international journal of nutritional research review article antioxidant … · 2021. 4. 6. ·...
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Archives of Life Science and Nutritional Research 1
Kiokias S*
Research Executive Agency (REA), Place Charles Rogier 16, 1210 Brussels, Belgium.
Received: 25 August, 2019; Accepted: 05 September, 2019; Published: 28 September, 2019
*Corresponding Author: Kiokias S, Research Executive Agency (REA), Place Charles Rogier 16, 1210 Brussels, Belgium. E-mail: [email protected]
Abstract Reactive oxygen species as initiators of oxidative stress account for LDL and DNA oxidative
changes that are respectively associated with the development of pathological conditions such as
atherosclerosis and carcinogenesis. This review paper first focuses on specific bio-indicators used to
monitor these harmful oxidative stress conditions and develop health strategies against the associated
human diseases. Subsequently, it provides an overview of the most recent available literature on the
protective role that certain antioxidant vitamins (vitamin C, vitamin E and provitamin A compounds)
have been reported to exert against the biochemical oxidative processes that govern the initiation of
these specific human diseases.
Key words:Provitamin A; Vitamin E; Vitamin C; DNA Damage; Oxidized LDL
Introduction Oxygen free radicals (i.e. as hydroxyl
radicals; superoxide radicals and other active
oxygen species such as singlet oxygen) have
been widely reported to adversely alter lipids
and proteins through biochemical oxidative
reactions and thereby trigger a number of
human diseases [1]. The ability of free radicals
to structurally modify cellular components,
gene expression and protein production has
led to the implication of their involvement in a
variety of health diseases [2]. More specifically,
these harmful oxygen species can generate
oxidative damage and adversely affect biological
membranes with pathological consequences [3].
This review mainly focuses on the following
two resulted pathological conditions:
(i) Oxidative modification of LDL (low- density
lipoproteins) a lipid peroxidation reaction driven
by free radicals that is Considered a key step in the
early stages of atherosclerosis and thereby the
development of cardiovascular diseases [4-6].
(ii) Cellular oxidative DNA damage for which a
body of research is trying to clarify how the
reported repair pathways may influence the cancer
transformation [7, 8].
International Journal of Nutritional Research
Review Article
Antioxidant Effects of Vitamins C, E and Provitamin A
Compounds as Monitored by Use of Biochemical
Oxidative Indicators Linked to Atherosclerosis and
Carcinogenesis
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Archives of Life Science and Nutritional Research 2
It is also known that the nature has
generously offered a wide range of nutrients
with strong antioxidant activities, among which
certain compounds of vitamin value can act as
radical scavengers in model biological systems
and in the human organism [9]. A large number
of studies have examined the effects of
antioxidant vitamins either individually or in
combination, on ex vivo LDL oxidation and in
vivo DNA damage with most information being
available for the effects of pro vitamins A,
vitamins C and vitamin E [10, 11].
Arvanitoyannis and co- authors (2009) [12]
reviewed the various available methods for the
determination of chain-breaking antioxidant
activity in food and biological systems. The
total peroxyl radical trapping parameter
(TRAP) and the oxygen radical absorbance
capacity assay (ORAC) have served as the most
commonly used methods of evaluating the
antioxidant capacity during the last two
decades [13,14].
This paper first provides an overview
of the link between LDL and DNA oxidative
changes with the development of the specific
harmful pathological conditions. The
biomarkers that are commonly used to monitor
these biochemical processes are also discussed.
Subsequently, building on the knowledge
presented by the most recent clinical studies in
this field, the paper summarises the most
important research findings concerning the use
of certain vitamins against oxidative stress.
More specifically, this work will investigate on
the effect of provitamins A carotenoids,
tocopherols (vitamin E) and ascorbic acid
(vitamin C) against both in vivo oxidative
damage of DNA and ex vivo LDL oxidative
modification.
Health adverse effects of oxidative
damage as monitored by certain
biochemical indicators
Oxidative damage and detrimental health effects
LDL oxidative modification and atherosclerosis
Over the last few years, extensive clinical
and epidemiologic research evidence has been
gathered on the role of oxidized LDL (low-density
lipoproteins) in the development of atherosclerosis
[15]. Atherosclerosis is a progressive disease of the
arterial tree that involves deposition of lipid,
mostly oxidized LDL, in the arterial intima leading
finally to a thickening of the arterial wall and
reduced luminal blood flow [16]. Oxidative
modification of LDL, a lipid peroxidation reaction
driven by free radicals is therefore a key step in the
early stages of atherosclerosis [17]. The
relationship between circulating ox-LDL and
subclinical atherosclerosis has been thoroughly
explored and confirmed in a case control study
performed by Fang and coworkers. [18]
DNA oxidative damage and cancer
It has recently become apparent that generation of
reactive oxygen species from mitochondria first as
the cellular response to oxidative stress and DNA
damage is close linked to carcinogenesis[19]. DNA
damage can take many forms, ranging from
specifically oxidized purine and pyrimidine bases
to gross DNA changes such as strand breaks, sister
chromatid exchange, and the formation of
micronuclei [20]. According to one of the proposed
oxidative mechanisms, hydrogen peroxide can
cause DNA strand breakage, by
generation of the hydroxyl radical (OH-) close to
the DNA molecule, via the Fenton reaction.
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Archives of Life Science and Nutritional Research 3
Equation (1): H2O2+ Fe2+→OH•+ OH- + Fe3+
This process may result in DNA
instability, mutagenesis and ultimately
carcinogenesis.
Health biomarkers of oxidative damage
Plasma levels of oxidized LDL
A convenient and very frequently used
method for monitoring the level of plasma
oxidized LDL is the process of copper- induced
LDL oxidation through the spectrophotometric
measurement of conjugated dienes (CDs)
absorption at 233 nm [21]. The chronology of
LDL oxidation by Cu2+ ions can be divided into
three consecutive time phases: During the lag
phase, LDL particles become progressively
depleted of its endogenous antioxidants, so
that they subsequently enter the propagation
phase in which the polyunsaturated fatty acids
(PUFAs) are rapidly converted to CDs [22].
In the final decomposition
stage, secondary reactions of LDL oxidation
leading to aldehydes (malondialdehyde,
hexanal, 4- hydroxynonenal etc.), are
accelerated by transition metal ions, such as
Fe2+, which may catalyze decomposition of
lipid hydro peroxides (LOOH) to alkoxyl
radicals (LO·)
Biomarkers of DNA oxidative damage
Among various types of DNA damage
that occur due to Reactive oxygen species
(ROS) and increase cancer risks, the most
studied base damage is 8- oxoguanine (8-
oxoG). Generation of 8-oxoG in DNA is a
mutagenic and potentially carcinogenic event
since the oxidized base has altered hydrogen
bonding or “code specificity”, preferentially
forming base pairs with adenine rather than
cytosine [23]. In addition, the deoxy-nucleoside
derivative 8- OH-dG 8-hydroxy-2’-
deoxyguanosine has been used as useful
marker of oxidative DNA damage [24].
Figure (1) Selective products of DNA oxidative
damage commonly used as biochemical indicators
of oxidative stress: (a) 8-OH-deoxyguanosine (b)
8-oxoadenine (c) 8-oxoguanine(Kiokias,2002)[24]
(a) 8-OH-deoxyguanosine
(b) 8-oxo adenine
(c) 8-oxo-guanine (Kiokias, 2002)[24]
The Japan Institute for the Control of Aging
has developed an in vitro enzyme-linked
immunosorbent assay (ELISA) for quantitative
measurement of the oxidative DNA adduct 8-OH-
dG in tissue or urine samples, thereby enabling a
reliable assessment of DNA oxidative damage.
Furthermore, the well-known COMET assay is an
alternative sensitive and valuable technique that
allows the determination of the level of DNA
damage by making use of repair enzymes to
introduce strand breaks at sites where oxidized
bases are present [25].
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Archives of Life Science and Nutritional Research 4
Other oxidative bio-indicators
During the last decade, the
development of immunochemical detection of
HNE-histidine cytotoxic adducts (4hydroxynon
enal (4-HNE)), has opened more advanced
methodological possibilities for qualitative and
quantitative detection of lipid peroxidation in
various human and animal tissues [26]. In
addition, the Thiobarbituric acid reactive
substances (TBARs) test is still the most
frequently used test to assess secondary
products of lipid peroxidation such as
malondialdehyde (MDA) that reacts with TBA
reagent on heating under acidic conditions to
give a red chromophore, which is measured by
UV spectroscopy at 532 nm or by fluorescence
at 553 nm [27].
Effect of vitamins on the oxidative
damage as monitored by LDL and
DNA biochemical indicators Antioxidant activity of Provitamin A
compounds
Provitamin A compounds (α, β-
carotenes and β-cryptoxanthin) belong to the
class of carotenoids (Figure 2). They are 40-
carbon terpenoids widely available in nature
with well-known scavenging activities against
free radicals that are trapped in their
conjugated structure [28]. Carrots and
tomatoes are the main sources of carotene in
the diet, while the daily consumption of leafy
vegetables (spinach, beets, lettuce)
significantly contributes to the
carotenoid daily intake [29]. The antioxidant/p
rooxidant potential of carotenoids is of
particular significance to human health, and a
critical factor in combating the oxidative
processes of various chronic disorders [30].
Figure (2) Structure of the provitamin A carotenoids (Kiokias 2002) [24]
-carotene
-carotene
-cryptoxanthin
Effect of Provitamin A against LDL oxidation
Major non-provitamin A carotenoids
(lycopene, lutein, and zeaxanthin) and provitamin A
compounds carotenoids have different biological
activities and efficacy, depending on their food
content, dietary intake, bioavailability, and
bioconversion [31]. Special attention has been
given to the potential protective role of carotenoids
in atherosclerosis, since these lipid soluble
pigments have shown remarkable antioxidant
capacity against LDL oxidation [32]. The disease-
preventing activity of β-carotene and other
provitamin A carotenoids could be ascribed either
to their conversion into retinoid or to their activity
against LDL oxidation. The molecular mechanisms
in the context of the anti- and pro-oxidant activity
of carotenoids in human are still not fully
understood [33].
It may be that β-carotene and other
carotenoids (e.g. astaxanthin) promote a good
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Archives of Life Science and Nutritional Research 5
health when supplemented at physiologic
amounts in foods, but could even present
adverse prooxidant harmful activities when
given in high doses and under highly oxidative
conditions. In the well known as “Rotterdam
study” the association between aortic
atherosclerosis and the levels of the major
serum carotenoids including both provitamin A
(α-carotene, β-carotene, α- cryptoxanthin) and
non provitamin compounds (lutein, lycopene,
and zeaxanthin) was investigated in a
subsample of the elderly population (n=108
cases and controls) [34]. In an age- and sex-
adjusted logistic regression model, serum
lycopene (but no other carotenoids) was
inversely associated with the risk of
atherosclerosis.
Effect of provitamin A against DNA oxidative
damage
Lorenzo and coworkers (2009) [35]
have investigated the biological properties of β-
cryptoxanthin, in cell culture model systems,
using the comet assay to measure DNA damage.
They reported that at low concentrations, close
to those found in plasma, β-cryptoxanthin does
not itself cause damage, but rather protects
transformed human cells from damage induced
by H(2)O(2) or by visible light in the presence
of a photosensitizer. Astley and coworkers
(2004) [36] supplemented healthy male
volunteers with lutein, beta-carotene or
lycopene (natural isolate capsules, 15 mg/d, 4
weeks) and observed that both beta carotene
and non provitamin A carotenoids exerted an
antioxidant protection by scavenging DNA-
damaging free radicals and modulation of DNA
repair mechanisms. On the other side, Collins
and Azqueta (2012)[37] stated that studying
reports from the last 5 years, revealed a clear
distinction between effects of pro-vitamin A
carotenoids (α,β-carotenes and β-
cryptoxanthin) and the effects of non- vitamin
A carotenoids (lycopene, lutein, astaxanthin
and zeaxanthin). Whereas the compounds of the
latter group are almost invariably reported to
protect against DNA damage, the provitamin A
carotenoids show a more varied spectrum of
effects, sometimes protecting and sometimes
enhancing DNA damage.
Antioxidant activity of Vitamin E
compounds Vitamin-E comprises a category of eight
monophenolic compounds (known as Tocopherols
and tocotrienols) with strong reported antioxidant
activities in food and biological systems. α-
Tocopherol is the most common compound found
in European dietary sources such as olive and
sunflower oils, while γ-tocopherol is frequently
present in the American diet because of higher
intakes of soybean and corn oil [38]. Vitamin E has
been reported to exert a role in reducing
inflammation and muscle soreness and protect the
cell membrane from oxidative damage [39].
Tocopherols mainly act as chain breaking
antioxidants that inactivate free radicals via their
hydrogen donating character [40].
Effect of vitamin E against LDL oxidation
Hodis and co-authors (2012) [41] reported
that α-tocopherol supplementation (400 IU/day)
significantly raised plasma vitamin E levels
(P<0.0001) whereas reduced circulating oxidized
LDL and LDL oxidative susceptibility. Studies that
included vitamin E supplementation support a
significant protection of LDL usually at doses higher
than 400 IU/day. As noted by Rizvi and co-workers
(2014) [42] Vitamin E is the major lipid-soluble
component in the cell antioxidant defense system
with numerous important roles within the body
because of its antioxidant activity. However, it has
also been suggested that when accompanying
antioxidants such as ubiquinone and vitamin C are
not available (to react and quench the vitamin E
radicals) a pro-oxidant tocopherol effect could be
induced [33]. Actually Niki (2010) [43] noted that
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Archives of Life Science and Nutritional Research 6
recent human clinical trials with vitamin E
have not yielded positive results against LDL
oxidative deterioration on the contrary to in
vitro experiments.
Effect of Vitamin E against DNA oxidative
damage
Makpol and coworkers (2010) [44]
observed that α-tocopherol protected against
H(2)O(2)-induced DNA damage and this
modulation was affected by donor age.
Another human trial [45] showed that an
intake of food rich in α-tocopherol could
decrease levels of DNA oxidative adducts.
Asgard (2014) [46] reported a significant
decrease of catechol- induced (1 mM) general
DNA damage in the presence of 20 μM of α-
tocopherol. On the contrary, Barcelos and co-
authors (2011) [47] supported that dietary
supplementation with α-tocopherol can even
induce DNA oxidative stress.
Antioxidant activity of Vitamin C compounds
L-Ascorbic acid (AH2) is an essential
nutrient, known as vitamin C, widespread
vitamin in nature in many fruits and
vegetables [48]. Although its role is not limited
to being an antioxidant, arguably its
antioxidant activity and its redox properties
are key to its over all biological function [49].
Ascorbic acid is commonly reported to act
synergistically with chain breaking
antioxidants (e.g. tocopherols, flavonoids)
resulting into enhancing effects against food
and biological oxidative deterioration [50].
Effect of Vitamin C against LDL oxidation
Ascorbic acid is a water-soluble
antioxidant, and as such is expected to be
removed from LDL during isolation. An earlier
study [51], did not find any significant effect of
dietary supplementation with vitamin C on LDL
oxidation in smoking volunteers. On the
contrary Harats [52], reported a beneficial
effect of dietary supplementation with 500
mg/d for 2 months [31] against LDL oxidative
deterioration. In addition, McRae (2008) [53] noted
that Vitamin C supplementation reduced serum
LDL and triglycerides levels. More recently, Shariat
and coworkers (2013) [54] noted a strong
antioxidant effect of vitamins C against the low
density lipoprotein oxidation mediated by mye-
lopero-xidase.
Effect of Vitamin C against DNA oxidative damage
A protective effect of vitamin C
supplementation in humans with plasma
levels>50μmol/l was observed by Sram (2012) [55]
in terms of 8-oxodG levels. More recently, Kontek
and coworkers (2013) [56] noted that vitamin C (in
a concentration range10- 100 μm) caused a clear
protecting effect against DNA damaging. More
specifically, they concluded that vitamin C
modulates DNA damage induced by hydrogen
peroxide in human colorectal adenocarcinoma cell
lines (HT29), estimated by COMET assay in vitro
(decrease ∼ 30%). Asgard (2014) [46] reported
that high plasma levels of ascorbate reduced the
levels of oxidative DNA damage (8-oxodG) in
mononuclear white blood cells. Overall, Konopacka
(2004) [57] highlighted that data concerning the
influence of vitamin C on oxidative DNA damage are
conflicting and some of the discrepancies can be
explained by the different experimental
ethodologies employed.
Antioxidant activity of Vitamin mixtures Effect of
vitamin mixtures against LDL oxidation
A growing body of human clinical
investigation has focused into combination of
various antioxidants in order to explore the
potential of interactions because of varying modes
and mechanisms of antioxidant action [10].
Interestingly, a few studies that were designed to
supplement subjects with mixtures of antioxidant
vitamins in generally observed an enhanced
beneficial effect on oxidative stability of LDL,
presumably resulting from a synergistic action
between the vitamins [58, 59].) A recently
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Archives of Life Science and Nutritional Research 7
conducted cross-sectional study [60] observed
that the total daily carotenoid intake of
provitamin A carotenoids (β cryptoxanthin, β
and α carotene lycopene) mixture with
xanthophylls (lutein plus zeaxanthin,) was
inversely associated (p<0.05) with
the plasma oxidized-LDL concentrations.
Kiokias and Gordon (2003) [61]
supplemented for 3 weeks 30 healthy
volunteers with a mixture of provitamin A
(palm oil carotenes) and xanthophylls
(paprika, lutein, bixin)providing in a total
amount of 30mg active carotenoid/day. The
authors reported an increased resistance
of LDL to oxidation
(monitored by CD at 233 nm) accompanied by
enhanced plasma carotenoid levels for the
supplemented groups compared with placebo
[61]. Boushehri and coauthors (2012) [61]
examined the effect of antioxidant vitamins on
serum oxidized LDL levels in male subjects
with cardiovascular disease risk factors. They
reported that a diet enriched in a combination
of vitamin C (500 mg), vitamin E (400 IU) and
ß-carotene (15 mg), was strongly associated
with lower serum oxidized LDL levels.
Similarly in an earlier study [63], a daily
supplementation for 2 months with a mixture
of vitamin E (200 mg) together with vitamin C
(400 mg) and β- carotene (20 mg) significantly
decreased the susceptibility of LDL to oxidative
deterioration.
Effect of vitamin mixtures against DNA
oxidative damage
An earlier study [64], had examined the
effect of antioxidant vitamin supplementation
on DNA damage and repair in human -
lymphoblastic cells. After a 24-hour
supplementation period with a mixture of
ascorbic acid and α-tocopherol, (60 micro M in
total) the level of endogenous DNA damage
was significantly lower than in the non-
supplemented culture, as assessed by the
comet assay. In addition a human clinical trial [65]
reported that supplementation of smokers and non-
smokers with an antioxidant mixture
(vitamin C-100 mg+vitamin E-280 mg +and β-
carotene-25 mg per day) significantly (p<0.002)
reduced base damage in lymphocyte DNA.
These findings agree with another human
trial [66] in which 23 healthy subjects (after 2
weeks of washout) were supplemented daily with
40 mg lycopene (weeks 3 and 4), 22.3 mg β-
carotene and 15.7mg α-carotene (weeks 5 and 6),
and 11.3 mg lutein (weeks 7 and 8) This
intervention has resulted into a significantly
decreased DNA damage in lymphocytes. Kiokias &
Gordon (2003) [61] conducted a double-blind,
placebo-controlled cross over study with 30
healthy subjects. Following a dietary
supplementation with 30 mg carotenoid mixture
/day (,-carotenes, lycopene, paprika, lutein,
bixin, total amount) they reported a significant
effect against production of urinary 8-OHdG
estimated by use of ELISA test. Zou and co-authors
(2014) [66] also highlighted that there could be a
synergistic effect when carotenoids are mixed
together because various compounds tend to
arrange in different sites of membranes and
lipoproteins, adding an enhanced protection
against oxidative damage. More recently, a cross-
sectional study [60] supplemented 296 healthy
middle-aged men with a mixture of all 3 provitamin
A compounds and two more carotenoids (lycopene
and lutein). In conclusion, the total daily carotenoid
intake based on five investigated carotenoids was
inversely associated with the production of urinary
8-OH-dG as oxidative stress biomarker
(p<0.05). Very recently, Ahmed and co-authors
(2018) [67] concluded a protective effect of
curcumin and α-tocopherol against propoxur-
induced oxidative DNA damage in human
peripheral blood mononuclear cells. An overview
on the most recent human trials (individually or in
mixtures) that reported protective effects of
vitamins against LDL and DNA oxidative changes is
given in (Table 1).
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Table (1) An overview of most recent human clinical evidence confirming positive effects of dietary
supplementation with vitamins against LDL and/or DNA oxidative changes.
Authors/studies(in date order)
Condition of Human Clinical trials
Protective effect of the vitamin mixture
Effect against LDL oxidation
Effect against DNA damage
Sram et al (2012) [55]
Vitamin C supplementation in
humans
---------- Protective effect of vitamin C
supplementation against DNA damage in terms of 8-oxodG levels
Hodis et al (2012) [41] reported
α-Tocopherol
supplementation (400 IU/day)
Supplementation significantly raised plasma
vitamin E levels (P< 0.0001) and reduced circulating
oxidised-LDL (P= 0.03) and LDL
oxidative susceptibility (P< 0.01).
----------
Boushehri et al (2012) [61]
Male subjects followed a diet enriched with a
combination of vitamin C (500 mg),
vitamin E (400 IU), ß- carotene (15 mg),
The antioxidant treatment resulted into significantly lower serum oxidized LDL
levels.
----------
Kontek et al (2013)[56] Vitamin C supplementation in
humans (in a concentration range
10-100 μm)
----------
Modulation of DNA damage estimated
by COMET (decrease ∼ 30%)
Asgard (2014)
[46]
47 type-2 diabetes subjects supplemented
for 12 weeks with 16 capsules/day (mixture of β- carotene + α- tocopherol)
----------
Significant decrease of catechol-
induced (1 mM) DNA damage in the presence of 20 μM of α-tocopherol.
Cocate et al. (2015)[60]
296 healthy middle- aged subjects were supplemented with a carotenoid mixture
(β-cryptoxanthin, lycopene, lutein plus
zeaxanthin α- β carotenes)
The carotenoid
supplementation resulted into reduced plasma
oxidised-LDL concentrations. (p<0.05)
----------
Ahmed et al (2018) [67]
Propoxur-induced oxidative DNA damage
in human peripheral blood
mononuclear cells:
----------
Protective effects of curcumin mixtured with α-tocopherol
Archives of Life Science and Nutritional Research 8
Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis Arch Lif Sci Nutr Res: 3(1): 104.
Conclusions/future work in this
scientific field Based on the analysis presented in the previous
section of this review, the following conclusions
can be drawn:
a) The association between plasma oxidized
LDL and DNA oxidative adducts with the
eventual risk of developing a cardiovascular
disease or cancer respectively are not
completely elucidated yet. Further
investigation is required in this field to
obtain more recent and valid clinical
intervention data further to the existing
epidemiological data. To this end, the set-up
of new methods and biomarkers to monitor
the level of DNA and LDL oxidative damage
is very essential and the use of innovative
technologies (e.g. Nano science and Nano-
tools) can be decisive in the development of
new monitoring tools. Such bio- indicators
can be used to test the efficiency of natural
antioxidants against oxidative stress and
thereby offer new strategies to combat
again the progression of atherogenesis and
certain types of cancer.
b) A recent body of clinical research evidence
has concluded that dietary combinations of
vitamins (e.g. vitamin E, vitamin C and
provitamins A) can be more effective
against oxidative damage of either LDL or
DNA than the supplementation of each
individual vitamin. Such an enhanced effect
of vitamins mixtures may relate to the
different mode of activities of the individual
compounds thereby allowing a synergistic
effect when combined in the diet. In
particular for carotenoids, a better
antioxidant effect against oxidative damage
has been reported when provitamin A
compounds (mainly hydrophobic α-and β-
carotene) are supplemented together with
preparations of more polar xanthophylls
(e.g. lutein or paprika) in recent human
clinical studies.
c) In order to design a new generation of
dietary supplements based on natural
vitamins with clear antioxidant activity, it is
essential to first explore and elucidate the
bioavailability of the individual compounds.
This would help to establish a clear
relationship between dietary intake and
health impact thereby facilitate
further optimization studies on the clinical
effects of vitamins supplementation against
oxidative pathological conditions.
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Citation: Sotirios K (2019), Antioxidant Effects of Vitamins C, E and Provitamin A Compounds as Monitored by Use of Biochemical Oxidative Indicators Linked to Atherosclerosis and Carcinogenesis. Int J Phar Inft Thrp; 3(1): 01-13.
DOI: 10.31829-2765-8368-alsnr2019-3(1)-104
Copyright: © 2019 Sotirios K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.