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COMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETY
Vitamin E in foodstuff: Nutritional, analytical, and food
technology aspects
Farah Zaaboul YuanFa Liu
State Key Laboratory of Food Science and
Technology, Jiangnan University, Wuxi,
People’s Republic China
Correspondence
Farah Zaaboul and YuanFa Liu, State Key
Laboratory of Food Science and Technol-
ogy,Jiangnan University, Wuxi ,
People’sRepublic China.
Email: farahzaaboul@jiangnan.edu.cn;
and yfliu@jiangnan.edu.cn
Abstract
Vitamin E is a group of isoprenoid chromanols with different biological activi-
ties. It comprises eight oil-soluble compounds: four tocopherols, namely, α-, β-,
γ-, and δ-tocopherols; and four tocotrienols, namely, α-, β-, γ,andδ-tocotrienols.
Vitamin E isomers are well-known for their antioxidant activity, gene-regulation
effects, and anti-inflammatory and nephroprotective properties. Considering
that vitamin E is exclusively synthesized by photosynthetic organisms, animals
can only acquire it through their diet. Plant-based food is the primary source
of vitamin E; hence, oils, nuts, fruits, and vegetables with high contents of vita-
min E are mostly consumed after processing, including industrial processes and
home-cooking, which involve vitamin E profile and content alteration during
their preparation. Accordingly, it is essential to identify the vitamin E content
and profile in foodstuff to match daily intake requirements. This review summa-
rizes recent advances in vitamin E chemistry, metabolism and metabolites, cur-
rent knowledge on their contents and profiles in raw and processed plant foods,
and finally, their modern developments in analytical methods.
KEYWORDS
analytical methods, antioxidant, metabolites, plant food, stability, tocopherols
1 INTRODUCTION
Vitamin E is a lipophilic, colorless, oily liquid that is sus-
ceptible to oxidation in the presence of light, oxygen, and
some metal ions (Peh et al., ). In , it was isolated
for the first time from wheat germ oil. However, the first
publication on vitamin E was actually published in
by Evans and Bishop. In this publication, vitamin E was
called factor X, and its anti-sterility effects on lab rats was
discussed (Evans & Bishop, ). Later, Evans named the
compound “tocopherol,” a word that is composed of the
Greek words “tocos,” meaning birth, and “ferein,” mean-
ing bringing, in reference to vitamin E’s essentiality for rats
to bear young; the “ol” suffix indicates that the compound
is an alcohol (Wisjaja, ). Other studies have shown
that in addition to its effects on fertility, vitamin E has var-
ious vital roles in developing tissues and organs, such as
the brain and nerves, muscle and bones, skin, bone mar-
row, and blood. Researchers have confirmed some of these
functions in humans, and others are still under investiga-
tion (Galli et al., ).
Vitamin E has eight isoforms, including four toco-
pherols and four tocotrienols; these isoforms vary in terms
of their functions and activities primarily because of their
bioavailability in the human body (Nowicka & Kruk, ).
The main and most recognized function of vitamin E
isoforms is their antioxidant action. Vitamin E isoforms
are excellent scavengers and quenchers of reactive oxygen
species (ROS) and reactive nitrogen species (RNS; Niki,
). However, in the last two decades, many researchers
have discovered that vitamin E and its long-chain metabo-
lites (LCMs) as well have several nonantioxidant activities.
Compr Rev Food Sci Food Saf. ;–. © Institute of Food Technologists R
1wileyonlinelibrary.com/journal/crf
2V E P
Given that animals cannot synthesize vitamin E, they
must obtain it from their diet. All vitamin E isoforms are
found in different food sources, particularly plant oils,
seeds, nuts, cereals, fruit, and vegetables (Eitenmiller &
Lee, ). Notably, plant oils are considered to be the pri-
mary dietary sources for meeting the recommended daily
intake of vitamin E (Eitenmiller & Lee, ).
Considering the importance of vitamin E in the human
diet and the necessity to identify the daily intake lev-
els for this vitamin, several separation techniques have
been developed to quantify vitamin E in different food
matrixes. The fundamental techniques are gas chromatog-
raphy (GC), normal phase high-performance liquid chro-
matography (NP-HPLC), reverse-phase HPLC (RP-HPLC),
supercritical fluid chromatography, and thin-layer chro-
matography (TLC; Saini & Keum, ). NP- and RP-HPLC
with ultraviolet (UV) fluorescent detection are primarily
used to analyze tocopherols in most food sources.
This review aimed to synthesize the current knowledge
regarding vitamin E and its isoforms, metabolism and
metabolites, content, and stability in various plant food-
stuffs ranging from raw plants to products on consumers’
tables.
2 VITAMIN E CHEMISTRY AND
METABOLISM
2.1 Chemistry of vitamin E
Vitamin E is the umbrella term for all tocochromanols
and tocols, which are isoprenoid chromanols of two
homologous series, namely, tocopherols (-methyl-
-[,,-trimethyltridecyl]-chroman--ol) with a
saturated side chain and tocotrienols (-methyl--
[,,-trimethyltrideca-,,-trienyl]chroman--ol)
with an unsaturated side chain, as well as some com-
pounds with low prevalence, including tocomonoenols
(Fiorentino et al., ), tocodienols (Siger et al., ),
desmethyltocotrienols, and didesmethyltocotrienol (Szy-
mańska & Kruk, )asshowninFigure. Tocopherols
and tocotrienols (Eitenmiller & Lee, ) comprise a
chromanol group attached to a saturated (tocopherol) or
unsaturated (tocotrienol) phytyl side chain. Their isomers
(α-, β,γ-, and δ-isomers) are determined by the numbers
and positions of the methyl groups at positions and
of the chromanol ring (Figure ). In nature, tocopherols
possess three chiral carbon atoms at position of the
chromanol ring and at and of the phytyl side chain.
Although each tocopherol yields eight different stereoiso-
mers synthetically, the R,R,R configuration remains
the only available form found in nature. Considering that
tocotrienols have only one chiral center at position of
their chromanol ring, only two tocotrienol isomers can
occur. However, similar to tocopherols, tocotrienols are
naturally available only in the R configuration. More-
over, although unsaturation at positions and of the
phytyl side chain can generate four different possible
geometric isomers, only the 3ʹ-trans,7ʹ-trans isomer is
found in nature. The importance of vitamin E originates
from its bioactivity, especially its activity in protecting
lipoproteins, polyunsaturated fatty acids (PUFA), and
cellular and intracellular membranes from oxidative stress
damage. The -hydroxy group of the chromanol ring is the
active site that is responsible for free-radical scavenging,
and in the case of tocotrienols, the side chain has an
important function because it allows efficient penetration
into tissues with saturated fatty layers when unsaturated
(Saini & Keum, ). Technically and indubitably, all
vitamin E isoforms are antioxidants. In vivo, however,
they are not all biologically available because their biolog-
ical availability depends on the methylation state of the
chromanol ring and the saturation grade of the side chain
at the liver level.
2.2 Vitamin E absorption and intestinal
uptake
Vitamin E absorption follows the same pathway described
for cholesterol and other fats, and their absorption rate
varies from % to % depending on the food matrix
(Rigotti, ). After exiting the stomach, vitamin E and
other fats interact with bile salts and form micelles to facil-
itate their transport in the intestinal lumen; in addition,
the esterified forms of vitamin E interact with pancre-
atic lipase in their very initial step of metabolism (Reboul,
) before finally migrating to intestinal epithelial cells
as shown in Figure (Schmölz et al., ). Scientists ini-
tially assumed that vitamin E absorption easily occurs via
passive diffusion through enterocyte apical membranes;
however, in , Reboul et al. found that α-andγ-
tocopherols may be transported into intestinal cells by the
scavenger receptor class B type I (SR-BI; Reboul et al.,
). SR-BI is closely related to high-density lipopro-
tein (HDL) metabolism and is abundantly expressed in
the brush borders of enterocytes (Bietrix et al., ). SR-
BI is highly suggested to have in vivo and in vitro vita-
min E uptake activity because in CaCo human cells, the
SR-BI inhibitor significantly decreases vitamin E uptake,
whereas in mice, the overexpression of SR-BI leads to a
notable increase in α-tocopherol bioavailability (Reboul
et al., ). Even though this hypothesis has been sug-
gested in other research (Reboul et al., ; Tachikawa
et al., ), the mechanism governing vitamin E transport
through SR-BI remains unknown.
V E P 3
FIGURE 1 Chemical structures of vitamin E isomers found in nature
In addition to SR-BI, other protein membranes are
involved in vitamin E efflux from the intestinal mucosa.
Vitamin E has been proposed to share the same diffu-
sion entryways as cholesterol and other fat components
given that it follows the same absorption pathway as these
biomolecules. For example, the main cholesterol trans-
porter protein, Niemann–Pick C NPC-like intracellu-
lar cholesterol transporter (NPCL), has been found to
participate in vitamin E migration to intestinal epithelial
cells (Kamishikiryo et al., ; Narushima et al., ).
Narushima et al. showed that α-tocopherol efflux is related
to NPCL expression, which can decrease in the pres-
ence of ezetimibe (Narushima et al., ). The integral
membrane protein cluster of differentiation (CD),
a class B scavenger receptor, is another molecule that is
suspected of involvement in vitamin E efflux (Goncalves
et al., ; Lecompte et al., ). Lecompte et al. investi-
gated the association between the single nucleotide poly-
morphisms of CD and the plasma concentration of α-
tocopherol in humans and found that CD indeed modu-
lates α-tocopherol concentrations in the blood. Therefore,
CD could be involved in the intestinal absorption or tis-
sue uptake of vitamin E (Lecompte et al., ).
As depicted in Figure , imported vitamin E molecules
are packed inside a specific lipoprotein named chylomi-
cron, which is synthesized in the endoplasmic reticu-
lum (ER) and Golgi apparatus via two steps that have
been well-documented in previous reviews (Demignot
et al., ; Giammanco et al., ). Chylomicrons are
capsules packed with triacylglycerols (TAGs), cholesterol,
cholesterol esters, and vitamin E, all surrounded by a
layer of phospholipids (PLs) embedded with the special
apolipoprotein ApoB. The newly formed chylomicron is
absorbed across the intestinal wall into the lacteal then into
the blood, where it gains additional Apo-proteins, mainly
Apo E and Apo C II, that later activate lipoprotein lipase
(LPL) and hydrolyzes TAGs (Feingold & Grunfeld, ).
Under the mediation of the LDL receptor via Apolipopro-
tein E (ApoE), the remaining vitamin E molecules in the
chylomicron are endocytosed into the liver, where the dis-
crimination between vitamin E isoforms begins (Kono &
Arai, ).
4V E P
FIGURE 2 The fate of vitamin E in the human body. Encapsulation of vitamin E in micelles or vesicles to enter the enterocyte via SR.BI,
CD, NPCL, and PP. Vitamin E is packaged with TAGs, cholesterol, and cholesterol esters into chylomicrons in the ER. These
chylomicrons are released into the lymphatic circulation and begin their journey to the liver. Apo B: apolipoprotein B; Apo CII:
apolipoprotein CII ; CD, cluster of differentiation; ER, endoplasmic reticulum; LPL, lipoprotein lipase; NPCL, NPC-like intracellular
cholesterol transporter ; PP, passive diffusion ; SR.BI, scavenger receptor class B type I; TAGS, triacylglycerols
2.3 The hepatic handling of vitamin E
Vitamin E metabolism is instigated in the liver, and α-
tocopherol is transported in lipoproteins for distribution to
other organs and tissues. At this stage, vitamin E isoforms
take two different pathways in parallel: the migration of
α-tocopherol from the liver to the bloodstream inside very-
low-density lipoprotein (VLDL) and the metabolism of the
remaining vitamin E isoforms in different cell compart-
ments. These two pathways have been suggested to be
the reason for the predominance of α-tocopherol in blood
and tissue (Desmarchelier & Borel, ). However, the
molecular mechanisms underlying this preference remain
poorly understood.
The hepatic cytosolic transport protein that is in charge
of the intracellular trafficking of hydrophobic molecules,
namely, the α-tocopherol transfer protein (α-TTP), has
been elucidated; this protein exhibits a solid affinity for
the α-tocopherol isoform, mainly the RRR (%), over
other isoforms (Hosomi et al., ; Manor & Morley, ;
Panagabko et al., ;Traberetal.,). The affinity of
α-TTP for tocopherols is ascribed to its hydrophobic pocket
and its correspondence with a phytyl pyrophosphate-
derived tail; its R-configuration at C-; and finally, its fully
methylated chromanol ring. Therefore, any change in this
protein configuration can lead to an incompatibility with
α-tocopherol. In humans and mice, the mutation or sup-
pression of the α-TTP gene causes severe vitamin E defi-
ciency that leads to neurodegenerative diseases (Ouahchi
et al., ; Yokota et al., ). For example, ataxia with
vitamin E deficiency (AVED), a rare neuromuscular dis-
ease that is characterized by the absence of the fine coor-
dination of voluntary movements, is mainly caused by
a mutation of the gene responsible for α-TTP regulation
(Becker et al., ). A study allocated individuals into
patient and control groups that received RRR and synthetic
SRR stereoisomers of α-tocopherol labeled with six (d)
or three (d) deuterium atoms, respectively. The results
showed that plasma and lipoprotein d-RRR-α-tocopherol
concentrations dropped rapidly in three patients and were
lower in the other four patients than in individuals in
the control group. These results suggested that α-TTP is
required to maintain plasma RRR-α-tocopherol concen-
trations because the patients were either unable to syn-
thesize this protein or had a marked defect in the RRR-
α-tocopherol binding region of the protein (Traber et al.,
). Jishage et al. () and Yokota et al. ()used
a mouse model with interrupted α-TTP expression to
investigate the relationship of α-TTP with vitamin E defi-
ciency. They found that α-TTP influenced vitamin E level
in plasma, and mice with dysfunctional α-TTP displayed
neurological symptoms associated with age-related AVED
V E P 5
FIGURE 3 The fate of vitamin E in the liver. Red pathway: Vitamin E is metabolized by CYPF-mediated ω-hydroxylation in the
endoplasmic reticulum to ′-hydroxychromanol, followed by one ω-oxidation and two cycles of β-oxidation in the peroxisome and three
cycles of β-oxidation in the mitochondria. In addition to the metabolic reactions, parallel conjugation of the formed metabolites occurs in the
peroxisome and mitochondria. Blue pathway: α-tocopherol transfer protein migrates to the late lysosome to bind to R-α-tocopherol and
protect it from metabolism and then transports it to the very-low-density lipoprotein
(Jishage et al., ; Yokota et al., ). However, the
predominance of the isoform in blood and tissues cannot
be ascribed to α-TTP because the discrimination against
γ-tocopherol can be suppressed by phytochemicals, such
as sesamin and alkylresorcinols (Ikeda et al., ; Ross
et al., ). Moreover, Parker et al. found that Drosophila
appears to have a particular preference for α-tocopherol
although they do not appear to express α-TTP (Parker &
McCormick, ). A very recent in vivo study demon-
strated that α-TTP has no power over the intracellular
distribution of vitamin E (Irías-Mata et al., ). Over-
all, although α-TTP is clearly indispensable for the deliv-
ery of vitamin E in the bloodstream, it is not the only
molecule responsible for discrimination among all iso-
forms. Some scholars have suggested that the predomi-
nance of α-tocopherol in the blood and tissues is the result
of the combined work between α-TTP and cytochrome
Ps.
After vitamin E endocytosis, all isomers undergo
metabolism inside liver cells (Figure ), with the excep-
tion of R-α-tocopherol, which can escape this metabolic
process due to its high affinity for α-TTP. α-TTP trav-
els to the late endosome/lysosome and binds to R-α-
tocopherol to protect it from metabolism and transport it
toward the plasma membrane (Figure ). At this stage, α-
TTP/α-tocopherol interacts with the head group of phos-
phatidylinositol bisphosphates (PIP); during this inter-
action, α-TTP exchanges α-tocopherol for PIP (Chung
et al., ; Kono et al., ). Finally, α-tocopherol in the
membrane is collected by the ATP-binding cassette trans-
porter A (ABCA) and secreted into circulation, where it
is spontaneously transferred into the nascent VLDL (Kono
&Arai,). Similar to chylomicrons, TAGs in VLDL are
hydrolyzed by LPL through Apo CII stimulation, result-
ing in the formation of intermediate-density lipoprotein
and then low-density lipoprotein (LDL), the carrier of
the major portion of plasma α-tocopherol (Schmölz et al.,
). HDL collects the released α-tocopherol out of extra-
hepatic tissues for transport back to the liver in the same
cycle adopted for cholesterol transport (Balazs et al., ).
On the other hand, non-R-α-tocopherol isomers
are escorted to sites where they are preferentially
ω-hydroxylated and then undergo β-oxidation in mito-
chondria to generate side-chain-shortened carboxyethyl
hydroxychromanol (CEHC) metabolites (Rizvi et al., ;
Sontag & Parker, , ). Vitamin E metabolism has
always been viewed as the maintenance of adequate vita-
min contents and the prevention of vitamin accumulation
to toxic levels by degrading excess vitamins (Torquato
et al., ). The urinary short-chain metabolite α-CEHC
is an indicator of sufficient vitamin E uptake. However,
vitamin E metabolites, including LCMs, are even more
6V E P
bioactive than their corresponding precursors. There-
fore, similar to vitamin A and D metabolism, vitamin E
metabolism may not only be an excretion pathway but
also an activation pathway (Galli et al., ).
2.4 Vitamin E metabolism and
metabolites
As mentioned above, in contrast to vitamin A metabolism,
vitamin E metabolism starts in the liver. The nomenclature
for α-, β-, γ-, and δ-metabolites is used (Figure ) consider-
ing that all vitamers are metabolized via the same pathway
with the consecutive shortening of their side chains with-
out the involvement of the chromanol ring (Schmölz et al.,
). The saturation of the side-chain and the methylation
pattern of the chromanol ring determine the affinity of the
metabolic reaction for different vitamin E isoforms, with
the dimethyl and unsaturated side chain isoforms being
preferentially metabolized. Mustacich et al. stated that
vitamin E metabolism begins in the hepatic ER with the
ω-hydroxylation of the side chain in a process that is medi-
ated by cytochrome CYPF or CYPA and results in the
formation of the LCM -hydroxychromanol (-OH); the
succeeding ω-oxidation by aldehyde dehydrogenase leads
to the formation of the LCM -carboxychromanol (-
COOH; Galli et al., ; Mustacich et al., ; Schmölz
et al., ). The -COOH group undergoes two separate
β-oxidation cycles in peroxisomes, leading to the forma-
tion of -COOH and -COOH, which are also consid-
ered LCMs (Mustacich et al., ). The last compartment
of vitamin E metabolism is the mitochondrion, wherein
the continuous cycle of β-oxidation cleaves LCMs into
intermediate-chain metabolites (ICMs) and finally into
SCMs, such as -COOH (Figure ).
The mechanism that is central to the transport of LCMs
from the ER to the peroxisome and from the peroxi-
some to the mitochondrion is still unknown. However,
scientists have proposed many hypotheses, among which
one states that the transport of -COOH may follow
the same pathway as that of long-chain, very long-chain,
or branched-chain fatty acids (Hardwick, ). Further-
more, the transport of -COOH and -COOH into the
mitochondria may follow the same pathway as that of vita-
min K metabolites or is even facilitated by α-TTP and/or
other hepatic α-tocopherol-binding proteins (Grebenstein
et al., ). Nevertheless, all these hypotheses still require
further investigation.
ω-Oxidation and β-oxidation are not the only reac-
tions that occur in the peroxisome and mitochondrion.
Q. Jiang et al. reported the presence of γ-tocopherol,
δ-tocopherol, and γ-tocotrienol LCMs and their conju-
gated forms, namely, SO--COOH, SO--COOH, and
SO--COOH, indicating that conjugation occurs con-
currently with oxidation as illustrated in Figure (Q.
Jiang et al., ). LCMs are mainly sulfated (Freiser &
Jiang, ; Q. Jiang et al., ). ICMs are either sul-
fated or glucuronidated (Johnson et al., ;Popeetal.,
). SCMs are found in a variety of conjugated forms,
including sulfate- (Tanabe et al., ), glutamine- (John-
son et al., ), glucoside- (Cho et al., ), glycine-,
glycine-glucuronide-, and taurine-conjugated metabolites
(Johnson et al., ). Soluble conjugated ICMs and SCMs
are predominantly excreted via urine (Bardowell, Ding,
Parker, ; Bardowell, Duan, et al., ;Zhaoetal.,
). By contrast, the remaining conjugated and non-
conjugated metabolites, as well as their precursors, are
excreted in feces; this route represents the major excretion
route (Bardowell, Duan, et al., ; Q. Jiang et al., ).
2.5 Biological activity of vitamin E and
its metabolites
Vitamin E has been intensively studied for its antioxi-
dant properties and free-radical scavenging capability. Its
ubiquitous presence at high concentrations throughout
the body makes it the most potent lipid-soluble, chain-
breaking antioxidant. The chromanol ring, particularly the
OH functional group at C, provides the power of vita-
min E isomers against ROS and RNS. This effect is not
the same for all vitamin E isomers because their antiox-
idant activity depends on the number of methyl groups
on the chroman ring; therefore, α-tocopherol is stronger
than other isoforms, and tocopherols are stronger than
tocotrienol (Karmowski et al., ). Many experiments
have been performed to verify the strength of each iso-
form, but their results varied because they used different
assays (Müller et al., ). The antioxidant activity of vita-
min E isomers has been suggested to be dependent on
the chemical structures of the isomers, as well as on vari-
ous environmental factors. The oxidative reaction between
vitamin E and ROS and/or RNS leads to the formation of
unstable tocopheroxyl radicals that can undergo radical–
radical coupling. Therefore, one tocopherol can react with
two free radicals. Two tocopheroxyl radicals can also react
with each other to form low-reactivity nonradical dimers
(Maulucci et al., ). Furthermore, tocopheroxyl can
be regenerated into tocopherol in the presence of other
antioxidants, such as ascorbic acid or phenolic compounds
(Kruk et al., ). This regeneration reaction has been
observed in vitro and in vivo. In one experiment, smok-
ers and nonsmokers received ascorbic acid or a placebo
inarandomizeddouble-maskedmannerfollowedbyoral
V E P 7
deuterated α-andγ-tocopherols for weeks. The results
showed that the rate of α-andγ-tocopherol disappearance
in smokers was significantly increased compared with that
in nonsmokers; however, the disappearance of these iso-
forms was attenuated by ascorbic acid supplementation.
On the basis of these results, vitamin C was suggested to
be capable of recycling tocopheroxyl radicals in vitro and
in vivo (Bruno et al., ).
Recent studies have implied that in addition to pos-
sessing antioxidant activities, vitamin E isomers have
a potent anti-inflammatory effect as reflected by its
capability to suppress cyclooxygenase (COX-) activity
(Q. Jiang et al., , ) and inhibit -Lipoxygenase
-LOX enzyme activity in vitro, with non-α-tocopherols
being far more potent than α-tocopherols (Z. Jiang et al.,
). It has been suggested that isoforms with unsubsti-
tuted -position such as γ-tocopherol are superior to α-
tocopherol in inflammatory diseases, and it has also been
suggested that they are potentially useful chemopreven-
tive agents against cancer (Q. Jiang, ). For example,
Q. Jiang et al. induced colitis with dextran sodium sulfate
and azoxymethane in a mice model. The results showed
that γ-tocopherol suppressed colon carcinogenesis pro-
moted by moderate colitis (Q. Jiang et al., ). Similarly,
in the same experimental model, another group reported
that γ-tocopherol-rich mixed tocopherols suppressed colon
tumorigenesis, inflammation, and eicosanoids (Ju et al.,
). In another type of cancer, Sanches et al. reported
that a γ-tocopherol-enriched diet decreased ventral pro-
static epithelial dysplasia and attenuated upregulation
of inflammatory markers in rats (Sanches et al., ).
In addition to cancer, a very recent study also used γ-
tocopherol-rich mixtures of vitamin E isomers. A ratio of
/ of a mixture of α-tocopherol and γ-tocopherol was used
to treat inflammatory markers in a mice model fed a high-
fat diet. The results showed that this ratio could atten-
uate adipose tissue enlargement, prevent high-fat diet-
induced hepatic steatosis, and upregulate hepatic perox-
isome proliferator-activated receptor αactivity (H. Lee &
Lim, ).
The anti-atherosclerosis effect of vitamin E has also
been demonstrated in vitro and in vivo. Recently, Meydani
et al. found that a low-fat and low-cholesterol diet supple-
mented with a low dose of vitamin E was effective in reduc-
ing atherosclerotic lesions and mortality in a group of LDL
receptor-deficient mice (Meydani et al., ). This effect
can be modulated by down-regulating CD and blocking
the uptake of oxidized LDL (Özer et al., ). Vitamin E
can down-regulate CD while up-regulating Peroxisome
proliferator-activated receptor gamma (PPARγ), Liver X
receptor alpha (LXRα), and ABCA. Moreover, vitamin
E can significantly inhibit early atherosclerotic lesions in
ApoE−/−mice (F. Tang et al., ).
The neuroprotective effect is among the first non-
antioxidant activities reported for vitamin E. As mentioned
above, vitamin E deficiency has been found to be associ-
ated with severe neurological and neuromuscular disor-
ders (Becker et al., ; Elkamil et al., ). It has also
been reported that vitamin E, particularly α-tocopherol,
has a high potential to reduce epileptogenesis when used
with other therapies. Further evidence and mechanisms of
action were presented by Ambrogini et al. in their recent
review. They discussed the preventive role of vitamin E in
epilepsy seizures by reducing the pathogenic triad repre-
sented in excitotoxicity, neuroinflammation, and oxidative
stress (Ambrogini et al., ). On the other hand, vita-
min E intake acts as a protective rather than curative fac-
tor in Alzheimer’s disease (Mangialasche et al., ; Mul-
lan et al., ; Zandi et al., ) and Parkinson’s disease
(Schirinzi et al., ).
The triangular relationship among the human diet, gut
microbiota, and physical and mental health has become
a hot topic (Morais et al., ; Pap et al., ; Sakkas
et al., ). Intestinal diseases that are characterized by
chronic inflammation, barrier dysfunction, and dysbiosis
are closely related to the distribution of the gut micro-
biota community (Li et al., ; Zheng et al., ). A
recent study has verified the effect of consuming differ-
ent contents of vitamin E mainly α-tocopherol isomer on
the microbiota community in mice (Choi et al., ).
The results of this study showed that α-tocopherol intake
can affect the distribution of the microbiota community,
resulting in a significant difference among the control, low
α-tocopherol consumption, and high α-tocopherol con-
sumption groups. However, the study is not yet sufficient
to provide a definite hypothesis on the effect of vitamin E
on gut microbiota and its relationship with inflammatory
bowel disease (Choi et al., ).
A well-received study investigated the effects of α-
and γ-tocopherol on inflammatory bowel disease in vitro
and in vitro (K. Y. Liu et al., ). The results of this
study showed that α-tocopherol and γ-tocopherol atten-
uated fecal bleeding, diarrhea, and interleukin eleva-
tion. In colitis-induced mice, γ-tocopherol exerted a pro-
tective effect on the integrity of the gut barrier by atten-
uating the colitis-induced increase in Lipopolysaccharide
binding protein (LPS-binding protein) in the plasma and
caused a beneficial change in the gut microbiota (K. Y.
Liu et al., ). In the same context, the effects of δ-
tocotrienol and its LCMs on gut microbiota during tumori-
genesis in mice were verified (C. Yang et al., ). The
above work revealed a novel activity of δ-tocotrienol and
its metabolite and suggested that δ-COOH may play
a role in the anticancer effect and gut microbe modula-
tion activity of δ-tocotrienol. Compared with the control
treatment, δ-tocotrienol and its metabolites inhibited the
8V E P
proliferation of large adenomas by % and %, respec-
tively. The two compounds promoted potentially benefi-
cial Lactococcus and Bacteroides species. In addition, delta-
tocotrienol ’-carboxychromanol (δTE-) counteracted
the azoxymethane/dextran-sulfate-sodium-induced deple-
tion of Roseburia, which is known to be reduced in patients
with inflammatory bowel disease (C. Yang et al., ).
This study is not the first to show that vitamin E metabo-
lites, particularly LCMs, are more biologically active and
potent than their precursors.
LCMs have been found to have superior biological
activity, and in the last two decades, several in vitro
studies have confirmed the hypothesis suggested by Galli
et al. (). Inflammation, a consequence of an overre-
acting immune response, is characterized by ROS and
RNS production. Inflammatory mediators, for example,
prostaglandins and leukotrienes, are also extensively
produced due to arachidonic acid degradation under the
mediation of proinflammatory enzymes, such as COX-
and -lipoxygenase. Inflammation is the main cause of
several diseases, including cancer, cardiovascular dis-
eases, and diabetes. Therefore, most studies on LCMs have
investigated their effects on the inflammation biomarkers
mentioned above. A study by Q. Jiang et al. is among the
first studies on the effect of vitamin E metabolites. In
this study, vitamin E metabolites were found to inhibit
arachidonic acid-stimulated COX activity in A cells
without affecting COX- expression. The partial diminu-
tion of cellular inhibition by sesamin is the main clue
suggesting that vitamin E metabolites were responsible
for this inhibitory effect (Q. Jiang et al., ). In vitro
tests on the LCMs -carboxychromanol and -COOH
and their conjugated forms confirmed the above sug-
gestions and illustrated that while the conjugated forms
lacked an anti-inflammatory effect, LCMs, especially
the forms, can block COX- activity by binding to
the substrate-binding site of COX; this mechanism is
different from the mechanism of action of α-tocopherol
described above (Jiang et al., ). Mazzini et al. used
semisynthetic α--OH and α--COOH derived from
garcinoic acid isolated from Garcinia kola (Mazzini et al.,
). Although these metabolites presented a motivating
anti-proliferative effect on glioma C cancer cells, their
regulatory mechanism was not examined. Wallert et al.
was the first to provide detailed evidence regarding the
anti-inflammatory and gene expression regulatory effect
of the above metabolites. Importantly, they revealed
for the first time that LCMs are released into the blood
circulation following the metabolism of α-tocopherols
in the liver (Wallert et al., ). These studies are only
the beginning of the numerous in vitro works on the
effects of LCMs on inflammation and inflammatory
diseases that used different cell models and verified
different mechanisms of action. These studies discovered
that LCMs, especially the longest forms, can inhibit
-LO/COX activity in cells preinduced with arachidonic
acid (Jang et al., ;Peinetal.,). Moreover, they
inhibit lipopolysaccharide-stimulated COX/inducible
nitric oxide synthase (iNos) Mrna and protein expres-
sion (Schmölz, Waller, Lorkowskiet, ; Wallert et al.,
) and decrease prostaglandin and nitric oxide release
(Schmölz, Waller, Rozzino, et al., ). Furthermore,
LCMs induce apoptosis in human liver cancer cells more
strongly than their precursors (Birringer et al., ).
LCMs can also induce autophagy with a stronger and
different mode of action than their precursors (Jang et al.,
).
Atherosclerosis is one of the major cardiovascular dis-
eases that affect arteries and cause blockage. It starts
with endothelial dysfunction, which leads to the efflux of
LDL into cells. LDL is oxidized and then interacts with
macrophages to form foam cells, which are the corner-
stone of plaque formation. α--COOH has been recently
shown to be capable of inducing lipid storage capacity and
thereby reducing susceptibility to lipotoxicity (Schmölz
et al., ). Moreover, α-′-COOH can induce the post-
translational regulation of LPL via angiopoietin-like and
protect macrophages from excessive lipid accumulation in
the presence of surplus VLDL (Kluge et al., ). To date,
most studies have been conducted in vitro. Therefore, the
in vivo biological activity of vitamin E metabolites remains
a topic of debate and has been discussed in detail in pre-
vious publications (Schubert et al., ; Torquato et al.,
;Q.Jiang,).
2.6 α-Tocopherol synthesis and
regulations
Given the importance of the antioxidant and biological
activities of RRR-α-tocopherol, the demand for this prod-
uct has rapidly increased over the past two decades, and
all efforts have been engaged in its industrial synthesis.
As illustrated in Figure , its production is subdivided
into three steps: the preparation of the aromatic build-
ing block (trimethylhydroquinone), the production of the
side chain component (all-racemic-isophytol or a corre-
sponding C derivative), and the condensation reaction
(Netscher, ). However, regardless of the advanced
research on optical stereoselectivity, no process for the
commercial total synthesis of naturally identical (RRR)-α-
tocopherol has seen the light yet. An equimolar mixture of
all eight stereoisomers is the only synthetic vitamin E that
has been successfully made available under the name of
“all-racemic-α-tocopherol.”
V E P 9
FIGURE 4 Synthesis of α-tocopherols according to Netscher ()
As mentioned earlier, not all vitamin E isoforms are
taken by human cells in the same way. Moreover, their
contents are highly variable across different food sources
and sometimes even within the same food group. There-
fore, a standard international unit (IU) based on their bio-
logical activity is needed. Earlier, milligram α-tocopherol
equivalent (mg α-TE) was defined to identify the rec-
ommended dietary intakes of vitamin E on the basis
of the biological activity of tocopherols and tocotrienols
as determined through the rat fetal absorption test. The
total mg α-TEs of food containing only RRR-isomers are
obtained by multiplying the amount of α-tocopherol by
., that of ß-tocopherol by ., that of γ-tocopherol by .,
that of α-tocotrienol by ., and that of γ-tocotrienol by
.. The conversion factors for all-racemic-α-TE and all-
racemic-α-tocopheryl acetate in fortified food are . and
., respectively (Eitenmiller & Lee, ). However, in
, the US Food and Drug Administration announced
new regulations for the evaluation of vitamin E activity.
The new daily value (DV) unit is mg α-tocopherol, and
the new conversion is mg of vitamin E in the form of
α-tocopherol = mg of natural α-tocopherol and mg of
vitamin E in the form of α-tocopherol = mg of synthetic
α-tocopherol. By changing the IU unit for vitamin E to mg
of α-tocopherol, the amount of natural α-tocopherol has
become twice that of synthetic α-tocopherol when used as
vitamin E (Food & Drug Administration, ).
3 VITAMIN E IN PLANT-BASED FOOD
Vitamin E is a dietary antioxidant that is found in plant
oils, nuts and seeds, vegetables, and fruit. The interest in
the vitamin E content of food products has dramatically
increased in the last two decades as concerns regarding
inflammatory and chronic diseases have increased. Vita-
min E is an essential compound that can be obtained only
through the diet. Therefore, a daily recommendation was
proposed to meet the everyday needs for this vitamin. The
recommended dietary allowance or DV for vitamin E is
mg for adults and children aged years and older (Food
& Drug Administration, ). Therefore, in this section,
the main vegetarian sources and contents of vitamin E are
discussed.
Vitamin E isomers are lipophilic antioxidants that are
synthesized only by photosynthetic organisms; they are
particularly abundant in seeds, where they protect stor-
age lipids from oxidation during germination and early
seedling development (Sattler et al., ). Oil bodies
(OBs) are the main store of tocopherols in all plants (Chen
et al., ). Fisk et al. demonstrated a strong association
between OBs and all tocopherol isoforms (Fisk & Gray,
) in three different varieties of soybean (Ustie, K, and
Elna). Washing with high concentrations of a chaotropic
agent, such as urea, significantly decreases the percent-
age of α-tocopherol, compared with the percentage of
other tocopherols. A similar study on peanut OBs showed
that increasing the recovery Ph can significantly affect
the concentration of α-tocopherols (Zaaboul, Raza, Chen,
&Liu,). Moreover, the release of intrinsic proteins,
such as caleosin and L-oleosin, is correlated with decre-
ments in the concentration of α-tocopherol, indicating that
α-tocopherols are likely to be associated with the mem-
branes of OBs. At the same time, other tocopherols are
merged into the TAG matrix and protected from repeated
washing as presented in Figure . Therefore, the largest
vitamin E-containing food groups, including oilseeds,
nuts, and kernels, originate from plants.
Oils and fats represent the most concentrated sources of
vitamin E in the human diet. The vitamin E content and
10 V E P
FIGURE 5 Soybean oil body model
showing the suggested localization of
α-tocopherol and other tocopherol (Zaaboul
et al., )
profile of specific plant oils varies depending on varieties,
genotypes, and growing and storage conditions (Trela &
Szymańska, ). Table shows the remarkable differ-
ences in vitamin E contents and profiles reported by dif-
ferent research groups that used different or the same
plant materials. These differences can be explained by
the influence of different factors on vitamin synthesis in
the plant or the resistance of vitamin E during indus-
trial processes or food preparation (additional details in
Section ). Furthermore, experimental conditions were
found to have significant influences on the final results of
each group. The highest concentrations are always found
in oils derived from cereals, such as wheat germ oil;
from seeds, such as safflower oil; from kernels, such as
almond oil; and from legumes, such as soybean oil and oils
extracted from fruits, for example, coconut and avocado,
have lower vitamin E concentrations than those extracted
from plant oils (Table ). Although oils and fats are gen-
erally rich in vitamin E, their bioavailability is assumed
to be limited because oil seeds are not easily digested by
the human gastrointestinal tract (Stahl et al., ). Grains
and cereals are consumed more often than nuts and seeds.
Therefore, cereals represent a source of tocotrienols and
tocopherols in the diets of people living in areas where
palm oil is not commonly consumed or available (Eiten-
miller & Lee, ). Seeds and nuts are the stock houses
of plant oils and vitamin E. However, they are not con-
sumed as much as cereals. Fruit and vegetables contain
the lowest amounts of available vitamin E, where spinach,
olives, and avocado show very high tocopherol contents,
compared with other vegetables and fruit (Table ).
These foodstuffs are not usually consumed in their raw
forms; they may go through different processes before
being available to the customer. Therefore, a detailed study
of the effects of all possible food preparation processes on
vitamin E content is needed.
4NATURAL AND INDUSTRIAL
FACTORS INFLUENCING THE VITAMIN E
CONTENTS IN PLANT-BASED FOOD
4.1 Natural factors
.. Geographic and weather conditions
and crop year, genotypes, and varieties
Setting a standard vitamin E content for each product is
always challenging because vitamin E content varies not
only within different species but also within varieties of the
same species. Several scholars compared the tocopherol
and/or tocotrienol contents of different varieties within
the same species, and their results were as expected. Sig-
nificant differences in the vitamin E contents and pro-
files of the analyzed samples were constantly found. A
recent study on four different pigmented maize genotypes
revealed significant differences in vitamin E profiles as rep-
resented by α-andγ-tocopherols and α-andγ-tocotrienols
(Suriano et al., ). This significant difference is unsur-
prising because several groups previously reported similar
observations. For example, Beyhan et al. showed remark-
able differences in the tocopherol contents of differ-
ent walnut genotypes from Turkey. Similar to that in most
plant seeds and nuts, γ-tocopherol is the predominant iso-
form in all walnut samples, with the highest content of
. mg/ g seen in genotype and the lowest con-
tent of . mg/ g seen in genotype . The highest α-
tocopherol content of . mg/ g was found in genotype
, and the lowest content of . mg/ g was found in
genotype (Beyhan et al., ). Similar trends have been
found in other plants, including barley, wherein vitamin E
content and antioxidant activity are dependent on genetic
makeup(T.D.T.Doetal.,), growth conditions, and
crop year (Irakli et al., ;Legzdin
,aetal.,;Siger
V E P 11
TABLE 1 Tocopherol and tocotrienol contents of various classes of plant food in mg/ g
Vitamin E content
Food source TαTβTδTγT3αT3βT3δT3γDetection method Reference
Oils
Almond oil . *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
.–. .–. –.–. – – – – HPLC coupled with
fluorescence detector
(Melhaoui et al.,
)
.–. .–. .–. .–. – – – – (Wang et al.,
)
.–. .–. .–. .–. – – – – (Fernandes et al.,
)
Apricot oil (Sweet) . – . . – – – – NP-HPLC coupled to
fluorescence detector
(Matthäus &
Musazcan
Özcan, )
(Bitter) . – . . – – – –
. *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
Avocado oil .–. – – – – – – – HPLC coupled with
ultraviolet
(UV)–visible detection
(Flores et al.,
)
.–. .–. –.–. – – – – HPLC coupled to
fluorescence detector
(Manaf et al.,
)
Argan oil . *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
.–. – .–. .–. – – – – HPLC coupled to
fluorescence detector
(Hilali et al.,
)
Camilia oil .–. .–. .–. – – – – – HPLC coupled with
UV−visible detection
(Ge et al., )
Coconut oil . . . . – – – – HPLC coupled to
fluorescence detector
(R. Liu et al.,
)
(Continues)
12 V E P
TABLE 1 (Continued)
Vitamin E content
Food source TαTβTδTγT3αT3βT3δT3γDetection method Reference
Corn oil . *. . RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
Cotton seed oil .–. – .–. .–. – – – – (Kouser et al.,
)
Flaxseed oil –*. . – – – – (Aksoz et al.,
)
.–. – – .–. ––––HPLC coupled with
fluorescence detector
(Choo et al.,
)
Grape seed oil
(Cold press)
.–. – – .–. .–
.
––.–
.
HPLC coupled with
Photodiode-Array
Detection (PDA)
detector
(Al Juhaimi &
Özcan, )
Grape seed oil
(soxhlet
extraction)
.–. – – .–. .–
.
– – .–
.
Hazelnut oil .–. .–. .–. .–. – – – – HPLC coupled with
fluorescence detector
(Fernandes et al.,
)
.–. *– .–. – – – – Liquid
chromatography-mass
spectrometry-
Electrospray
ionization(MS-ESI)
(Ta & Gökmen,
)
. *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
Hemp seed oil . *. . – – – – (Aksoz et al.,
)
Line seed oil . – . . – – – – HPLC coupled to
fluorescence detector
(Matthäus &
Musazcan
Özcan, )
Oat oil .–. .–. –.–. – – – – (Musa Özcan
et al., )
(Continues)
V E P 13
TABLE 1 (Continued)
Vitamin E content
Food source TαTβTδTγT3αT3βT3δT3γDetection method Reference
V:.–.–––––––Solid-phase
microextraction and
gas
chromatography–MS
(Aresta &
Zambonin,
)
EV: .–.
Olive oil . . . HPLC coupled to
fluorescence detector
(Yalcin &
Schreiner,
)
EV: . *. . RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
R: . *. .
Palm oil . –––. –. . HPLC-fluorescence
method using a C
silica coupled to MS
and Nuclear magnetic
resonance (NMR)
(Ng et al., )
Peanut oil . . . . . – – – HPLC coupled with
fluorescence detector
(Matthäus &
Musazcan
Özcan, )
. . . . . . . . (Zhu et al., )
Pecan oil –––. – – – – HPLC coupled with PDA
detector
(Juhaimi et al.,
)
. – . −. . −. – – – – HPLC coupled with
fluorescence detector
(Fernandes et al.,
)
Pistachio oil – *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
Pumpkin oil . *. . – – – –
Rapeseed oil .–. – .–. .–. – – – – RP-HPLC coupled to UV
detector on a C
column
(Wuetal.,)
(Continues)
14 V E P
TABLE 1 (Continued)
Vitamin E content
Food source TαTβTδTγT3αT3βT3δT3γDetection method Reference
Rice bran oil .–. .–. .–. .–. .–
.
.–. .–
.
.–
.
HPLC (Endo &
Nakagawa,
)
Safflower oil .–. – – .–. – – – – HPLC coupled to DAD
detector
(Günç Ergönül
and Aksoylu
Özbek, )
. *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
Sesame oil . *. . – – – – (Aksoz et al.,
)
–.–. .–. – – – – HPLC coupled to DAD
detector
(Mohamed
Ahmed et al.,
)
Soybean oil . . . . – – – – Supercritical-fluid
chromatography
coupled to
high-resolution mass
spectrometry
(Méjean et al.,
)
Sunflower oil . *. . – – – – RP-HPLC coupled with
fluorescence detector
(Aksoz et al.,
)
Walnut oil . *. . ––––
Wheat germ oil . *. . – – – –
.–. .–. – – – – – – HPLC coupled to
fluorescence detector
(Magariño et al.,
)
(Continues)
V E P 15
TABLE 1 (Continued)
Vitamin E content
Food source TαTβTδTγT3αT3βT3δT3γDetection method Reference
Fruit and vegetables (wet weight unless we mention otherwise)
Avocado .–. – – – – – – – RP-HPLC coupled with
DAD
(Peraza-
Magallanes
et al., )
Apricot .–. .–. –.–. – – – – RP-HPLC/Fluorescence
Detector (FLD) and
Reversed Phase Ultra
Performance Liquid
Chromatograph-
Electrospray
ionization/Mass
spectrometry-
Electrospray ionization
RP-UPLC ESI/MS
(Górnaś et al.,
)
Olives . *– . – – – – RP-HPLC coupled to
fluorescence detector
(Tekaya et al.,
)
Tomato .–. .–. .–. .–. – – – – HPLC coupled to
fluorescence detector
(Petropoulos
et al., )
. . . . – – – – HPLC coupled with DAD (Knecht et al.,
)
Broccoli .–. .–. .–. – – – –
Carrot .–. .–. – .–. – – – – HPLC coupled with DAD (Knecht et al.,
)
Cauliflower . – – . – – – – NP-HPLC coupled with
fluorescence detection
(Piironen et al.,
)
. – – . . NP-HPLC coupled with
spectrofluorometric
detector
(Chun et al.,
)
Cauliflower
(dry weight)
.–. – – .–. – – – – HPLC coupled with DAD (Diamante et al.,
)
Parsley . – – . – – – – NP-HPLC coupled with
spectrofluorometric
detector
(Chun et al.,
)
Parsley (dry
weight)
.–. – – .–. – – – – HPLC coupled to
fluorescence detector
(Fernandes et al.,
)
Red sweet
pepper
.–. .–. .–. .–. – – – – HPLC coupled with DAD (Knecht et al.,
)
Green sweet
pepper
. – – – – – – –
Spinach . – – . – – – –
(Continues)
16 V E P
TABLE 1 (Continued)
Vitamin E content
Food source TαTβTδTγT3αT3βT3δT3γDetection method Reference
Nuts, cereals, and legumes
Almond .–. – – – – – – – HPLC coupled with
fluorescence detector
(Yada et al., )
Hazelnut Raw .–. *.–. .–. – – – – HPLC coupled with
fluorescence detector
(Król et al., )
Hazelnut
Roasted
.–. *.–. .–. – – – –
Yellow maize . – – . . – – . RP-HPLC coupled to
fluorescence detector
(Suriano et al.,
)
Red maize . – – . . – – .
Blue maize . ––. . – – .
Purple maize . – – . . – – .
Peanut .–. .–. .–. .–. – – – – HPLC coupled to
fluorescence detector
(Hashim et al.,
)
Ripe Pistachio
kernels
. – – . ––––HPLCcoupledto
Diode-Array Detection
(DAD) detector
(Ballistreri et al.,
)
Dried ripe
Pistachio
kernels
. – – . – – – –
Walnuts .–. *..–. .–. – – – – RP-HPLC coupled with
fluorescence detector
(Kafkas et al.,
)
Note: Tocopherol contents (mg/ g).
Abbreviations: V, virgin; EV, extra virgin; R, refined.
*Means βand γare counted together.
V E P 17
et al., ). Abdallah et al. also studied the tocopherol
content of six different walnut varieties. They similarly
discovered a very high content of γ-tocopherol; however,
the α-tocopherol content found by this group was lower
than that reported by Omer’s group (Abdallah et al., ).
This difference could be related to other factors that will
be discussed later. Lavedrine et al. revealed that variety is
responsible for the variation in tocopherol content within
the same species. However, geographical origin may have
a more substantial influence than other factors consid-
ering the significant differences in tocopherol contents
within the same variety cultivated in different geograph-
ical regions (Lavedrine et al., ). The possible reason
behind the influence of geographical regions on variations
in vitamin E isomers content within the same variety was
explained in the study conducted by Skłodowska et al. on
tomato plants subjected to different degrees of NaCl stress.
They found that the content of tocopherols increased with
the increase in the stress level in the environment wherein
the tomatoes were planted (Skłodowska et al., ). Loy-
ola et al. also explained this behavior when they proved
that α-tocopherol biosynthesis is one of the mechanisms
underlying adaptation to harsh environmental conditions,
such as drought stress (Loyola et al., ). Similarly, Watts
et al, collected seed samples of emmer wheat from
two different groups exposed to two different stress lev-
els. The high-stress group was exposed to high solar radia-
tion, temperature, and drought. The results showed signifi-
cant differences in vitamin E contents and profiles between
the seeds of the two groups of wild emmer wheat. In par-
ticular, the percentages of α-tocopherol and α-tocotrienol
were high under low-stress conditions, whereas the per-
centages of δ-tocopherol and δ-tocotrienol were high under
high-stress conditions, suggesting that high stress reduced
methylation (Emily Watts et al, ). Therefore, the dif-
ferences in vitamin E content within the same genotype
or variety can be ascribed to the conditions under which
the plant is grown because two plants planted in the same
region can experience different degrees of oxidative stress.
Consequently, they express their defense mechanisms dif-
ferently as well. However, this situation is not always
the case considering that a study conducted by T. T. D.
Do et al. showed consistency between the vitamin E con-
tents of two varieties of barley grown in different years and
different locations (T. T. D. Do et al., ).
The vitamin E content of oils appears to be affected by
the seed variety used for extraction. A recent study showed
that the total tocopherol contents of oil extracted from
four different almond varieties from Morocco were signifi-
cantly different, with the highest α-tocopherol content of
approximately . mg/ g found in the Beldi variety
and the lowest content of approximately . mg/ g
found in the Ferragnes/Feraduel variety (Melhaoui et al.,
). Α-Tocopherol contents were directly related to the
contents of vitamin E in the almonds themselves. The same
observations were seen in several seeds, fruits, and kernel
oils, such as apricot kernels, pumpkin seeds, avocado, and
olives (Manaf et al., ; Matthäus & Musazcan Özcan,
; Matthäus et al., ; Nakić et al., ; Özcan et al.,
; Wen et al., ).
.. Ripening and harvest time
Besides geographical and environmental conditions and
varietal type, harvest time at different ripening stages can
significantly affect vitamin E contents and profiles. For
example, Kumar et al. observed the development of toco-
pherols content in soybean seeds at four different stages
of maturity, namely, the first collection stage (R), the sec-
ond collection stage (R), the last collection stage before
full maturity (R), and full maturity. They found that toco-
pherol isomers and total tocopherol content varied signifi-
cantly across harvest stages. All tocopherol isomers were
present since the R; surprisingly, δ-tocopherol was the
predominant form, accounting for approximately % of
the total concentration of tocopherol isomers. This pre-
dominance started to wane as the content of other iso-
mers dramatically increased throughout R to R to com-
pletely change the tocopherol profile of the final products,
wherein γ-tocopherol accounted for approximately .%
of the total tocopherols content (Kumar et al., ). The
changes in the total vitamin E content in the seed must be
directly related to the plant’s needs and oil content as previ-
ously reported (Loyola et al., ). Vitamin E production
is an adaptation and defense mechanism that is adopted
by plants in need. With seed development, moisture con-
tent decreases, oil and polyunsaturated fatty acid contents
increase; thus, the risk of oxidation rises (Kamal-Eldin &
Appelqvist, ). The correlation of the changes in fatty
acid and vitamin E profiles with the different stages of seed
growth was studied in flaxseed. The results for flaxseed
were in line with those for soybean, wherein vitamin E,
which was mainly present in the form of γ-tocopherol and
γ-tocotrienol, dramatically increased with seed matura-
tion and the increase in polyunsaturated fatty acid con-
tent (Herchi et al., ). Hence, the increase in vitamin
E content along with seed growth was verified. However, a
study done on marula kernels revealed the opposite behav-
ior. The vitamin E content of the four tocopherol isomers
drastically dropped to almost by full maturity; this unex-
pected reduction could be attributed to the consumption
of tocopherols during ROS scavenging and fatty acid pro-
tection (Mariod et al., ). A similar trend was seen in
pistachio kernels at three different developmental stages.
The total tocopherol content, which was represented by