VITAMIN E
Fat soluble
RDA – vitamin E requirement and twice the coefficient of variation
Men: 15 mg alpha-tocopherol
Women: same
UL: 1,000 mg
Chemical Structure: there are eight compounds and each contain a phenolic functional
group on a chromanol/chromane ring and a phytyl tail.
This is the only vitamer with biologic activity
They are divided into two categories and all are found in RRR stereochemistry in
nature:
Tocopherols: have saturated 16 carbon side chains
Tocotrienols: have unsaturated 16 carbon side chains
R1 R2 R3
alpha CH3 CH3 CH3
beta CH3 H CH3
gamma H CH3 CH3
delta H H CH3
Contains a S: no
Nomenclature/ Bioactive Forms
Plants:
Chloroplast portion from plants (mostly alpha-tocopherol with some
gamma- tocopherol)
Nonchloroplast regions of plants (main sources of gamma, delta and beta-
tocopherol)
Animals: alpha- tocopherol (mostly – in the fatty tissues)
Dietary Sources
Foods:
Oils from plants (richest sources) – canola, olive, sunflower, safflower,
and cottonseed (alpha-tocopherol), soybean and corn olis (mostly
gamma-tocopherol); salad dressings, mayonnaise, margarine, and
peanut butter (good sources); whole grain cereals, legumes, and
some fruits and vegetables.
Legumes, wheat, barley, rice oats – especially bran and germ sections
(have tocotrienols)
Supplements: Have eight stereoisomers (RRR, RSR, RRS, RSS, SRR, SSR, SRS,
and SSS – not as effective as natural form) of the synthetic ester forms of
vitamin E (all-rac alpha- tocopheryl acetate and all-rac alpha- tocopheryl
succinate)
Activity is limited to RRR, RSR, RRS, and RSS of alpha-
tocopherol
Other:
80% of total dietary vitamin E is in the form of alpha- tocopherol
Most food tables report vitamin E content as alpha- tocopherol equivalents
(which includes all vitamers) but there is no direct coversion from
alpha-tocopherol equivalents to alpha-tocopherol
Digestion
Location: jejunum (primarily)
Amount: 20-80% (unclear)
Form on absorption: tocopherols (free form), tocotrienols (must be hydrolyzed)
and synthetic ester forms (need to be digested)
Hydrolization and digestion happens by pancreatic or duodenal
mucosal esterases (in the lumen or at the brush border)
Transporter
Low concentrations: passive diffusion
This needs bile salts for emulsification, solubilization and micelle
formation (to pass though water) so absorption with lipids
improves it
High concentrations: same as above – it is unsaturable
Other:
RRR and SRR alpha-tocopherol, and RRR and all-rac alpha-tocopherol
have similar absorption efficiencies
RRR alpha-tocopherol half life is 24 hours
SRR alpha-tocopherol half life is 13 hours
Blood
Transport: chylomicrons (put there in enteroytes which then travel though the
lymph to the blood); HDLs and LDLs (have the highest concentration);
VLDLs (only alpha-tocopherol)
Form: tocopherol and tocotrienols
Other:
Chylomicrons take the vitamin E to the liver and the liver uses alpha-
tocopherol transfer protein to transfer tocopherols into VLDLs (to
take to the tissues)
Tissues take up tocopherol when they take up lipoproteins
A transport protein is thought to be needed when transferring vitamin E
from lipoproteins to tissues
In tissues: vitamin E binds to tocopherol-binding proteins for transport
(but it’s found mostly in cell membranes)
Storage
Amount: not specified
Location: adipose tissue (mostly); liver, lung, heart, muscle, adrenal glands,
spleen and brain (smaller amounts)
Form: unesterified
Other:
The concentration in adipose tissues increases linearly with dosage but
other tissues remain constant
Adipose tissue releases vitamin E slowly (even when in need)
Metabolic Functions: maintenance of membrane integrity (including physical stability)
in cells by preventing oxidation of the unsaturated fatty acids in the phospholipids
of the membranes (especially lungs, brain and RBCs)
Antioxidant role:
Free radical termination: the phenolic ring donates H to free ions
Alpha-tocopherol is more effective than the other vitamers
Three phases:
Initiation – can form lipid carbon-centered radicals
LH + •OH → L• + H2O
LH + O2 → L• + HO2•
Propagation – ongoing generation
L• + O2 → LO2•
LO2• +L’H → L’• + LOOH
Termination – this involves reduced vitamin E (EH)
LO2• + EH → LOOH + E•
L• + EH → LH + E•
It is less effective in terminating •OH or RO• than LO2•
Regenerating requires vitamin C, reduced glutathione,
NADPH, ubiquinol and dihydrolipoic acid
Works synergistically with vitamin C to inhibit oxidation
Single molecular oxygen destruction:
From: lipid peroxidation, light energy, respiratory burst
Reacts with: proteins, lipids, and DNA
Physically quenches the singlet oxygen by using the free
hydroxyl group in position 6 of the chromane ring
alpha-tocopherol is more effective than beta,
gamma or delta (in this order)
Beta-carotene is twice as good at quenching
Other roles:
Affect cholesterol metabolism by suppressing HMG CoA
reductase
Suppression of tumor growth and cell proliferation (but not an
association with lower cancer risks)
Inhibition of protein kinase C (for signal transduction and cell
growth)
Breakdown
Metabolism:
From alpha-tocopherol to tocopheroxyl chromanoxy radical which is then
oxidized to tocopheryl quinine, then in the liver its reduced by
alpha- tocopheryl reductase (with NADPH) to tocopherol
hydroquinone which is then oxidized to alpha-tocopheronic acid;
this is conjugated with glucuronic acid and excreted
Most of bile vitamers are conjugated with glucuronic acid before excretion
Excretion: urine (alpha- tocopheronic acid conjugated with glucuronic acid,
alpha-CEHC, gamma-CEHC and alpha-tocopheronolactone); bile to feces
(major rout for alpha-tocopherol)
Deficiencies:
At risk: fat malabsorption disorders (cystic fibrosis), hepatobiliary system
disorders (chronic cholestasis), genetic defects in lipoproteins or vitamin E
transfer protein (abetalipoproteinemia)
Sx: skeletal muscle pain and weakness, ceroid pigment accumulation, hemolytic
anemia, and degenerative neurological problems (ataxia, loss of vibratory
sense, and loss of coordination)
Plasma concentrations of tocopherol 20% deficient)
Other:
It’s susceptible to destruction during: preparation, processing and storage
(oxidized if they sit out too long, and exposure to light, heat and metals
will destroy them)
Vitamin E intake has been associated with lowering the risk of coronary heart
disease and lowering the rate of heart attacks for those with the disease (by
stopping the development of artherosclerotic lesions)
Vitamin E can also help with: cataracts, and for people with increased lipid
peroxidation (iron toxicity or DM)
Interactions with other nutrients:
Selinium – higher concentrations of one nutrient can reduce the effects of
lower concentrations of the other
Sulfur containing amino acids – cysteine is needed to make glutathione
which is reduces vitamin E
Polyunsatturated fatty acids – the vitamin is needed for the degree of
unsaturation of fatty acids in body tissues
B-carotene – absorption and conversion to retinol is inhibited by vitamin E
Vitamin K – absorption or regeneration of the reduced form is inhibited by
vitamin E