International Journal of Ethnopharmacology

Vol. 2(1), pp. 014-020, July, 2016. www.premierpublishers.org, ISSN: 1357-4285

IJE

Research Article

Antioxidant potentials of tannic acid on lipid

peroxidation induced by several pro-oxidants in
cerebral and hepatic lipids
Tajudeen O Jimoh1*, Temidayo Ogunmoyole2, Emmanuel A Aladejana1, Ige J Kade3
1

Department of Biochemistry, Adekunle Ajasin University P.M.B 001, Akungba-Akoko, Ondo State, Nigeria.
Ekiti State University, P.M.B 5363, Ado-Ekiti, Ekiti State, Nigeria.
3
Federal University of Technology, Akure, P.M.B. 704, Akure 340001, Nigeria.
2

Various prospective studies have indicated the antioxidant potency of tannic acid in several
models. However, there is no clear-cut evidence revealing that the reported antioxidant
properties of tannic acid remains potent regardless of the lipid sources and pro-oxidants
employed for the oxidative assault. Hence, this study sought to investigate the antioxidant
properties of tannic acid against cerebral and hepatic lipid peroxidation induced by several
pro-oxidants (Iron (II) sulfate, Sodium nitroprusside, cyclophosphamide and acetaminophen)
in vitro. Rats were decapitated under mild ether anesthesia and the tissues were
rapidly dissected, placed on ice, weighed and immediately homogenized in cold 50 mM
Tris-HCl, pH 7.4 (1/10, w/v). The homogenates were centrifuged for 10 min at 4000 g to yield
a pellet that was discarded and a low-speed supernatant (S1). Our results indicated that Fe
(II) showed the highest pro-oxidative effects in both tissues lipids. Furthermore, tannic acid
demonstrated potent inhibitory effects against lipid peroxidation in both tissues lipids
regardless of the pro-oxidant employed. To this end, there is a dire need to exploit the
protective benefits of tannic acid as a potential exogenous antioxidant against lipid
peroxidation with a view to providing solution to the global oxidative stress menace.
Keywords: Antioxidant, tannic acid, hepatic, pro-oxidants, lipid peroxidation; cerebral, free radicals.

INTRODUCTION
The
pathogenesis
of
metabolic
and
neurological diseases such as diabetes mellitus,
Alzheimer and Parkinson diseases are primarily due to
the imbalance between the pro-oxidants and
antioxidants homeostasis (Halliwell and Whiteman
2004). In order to counteract this imbalance,
exogenous supply of antioxidants becomes paramount
while tannic acid a polyphenol having molecular
formula C76H52O46 consisting of a D-glucose to which
five gallic acid residues are linked through ester bonds
becomes handy. However, the polyphenolic structure of
tannic acid has been reported to be responsible for its
antioxidant and antimutagenic activities (Andrade et al.,
2005). Meanwhile, the protection of cell constituents
against destructive oxidative damage, inhibition of
hydrolytic and oxidative enzymes including lipid

peroxidation coupled with the reduction of the risk

factors of various degenerative diseases associated
with oxidative stress have been linked with the roles of
antioxidants in cell (Vinary et al., 2010).

*Corresponding Author: Tajudeen O Jimoh,

Department of Biochemistry, Adekunle Ajasin
University P.M.B 001, Akungba-Akoko, Ondo State,
Nigeria. E-mail: jimmmypeace@gmail.com, Tel.:
+2348066091263.

Antioxidant Potentials of Tannic Acid on Lipid Peroxidation Induced by Several Pro-oxidants in Cerebral and Hepatic Lipids

Jimoh et al.

014

Oxidative stress occurs when excessive free

radicals react with proteins, cell walls and DNA causing
damage to cell structures that are critical to the immune
system (Alia et al., 2003). During normal metabolism
body cells use oxygen and form highly reactive
molecules known as free radicals, and under normal
circumstances, the body maintains equilibrium between
pro-oxidants (free radicals) and antioxidants (Oboh,
and Rocha, 2007). A disturbance in the systems
equilibrium where pro-oxidants outweigh antioxidants
causes the body to lose its ability to neutralize free
radicals resulting in oxidative stress (Oboh, 2005) and
this has been implicated in the pathophysiology of
various diseases including hepatic injury (Jarrar et al.,
2000) and chronic renal damage (Baker et al., 1985;
Galle, 2001). These free radicals could as well be
produced by inflammatory response, stress and
environmental pollution. When the free radicals are not
neutralized and the cell damage is not repaired, cell
death occur leading to a higher propensity for diseases
(Moskovitz et al., 2002). This may however be
responsible for the oxidation of biomolecules explaining
the key mechanisms responsible for the metabolic
changes observed in hepatic injury (Kojima et al.,
2007).
On the other, the high concentration of
polyunsaturated fatty acids in membrane lipids,
presence of iron ions and low capacity of antioxidant
enzymes make the cerebral system very susceptible to
lipid peroxidation involving the interaction of oxygenderived free radicals with polyunsaturated fatty acids
(REED, 2011). Double bonds of polyunsaturated fatty
acids in biological membranes are easily attacked by
free radicals, they undergo degradation by a chain
reactions and form lipid hydroperoxides. This complex
process yields a mixture of epoxy-fatty acids, alkanes,
alkenes, alkanals, 4-hydroxy-2-alkenals (HAKs),
alkenals, and aldehydes including malondialdehyde
(MDA), which represents about 70 % of the total
aldehydes
produced
during
membrane
lipid
peroxidation (Esterbauer et al., 1991). The build-up of
superoxide, hydroxyl peroxide and other free radicals
which are highly reactive could offer a potential threat
to the integrity of critical macromolecules such as lipids
which is a vital component of the membrane ultimately
resulting in the alteration of critical membrane function.
Moreover, it is vital to express the potentials of
tannic acid which is a specific commercial form of
tannin and a type of polyphenol. Tannins are
antioxidants often characterized by reducing power (MiYea et al., 2003) and scavenging activities (Minussi et
al., 2003). The antioxidant capabilities of tannins
depend on: (1) the extent of their colloidal state; (2) the
ease of interflavonoid
bond cleavage
or
its
stereochemical structure; (3) the ease of the pyran ring
(C-ring) opening; and (4) the relative number of OH
groups on A and B rings (Noferi et al., 1997).
Compounds with a trihydroxyl structure in the B-ring
have the greatest antioxidant activity (Rice-Evans et al.,
1996). The total phenolic contents of most previously
studied plants were in most cases determined using

tannic acid as a standard phenolic compound as this

may be due to its antioxidant properties. More so,
tannic acid exhibits antioxidant, antimutagenic and
anticarcinogenic properties (REED, 2011). One of its
common applications is in the pharmaceutical
production of albumin tannate; an antidiarrheal agent
and it is also used to produce tannate salts of certain
antihistamine and antitussive products to impart
increased stability or slow release properties to the
active pharmaceutical ingredient. It exerts many
physiological effects, such as to accelerate blood
clotting, reduce blood pressure, decrease the serum
lipid level, reduce liver necrosis, and modulate immune
responses (Chung et al., 1998). Therefore, these may
be the possible underline principle responsible for the
use of tannic acid in folkloric medicine (Cox and Cox,
2009).
Meanwhile, antioxidants and free radical
scavengers
have
been
suggested
to
offer
cytoprotective and therapeutic benefits (Pulido et al.,
2000) as this will however, reduced or impaired the
oxidative chain reactions. To this end, there is an ever
increasing search for substances that could inhibit the
deleterious effects of free radicals. More importantly,
there is no clear-cut evidence revealing that the
reported antioxidant properties of tannic acid remains
potent regardless of the lipid sources and pro-oxidants
employed for the oxidative assault. Hence, this study
sought to investigate the in vitro antioxidant properties
of tannic acid against cerebral and hepatic lipid
peroxidation induced by several pro-oxidants (Iron (II)
sulfate, Sodium nitroprusside, cyclophosphamide and
acetaminophen.

MATERIALS AND METHODS

Chemicals
Tannic acids and thiobarbituric acid (TBA) were
obtained from Sigma Chemical Co. (St. Louis, MO,
USA). All other chemicals were of analytical grade and
were obtained from standard commercial suppliers.
Animals
Twenty one male adult Wistar rats (200 250
g) from ours breeding colony were used. Animals were
kept in separate animal cages, on a 12 h light: 12 h
o
dark cycle, at a room temperature of 22 24 C, and
with free access to food and water. They were
acclimatized under these conditions for two weeks prior
to the commencement of the experiments. The animals
were used according to standard guidelines of the
Committee on Care and Use of Experimental Animal
Resources.
Tissue preparation
Rats were decapitated under mild ether anesthesia and
the cerebral and hepatic tissues were rapidly removed,
placed on ice and weighed. The tissues were
immediately homogenized in cold 50 mM Tris HCl, pH

Antioxidant Potentials of Tannic Acid on Lipid Peroxidation Induced by Several Pro-oxidants in Cerebral and Hepatic Lipids

Int. J. Ethnopharmacol.

7.4 (1/10, w/v). The homogenate was centrifuged for 10

min at 4000 rpm to yield a pellet that was discarded
and a low-speed supernatant (S1).

THIOBARBITURIC
(TBARS) ASSAY

ACID

REACTIVE

SPECIES

An aliquot of 100 l of S1 was incubated for 1 h

o
at 37 C in the presence of tannic acid (concentrations
range of 0100 M), with and without the pro-oxidants;
Iron sulphate (final concentration 10 M), sodium
nitroprusside (SNP) (final concentration 30M),
Cyclophosphamide (final concentration 10 M) and
Acetaminophen (final concentration 20 M). This was
then used for lipid peroxidation determination in the
tissues. Productions of thiobarbituric acid reactive
substances (TBARS) were also determined as
described by method of (Ohkawa et al., 1979). The
colour reaction was developed by adding 300 l 8.1%
sodium dodecyl sulphate to S1, followed by sequential
addition of 500 l acetic acid and 500 l 0.8% of
thiobarbituric acid (TBA). This mixture was centrifuged
o
and incubated at 95 C for 1 h. TBARS (thiobarbituric
acid reactive species) produced were measured at
532nm and the absorbance was compared with that of
standard curve using
MDA
(Malondialdehyde).
Statistical analysis
All values obtained were expressed as mean
standard error of the mean. The data were analyzed by
one way ANOVA followed by Duncans multiple range
tests where appropriate and this is indicated in the text
of results. The differences were considered significant
when p < 0.05.

RESULTS
Figures 1 - 4 revealed the effect of tannic acid
on lipid peroxidation subjected to oxidative assaults
induced
by cyclophosphamide,
acetaminophen,
Sodium nitroprusside, and Iron (II) sulphate
respectively. Our results showed that when liver and
brain lipids were subjected to stress induced lipid
peroxidation caused by all the four pro-oxidants in the
presence of tannic acid, iron (II) sulphate showed the
highest pro-oxidative effects in both the liver and brain
lipids. However, one-way ANOVA revealed that
irrespective of the pro-oxidant or lipid types, the
inhibitory effect of tannic acid was significant at the
lowest volume of the pro-oxidants tested (P < 0.05).
This however, showed that tannic acid uses diverse
mechanisms to protect critical macromolecules from
free radical attack.

DISCUSSION
Lipid peroxidation has been reported to
proceed through free radical chain reactions (Donnell et

015

al., 1997) and its roles in the pathogenesis of several

pathologies such as: neurodegenerative (Domnguez et
al., 2008; Famulari et al., 1996; Fiszman et al., 2003),
inflammatory (Farooqui and Farooqui, 2011), infectious
(Repetto et al., 1996) and gastric related diseases
(Repetto et al., 2003) has been associated with the
alteration in the biomembrane structure. However,
since free radical overproduction involvement in the
onset, progression and complications of several
pathological conditions cannot be under-estimated,
research efforts geared towards the discovery of
antioxidant containing compounds that could be
exploited as panacea to the free radical menace has
been on the increase (Azizan, 2006). Although, the
antioxidant potential of tannic acid has been much less
marked than those of flavonoids, but its higher degree
of polymerization is related to its antioxidant activity.
The condensed and hydrolysable tannic acid
(ellagitannins) was reported to be up to fifteen to thirty
times superior in antioxidant activity to simple phenols
(Hagerman et al., 1998).
Moreover, oxidative damage in liver has
been linked with hepatic lipid metabolism, and may be
affecting the absorption and transport mechanisms of
vital substances
in
this organ.
Specifically,
morphological damage in the liver has been traced to
hepatic lipid peroxidation and the consumption of
endogenous antioxidants. Similarly, in the kidney and
heart, lipid peroxidation and oxidative damage
preceded necrosis (Repetto et al., 2010). The
increased oxidation of the cell biochemical constituents
is associated with ultra-structural changes in
mitochondrial morphology with mitochondrial swelling
and increased matrix volume (Boveris et al., 2008). In
human liver, the morphological changes can affect the
organ structure and function as it is the case for the bile
canaliculi that are damaged in liver transplanted
patients; a fact interpreted as the consequence of
oxidative damage which is associated with ischemia
reperfusion (Cutrin et al., 1996). Interestingly, there are
reports in rat liver experimental models of increased
peroxidation secondary to increased mitochondrial
production of O2- and H2O (Fridovich, 1978; Navarro
and Boveris, 2007; Navarro et al., 2009). Nevertheless,
since free radical can be generated from pro-oxidants
then, several pro-oxidants were employed in the
present study to test the antioxidant power of tannic
acid against lipid peroxidation.
Cyclophosphamide, an alkylating agent widely
used in cancer chemotherapy, is an inactive cytostatic
drug which is metabolized into active metabolites
mainly in the liver. During bio-activation, reactive
oxygen species are also formed, which can modify the
components of both healthy and neoplastic cell leading
to decreased antioxidative capacity (Stankiewicz et al.,
2002). Previous reports affirmed that cyclophosphamide
produces genotoxicity and oxidative stress in mice
(Premkumar et al., 2001) and early lung injury in rats
(Venkatesan and Chandrakasan, 1994). It also causes
fatal cardiotoxicity (Sudharsan et al., 2005). It is not
known however, whether lipid peroxidation is involved
in the mechanism of its toxicity. Meanwhile, (Figure 1)

Antioxidant Potentials of Tannic Acid on Lipid Peroxidation Induced by Several Pro-oxidants in Cerebral and Hepatic Lipids

Jimoh et al.

016

Figure 1. Shows the inhibitory effect of tannic acids against lipid peroxidation induced by cyclophosphamide in brain
and liver homogenates. Values averages from 3 to 4 independent experiments performed in triplicate. b and c
indicate a significant difference from the control a at p < 0.05.

Figure 2. Shows the inhibitory effect of tannic acids against lipid peroxidation induced by Acetaminophenin brain
and liver homogenates. Values averages from 3 to 4 independent experiments performed in triplicate. b and c
indicate a significant difference from the control a at p < 0.05.

indicates that cyclophosphamide induced lipid

peroxidation in the cerebral and hepatic tissues of
albino rats in vitro, as this assay measures the capacity
of an antioxidant sample to scavenge lipophilic radicals.
Interestingly, tannic acid exhibited a significant
inhibitory effect on the cyclophosphamide - induced
lipid peroxidation (Figure 1). This observation may be
indicating the critical underline principle responsible for
its potent DPPH radical scavenging ability (Omololu et
al., 2011). Apparently, the side effects of
cyclophosphamide can be minimized by the
incorporation of tannic acid in its compounding thereby
helping to inhibit its toxic effects by inhibiting the
formation of toxic metabolites that would have caused
lipid peroxidation.

excess level of ROS formation by N-acetyl-pbenzoquinone imine (NAPQI) leads to enhancement of

lipid peroxidation and reduction of antioxidant enzyme
which attack biomolecules such as DNA and
phospholipids (Hinson et al., 2004). Hence, search for
agents that could help minimizing acetaminophen
toxicity is on the increase. Interestingly, tannic acid
demonstrated a very significant inhibitory effect
especially on hepatic lipids (Figure 2) indicating its
potential antioxidative effectiveness towards shielding
the liver from acetaminophen toxicity. This finding could
be related with the underline mechanism responsible
for tannic acid ability to prevent the formation of toxic
intermediates probably by its potent reducing power
(Omololu et al., 2011).

Furthermore, acetaminophen has been widely

reported as a specific hepatotoxic agent, its effect being
confined to the liver. Other reports have indicated that

Sodium nitroprusside is an anti-hypertensive drug that

acts by relaxation of vascular smooth muscle and
consequently dilates peripheral arteries and veins

Antioxidant Potentials of Tannic Acid on Lipid Peroxidation Induced by Several Pro-oxidants in Cerebral and Hepatic Lipids

Int. J. Ethnopharmacol.

017

Figure 3. shows the inhibitory effect of tannic acids against lipid peroxidation induced by sodium nitroprusside in brain and liver
homogenates. Values averages from 3 to 4 independent experiments performed in triplicate. b and c indicate a significant difference
from the control a at p < 0.05.

Figure 4. shows the inhibitory effect of tannic acids against lipid peroxidation induced by FeSO4 in brain and liver homogenates. Values
averages from 3 to 4 independent experiments performed in triplicate. b and c indicate a significant difference from the control a at p
< 0.05.

(Fahmy, 1985). Meanwhile, reports have shown that

sodium nitroprusside elicit cytotoxic effect through the
release of cyanide and/or nitric oxide (NO) (Rauhala et
al., 1998). NO has been implicated in the
pathophysiology of strokes, traumas, seizures,
Alzheimer's and Parkinson's diseases (Castill et al.,
2000; Prast and Philippou, 2001). Besides, light
exposure promotes the release of NO from SNP
through a photodegradation process (Arnold et al.,
1984; Singh et al., 1995) and data from the literature
have shown that after the release of NO and SNP,
2
[NOFe(CN) 5-] is converted to iron containing
3
2
[(CN) 5Fe] and [(CN) 4 Fe] species (Loiacono
and Beart, 1992). After the release of NO, the iron

moiety may react with SNP, which could lead to the

formation of highly reactive oxygen species, such as
hydroxyl radicals via the Fenton reaction (Graf et al.,
1984). However, tannic acid was able to inhibit SNP
induced lipid peroxidation in the cerebral and hepatic
tissues of albino rats (Figure 3), suggesting that tannic
acid may be utilizing multiple mechanisms (probably a
combination of iron chelation, reducing power and
radical scavenging (Saravanan and Parimelazhagan,
2014) to combat free radicals released as result of
degradation of SNP therefore prevent lipid peroxidation.
The chemical structure of iron and its capacity
to drive a one-electron reaction makes it a key factor in
the formation of free radicals (Fraga and Oteiza, 2002).

Antioxidant Potentials of Tannic Acid on Lipid Peroxidation Induced by Several Pro-oxidants in Cerebral and Hepatic Lipids

Jimoh et al.

018

It has its role in the causation of deleterious

effect on biological macromolecules by reacting with
superoxide anion (O2) and hydrogen peroxide (H2O2)
to produce hydroxyl radical (OH) via the Fenton
2+
chemistry (Graf et al., 1984). Fe is a powerful prooxidant, capable of inducing generation of ROS and
initiating lipid peroxidation chain reaction (Prast and
Philippou, 2001). This study has shown that the tannic
acid was able to prevent the progression of lipid
peroxidation by inducing a reduction in MDA content of
the cerebral and hepatic tissues in a concentration
dependent manner (Figure 4). Antioxidant containing
compounds participate in coordinating chemical
reactions by forming complexes with ligand molecules
2+
2+
like Fe and this can therefore prevent Fe -induced
ROS generation and lipid peroxidation. Hence, the
inhibition of iron induced cerebral and hepatic tissues
lipid peroxidation by the tannic acid could be as a result
2+
of its Fe chelating ability and/or radical scavenging
ability (Omololu et al., 2011). In this study, tannic acid
2+
demonstrated a significant inhibitory effect against Fe
induced lipid peroxidation regardless of the tissue
involved (Figure 4). This could be due to its potent ferric
reducing power (Pulido et al., 2000) which prevents
free radicals generation and consequently inhibit lipid
peroxidation.

CONCLUSION
This study revealed the inhibitory effects of tannic acid
against lipid peroxidation in both cerebral and hepatic
lipids regardless of the four pro-oxidants employed.
This could however, offer a promising source of
therapeutic
approach
towards
the
management/treatment
of
diseases/disorders
associated with peroxidation of lipids.

ACKNOWLEDGMENT
This research was supported by Alhaji and Alhaja
Obajuaye Jimohs grant (2009-2010) for the
Biochemical Research programme through Adekunle
Ajasin University Akungba-Akoko, Ondo State, Nigeria.

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Accepted 15 July, 2016.
Citation: Jimoh TO, Ogunmoyole T, Aladejana EA,
Kade IJ (2016). Antioxidant Potentials of Tannic Acid
on Lipid Peroxidation Induced by Several Pro-oxidants
in Cerebral and Hepatic Lipids. International Journal of
Ethnopharmacology, 2(1): 014-020.

Copyright: 2016 Jimoh et al. This is an open-access

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Antioxidant Potentials of Tannic Acid on Lipid Peroxidation Induced by Several Pro-oxidants in Cerebral and Hepatic Lipids