitamin E protect against in regards to free radicals?

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A

Vit E is lipid soluble and found in membranes so protects against lipid oxidative stress

21
Q

Metabolic Functions of Vit E

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A

Lipophillic antioxidant
* Vit E is unique because of its location in the membrane so effective at breaking free radical chains and will react more readily with peroxyl radicals than PUFA and the tocopherol radical produced is less reactive.

22
Q

How much vit E is needed to be effective?

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A

Effective at low concentration (1 Vit E per 100s of PL)
* waits for radicals to occur

23
Q

Outcome of vit E anti-oxidant acitivty

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A

Thus, protects lipids and maintains membrane integrity

24
Q

How can vit E benefit food sources?

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A

Stability of highly unsaturated vegetable oils
* not applicable to foods fortified with esterified tocopherol

25
How does the lipid oxidation chain reaction occur?
1. hydroxyl radical occurs in aqueous solution which can attack lipids, proteins and DNA causing a lot of damage. 2. **Initiation (oxidation of membranes)**: hydroxyl radical will react to the double bonds in PUFA so get an unbalance of the electrons and it becomes reactive lipid radical. 3. The lipid radical can then react with oxygen making the lipid peroxide radical which is very reactive species 4. **Propagation (continueing chain reaction)**: The lipid peroxide radical can then attack another lipid resulting in lipid hydro peroxide + another radical produced which continues down the membrane.
26
How does vit E work to protect against the propagation of lipid oxidation?
Vit E quenches the chain reaction by scavenging free radicals * can react with the lipid radical and become one itself. We still get the lipid hydroperoxide but we stop the lipid radical from forming and the vit E radical does not react with other things.
27
How is the LOOH removed?
Can be reduced to a lipid alcohol via the glutathione peroxidase system which is less reactive
28
How is the tocopheroxyl radical recovered?
reduced back to 𝝰-toco by vitamin C * Cox then reduced by 2 GSH * GSSG then reduced by glutathione reductase
29
Rich sources of tocopherols
* animal fats * Oil seeds and vegetable oils (especially safflower) * Leafy green vegetables (Broccoli, spinach) * Fortified breakfast cereals
30
Tocochromanol DRIs
DRIs are for the 𝝰-tocopherol form only in mg/d * M/F - 15 mg/d * ↑ in pregnancy and lactation
31
How is Vitamin E status measured?
Measurement of plasma α-tocopherol concentration * normal plasma [Vit E]: 20 – 30 μM * linearly related to intake up to ~ 20 mg/day * Suppl. to 400 mg/day needed to double plasma [Vit E] * max50–60μM * Often measured as ratio to cholesterol
32
Functional test for vitamin E
Erythrocyte hemolysis upon oxidative stress * Give oxidative stress to RBCs and measure it. If low vit E than more oxidative stress would occur
33
Tocochromanol Deficiency
Deficiencies are very rare but usually functional deficiencies * due to widespread availability of vitamin E * due to recycling of vitamin E
34
Populations at risk
* familial α-TTP deficiency (cant move it around) * familial abetalipoproteinemia (Problems with lipoprotien metabolism or lipid absorption) * lipid malabsorption (CF; cholestasis)
35
What concentration of vit E is associated with erythrocyte hemolysis
[Serum]< 12 μM associated with erythrocyte hemolysis * Degeneration of CNS and peripheral nerves → ataxia * shorter life-span of RBCs
36
Tocochromanol Toxicity
UL is 1000 mg/d but relatively non-toxic * Quickly metabolised and excreted
37
Symptoms of toxicity
* Inhibition of blood clotting action of Vit K - Increases blood coagulation time * Reduces bioactivity of xenobiotics metabolized by CYP450
38
Interaction of vit E with other nutrients
* Function of Vit E closely tied to selenium in glutathione peroxidase (complementary action) * Complementary action of Vit E and C (Vit C can reduce Vit E radical back to Vit E) * Inhibits β-carotene absorption and metabolism in intestine * Impairs Vit K absorption and metabolism
39
How does vit E impair vit K absorption
* incl. phylloquinone (K1) → menoquinone * Increased risk for bleeding (interfering with Vit K-dependent clotting)
40
Vit E role in CVD Prevention
reduced CVD risk at higher intake of VitE * Fewer atherosclerotic plaques * Lower risk of CVD-induced mortality LDL goes into interstitial space and gets oxidized forming foam cells and vessel eventually gets blocked (oxidative process); higher vitamin E may lower risk of athersclerosis
41
Potential mechanisms of vit E preventing atherosclerosis
* Reduces free radical-induced oxidation * Protects against LDL oxidation * Decreases blood clotting
42
Evidence for the impact of vit E on CVD
CVD is a complex pathophysiology with multiple factors and vit E might be too simplistic * Overall mixed impact on myocardial infarction/ stroke [Very little benefit] as biomarkers were not used so do not know where the vit E went * Decreased biomarkers of lipid peroxidation: dependant on vitamin C status
43
Vit E: Role in Cancer
may be benefit in prostate cancer
44
Vit E on all cause mortality
No effect on all-cause Mortality Meta of all cause mortality intervention
45
What is vit E used as a therapy in?
currently one of very few therapies used clinically to treat Nonalcoholic Steatohepatitis (NASH) but this treatment doesn’t work if person has T2DM. * 360 mg/d for 96 weeks * PIVENS study
46
What happens in non-alcoholic fatty liver disease?
Oxidation eventually occurs in the liver and over decades get fibrosis and function degrades. * no treatment for the fibrosis part in clinical trials * 60-70% of obese people have this to some extent and really no treatment except weight loss * vitamin E is clinically accepted treatment however
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