PHYTOTHERAPY RESEARCH

Phytother. Res. 17, 925–929 (2003)

Published online in EFFECTS
Wiley InterScience (www.interscience.wiley.com).
OF CURCUMIN AND IC ON CIRCULATORYDOI: 10.1002/ptr.1254
LIPIDS AND LPO 925

Protective Effects of Curcumin and Photo-

Irradiated Curcumin on Circulatory Lipids and
Lipid Peroxidation Products in Alcohol and
Polyunsaturated Fatty Acid-induced Toxicity

R. Rukkumani, M. Sri Balasubashini and Venugopal P. Menon

Department of Biochemistry, Faculty of Science, Annamalai University, Annamalainagar, Tamil Nadu, India

Alcohol is a neurotoxin associated with significant morbidity and mortality. Ethanol is found to induce a dose
dependent increase in lipid peroxidation (LPO). The elevation in lipid peroxidative products and the loss of
antioxidant defense potential are enhanced when alcohol is taken along with polyunsaturated fatty acid (PUFA)
or heated PUFA. The present study was undertaken to evaluate the effects of curcumin and photo-irradiated
curcumin on alcohol and PUFA induced LPO and lipid profiles in plasma. The levels of vitamin C and E were
decreased significantly in alcohol + raw as well as heated PUFA groups. The treatment with curcumin and
photo-irradiated curcumin (IC) increased their levels significantly. The increase was more significant in the IC
group than the curcumin group. The levels of cholesterol, phospholipids (PL), triglycerides (TG), free fatty
acids (FFA), thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HP) were increased signi-
ficantly in alcohol + raw as well as heated PUFA groups and the treatment with curcumin and IC, brought back
the levels. But the IC reduced the levels more significantly than curcumin. Thus, our results indicate that IC
is a more potent antioxidant than curcumin. Copyright © 2003 John Wiley & Sons, Ltd.

Keywords: Alcohol; PUFA; curcumin; photo-irradiated curcumin; lipid peroxidation; circulatory lipids.

(Sharma, 1976). Moreover, curcumin also decreases

INTRODUCTION
It is well-established that alcoholic patients and experi-
mental animals exposed to ethanol display biochemical
signs of oxidative damage. The primary mechanisms
of oxidative damage include aldehyde derived protein
modifications resulting from ethanol metabolism and
lipid peroxidation. Fat is a dietary component and the
actual lipid content, especially the fatty acid composi-
tions of diets, are significant. In recent years there has
been an increased focus on replacing some of the indi-
vidual fat intake with unsaturated fat. Current data in-
dicates that the newer heart-friendly oils like sunflower
oil posses a high PUFA n-6 content and high n-6/n-3
ratio, which are actually detrimental to health (Sircar
and Kansra, 1998). Moreover heating of edible fats is
known to alter their nutritional properties, especially
when fat is rich in PUFA. During deep fat frying many
volatile and non-volatile products are produced, some
of which are toxic, depending on the level of intake
(Alexander, 1981). Thus, it is evident that the lipid
peroxidation is more prominent when alcohol is taken
along with PUFA and heated PUFA.
Curcumin (Diferuloyl methane), the active ingredi-
ent of turmeric (Curcuma longa), inhibits LPO in vitro
serum cholesterol levels in hyperlipidemic rats (Rao
et al., 1970). When curcumin is irradiated, stable pho-
toproducts like vanillin and ferulic acid (FA) are pro-
duced (Dahl et al., 1994). In the present investigation
the efficiency of curcumin in inhibiting peroxidation
of lipids under the influence of known free radical
inducing alcohol + PUFA as well as heated PUFA has
been studied and compared with the efficiency of irra-
diated curcumin, whose antioxidant property is not well
established.
MATERIALS AND METHODS
Female Albino rats, Wistar strain of body weight
ranging 140–150 g bred in the central Animal House,
Rajah Muthiah Medical College, were fed on pellet diet
(Agro Corporation Private Ltd, Bangalore, India) and
water, ad libitum. The standard pellet diet comprised
21% protein, 5% lipids, 4% crude fibre, 8% ash, 1%
calcium, 0.6% phosphorus, 3.4% glucose, 2% Vitamins
and 55% Carbohydrates and provides metabolisable
energy of 3600 Kcal/Kg. The animals were housed in
plastic cages under controlled conditions of 12 h light/
dark cycle, 50% humidity and at 30 ± 3 °C.

Materials Used.
* Correspondence to: Dr V. P. Menon, Department of Biochemistry,
Faculty of Science, Annamalai University, Annamalai Nagar-608 002,
Sunflower Oil: Sunflower oil marketed by Gold Win-
Tamil Nadu, India. Tel: 0091 4144 38343 (0). Fax: 0091 4144 38343. ner was purchased from local market,
E-mail: cmrana@md3.vsnl.net.in Chidambaram, Tamil Nadu, India.
Copyright © 2003 John Wiley & Sons, Ltd. Received
Phytother. Res. 9 April(2003)
17, 925–929 2002
Accepted 5 August 2002
Copyright © 2003 John Wiley & Sons, Ltd.
926 R. RUKKUMANI ET AL.

Curcumin (C): Curcumin was obtained from central
drug house private limited, Mumbai,
India.
Heated PUFA: Sunflower oil was subjected to heating
at 180 °C for 30 min, twice.
Irradiated
Curcumin (IC): Curcumin was subjected to photo-
oxidation by exposing curcumin to
bright sunlight for 5 h continuously.
(All other chemicals and solvents used were of ana-
lytical grade)
Animals and Treatment.
Group 1: Control rats (Rats given standard pellet diet
and glucose solution isocalorific to ethanol
and high fat diet).
Group 2: Rats given 20% ethanol (Rajakrishnan et al.,
1997) and a high fat diet (15%) [Raw Sun-
flower oil].
Group 3: Rats given 20% ethanol and a high fat
diet (15%) [Thermally oxidised sunflower
oil].
Group 4: Rats given curcumin (80 mg Kg−1 body
weight) (Rajakrishnan et al., 2000), dissolved
in 20% ethanol (7.9 g Kg−1 body weight) and
a high fat diet [15% raw sunflower oil].
Group 5: Rats given curcumin (80 mg Kg−1 body
weight) dissolved in 20% ethanol (7.9 g Kg−1
body weight) and a high fat diet [15% heated
sunflower oil].
Group 6: Rats given photo-irradiated curcumin
(80 mg Kg−1 body weight) dissolved in 20%
ethanol (7.9 g Kg−1 body weight) and a high
fat diet [15% heated sunflower oil].
At the end of the experimental period (45 days), the
rats were sacrificed by decapitation after an overnight
fast. Blood was collected in heparinised tubes and
(Table 1) plasma was separated for various analyses.
Biochemical Estimations. The activities of Alkaline
phosphatase (ALP) (E.C.3.1.3.1) by p-nitro phenyl
phosphate (PNPP) method (King and Armstrong,
1988) using a reagent kit and γ -glutamyl transferase by
the fixed time method of Orlowski and Meister (Fiala
et al., 1972) and the levels of TBARS by Thiobarbituric
assay method (Niehaus and Samuelson, 1968), lipid
hydroperoxides (Jiang et al., 1992), ascorbic acid (Roe
and Kuether, 1943), α-tocopherol (Baker et al., 1980),
Plasma cholesterol (Allain et al., 1974) using a reagent
kit, plasma triglycerides (TG) (Foster and Dunn, 1973),
Phospholipids (Zilversmit and Davis, 1950) and Free
fatty acids (Falholt et al., 1973) were analyzed.
Statistical Analysis. The data given in the tables are
average values ± standard deviation (SD). Data were
analyzed statistically by analysis of variance (ANOVA)
and groups were compared by least significant differ-
ence (LSD).
RESULTS
In this study, the levels of liver markers (ALP, GGT)
(Table 2), lipid peroxidative end products (TBARS,
HP) (Table 3) and lipids (Cholesterol, PL, TG, FFA)
(Table 4), were increased significantly in the plasma of
both alcohol + raw as well as heated PUFA groups.
The treatment with curcumin significantly decreased the
levels, but photo-irradiated curcumin treatment was
found to be more effective than curcumin. Similarly,
the antioxidant levels (Vitamin C and Vitamin E)
(Table 3), were decreased significantly in alcohol + raw
as well as heated PUFA groups, which improved
significantly on curcumin treatment. The improvement
was more significant in IC group compared to curcumin.
DISCUSSION
Chronic ethanol intoxication may be related to delete-
rious changes that occur at the cellular level. The inter-
action of ethanol with biological membranes alters
membrane fluidity, modulates fatty acid composition
and thus alters its function. Moreover, poly unsaturated
edible oils are more prone to lipid peroxidation and
further damages the cellular structures (Ibrahim et al.,
1998) and makes the membrane leaky to liver markers
when given along with alcohol. The lipid peroxides
generated during cooking and frying of oils can cause
membrane damage and increase lipid infiltration
(Jethmalani et al., 1989), so the hepatic injury caused

Table 1. Experimental design

Group No. of rats Treatment Dose administered

Normal (N) 6 Glucose 36.2 g Kg−1 body weight (b.w.)

Alcohol + raw PUFA (A + R)
Alcohol + Heated PUFA (A + H)
Alcohol + raw PUFA + curcumin
(A + R + C)
Alcohol + heated PUFA+ curcumin
(A + H + C)
Alcohol + heated PUFA +
photo-irradiated curcumin
(A + H + I.C.)
6 20% alcohol + high fat diet
6 20% alcohol + high fat diet
6 20% alcohol + high fat
diet + curcumin
6 20% alcohol + high fat
diet + curcumin
6 20% alcohol + high fat
diet + irradiated curcumin
7.9 g Kg−1 b.w. ethanol + 15% fat (raw
sunflower oil)
7.9 g Kg−1 b.w. ethanol + 15% fat (heated
sunflower oil)
7.9 g Kg−1 b.w. ethanol + 15% fat (raw
sunflower oil) + 80 mg Kg−1 b.w. curcumin
7.9 g Kg−1 b.w. ethanol + 15% fat (heated
sunflower oil) + 80 mg Kg−1 b.w. curcumin
7.9 g Kg−1 b.w. ethanol + 15% fat (heated
sunflower oil) + 80 mg Kg−1 b.w.
photo-irradiated curcumin

Average food intake/day: Ω 15 g/150 g rat.

Total calories/day: 508 Kcal/150 g rat.

Copyright © 2003 John Wiley & Sons, Ltd. Phytother. Res. 17, 925–929 (2003)
 EFFECTS OF CURCUMIN AND IC ON CIRCULATORY LIPIDS AND LPO 927

Table 2. Activities of marker enzymes in plasma [Values are mean ± SD from 6 rats in each
group]

Groups GGT (IU/L) ALP (IU/L)

1. Normal 0.597 ± 0.06 85.880 ± 7.00

2. Alcohol + raw PUFA 1.658 ± 0.16a 174.020 ± 15.85a
3. Alcohol + heated PUFA 2.508 ± 0.14a 239.560 ± 22.14a
4. Alcohol + raw PUFA + curcumin 0.783 ± 0.13bd 119.780 ± 10.21ad
5. Alcohol + heated PUFA + curcumin 1.433 ± 0.12ag 177.410 ± 16.28ag
6. Alcohol + heated PUFA + 1.150 ± 0.16agj 149.147 ± 12.13agk
irradiated curcumin
F – ratio 160.764 77.259

ANOVA followed by LSD

Groups 2,3,4,5,6 are compared with group 1; a
= p ≤ 0.001; b = p ≤ 0.01; c
= p ≤ 0.05;
Group 4 is compared with group 2; d
= p ≤ 0.001; e = p ≤ 0.01; f
= p ≤ 0.05;
Groups 5,6 are compared with group 3; g
= p ≤ 0.001; h = p ≤ 0.01; i
= p ≤ 0.05;
Group 6 is compared with group 5; j
= p ≤ 0.001; k = p ≤ 0.01; l
= p ≤ 0.05;
n
= no significance.

Table 3. Levels of nonenzymic antioxidants and extent of lipid peroxidation in plasma [Values are mean ± SD from 6 rats in each group]

Vitamin C Vitamin E TBARS Hydroperoxides

mg/100 ml mg/100 ml mM/100 ml ×10−5 mM/100 ml
Groups plasma plasma plasma plasma

1. Control 1.850 ± 0.11 1.621 ± 0.07 0.130 ± 0.02 9.933 ± 1.00

2. Alcohol + raw PUFA 1.167 ± 0.13a 0.898 ± 0.39a 0.370 ± 0.04a 19.477 ± 1.76a
3. Alcohol + heated PUFA 0.767 ± 0.05a 0.533 ± 0.06a 0.415 ± 0.02a 25.915 ± 2.05a
4. Alcohol + raw PUFA + curcumin 1.383 ± 0.25ad 1.412 ± 0.07nd 0.183 ± 0.02ad 13.115 ± 0.68bd
5. Alcohol + heated PUFA + curcumin 1.100 ± 0.09ag 1.018 ± 0.07ag 0.228 ± 0.02ag 18.962 ± 1.92ag
6. Alcohol + heated PUFA + 1.233 ± 0.08agl 1.249 ± 0.12bgl 0.200 ± 0.01agl 16.777 ± 1.20agl
irradiated curcumin
F – ratio 76.088 29.078 173.789 79.387

ANOVA followed by LSD

Groups 2,3,4,5,6 are compared with group 1; a
= p ≤ 0.001; b = p ≤ 0.01; c
= p ≤ 0.05;
Group 4 is compared with group 2; d
= p ≤ 0.001; e = p ≤ 0.01; f
= p ≤ 0.05;
Groups 5,6 are compared with group 3; g
= p ≤ 0.001; h = p ≤ 0.01; i
= p ≤ 0.05;
Group 6 is compared with group 5; j
= p ≤ 0.001; k = p ≤ 0.01; l
= p ≤ 0.05;
n
= no significance.

Table 4. Lipid levels in plasma [Values are mean ± SD from 6 rats in each group]

Cholesterol Triglycerides Phospholipids Free fatty acids

Groups mg/100 ml Plasma mg/100 ml Plasma mg/100 ml Plasma mg/100 ml Plasma

1. Normal 89.813 ± 4.18 81.333 ± 7.87 92.500 ± 9.08 72.622 ± 4.13

2. Alcohol + raw PUFA 165.747 ± 12.86a 136.000 ± 4.73a 165.000 ± 10.75a 136.867 ± 10.23a
3. Alcohol + heated PUFA 207.402 ± 15.64a 170.667 ± 4.13a 223.833 ± 17.22a 172.190 ± 9.48a
4. Alcohol + raw PUFA + curcumin 114.802 ± 12.01bd 101.333 ± 6.53ad 116.250 ± 7.87bd 87.822 ± 6.14cd
5. Alcohol + heated PUFA + curcumin 158.500 ± 17.70ag 137.333 ± 11.15ag 166.250 ± 12.92ag 129.166 ± 14.50ag
6. Alcohol + heated PUFA + 129.342 ± 6.78agj 121.667 ± 9.91agk 142.500 ± 10.60agj 105.483 ± 10.27agj
irradiated curcumin
F – ratio 67.305 333.115 89.882 83.323

ANOVA followed by LSD

Units – Enzyme reaction, which gives 50% inhibition of NBT reduction/min.
Groups 2,3,4,5,6 are compared with group 1; a
= p ≤ 0.001; b = p ≤ 0.01; c
= p ≤ 0.05;
Group 4 is compared with group 2; d
= p ≤ 0.001; e = p ≤ 0.01; f
= p ≤ 0.05;
Groups 5,6 are compared with group 3; g
= p ≤ 0.001; h = p ≤ 0.01; i
= p ≤ 0.05;
Group 6 is compared with group 5; j
= p ≤ 0.001; k = p ≤ 0.01; l
= p ≤ 0.05;
n
= no significance.

by alcohol and heated PUFA may disorganize mem-
brane and release enzymes from the cell.
The hike in TBARS and HP is due to the induction
of hepatic cytochrome p450 monooxygenases activity
by ethanol (Wisniewska and Wronska, 1994), which
leads to the production of free radical species that cause
Copyright © 2003 John Wiley & Sons, Ltd.
membrane damage through lipid peroxidation pro-
ducts. The changes in the composition of erythrocytes,
with increased erythrocyte deformability exvivo have
been reported with increased intake of PUFA (Nordey
and Goodnight, 1990). The increase in dietary unsat-
urated fat increases the degree of unsaturation in the
Phytother. Res. 17, 925–929 (2003)
928 R. RUKKUMANI ET AL.
membranes (Jaya et al., 1993), since unsaturated bonds
are more susceptible to lipid peroxidation, in alcohol +
raw PUFA group, the TBARS and HP levels are higher.
It has been reported that heated PUFA contains detec-
table amounts of TBARS and HP (Hageman et al.,
1991), which aggravates damage when given along with
alcohol. Thus, the largest increase in lipid peroxidative
indices were seen in alcohol + heated PUFA group.
There appears to be an inverse correlation between
alcohol + PUFA (raw and heated) mediated oxidative
stress and antioxidant defenses. The alcohol and PUFA
(raw and heated) actually challenge the Vitamin C and
Vitamin E, by increasing the susceptibility of tissues
to free radical mediated oxidative damage. In vitro
experiments have shown that Vitamin C at higher levels
act as an effective antioxidant (Steinberg and workshop
participants, 1992) and Vitamin E is known to pro-
vide protection by directly terminating lipid peroxidat-
ive side chain (Cohly et al., 1998). Thus their counter
balancing action against lipid peroxidative products
decreases their levels.
Marked alterations in lipid metabolism have been
reported in chronic ethanol feeding (Day et al., 1993).
Reports show that chronic ethanol ingestion results
in moderate hypercholesterolemia and hypertrigly-
ceridemia (Antonenkov et al., 1983). Chronic admin-
istration of ethanol increases tissue cholesterol and FFA.
Increase in cholesterol may be due to the accumula-
tion of fat in tissues and excess cholesterol leaking out
into the blood. High blood cholesterol concentrations
have been reported in diets rich in PUFA (Hocquette
and Bauchart, 1999). Moreover reports show that
the higher plasma cholesterol has been observed in
heated oil fed rats (Narasimhamurthy and Raina, 1999).
Thus both in alcohol + raw as well as heated PUFA
groups the cholesterol levels were higher.
Fielding et al. have found increased plasma TG con-
centration after acute ethanol ingestion (Fielding et al.,
2000). In vitro alcohol has been shown to exert a direct
effect on lipid metabolism, causing an increase in fatty
acid esterification and a decrease in oxidation, thus
accumulating TG. The increased TG levels after PUFA
ingestion may be due to the increased availability of
substrate, FFA for esterification. Since the availability
of FFA is more in heated PUFA group, the TG levels
are also comparatively higher.
Phospholipids are the vital components of bio mem-
branes. They are the primary targets of peroxidation
and can be altered by ethanol (Yamada et al., 1985).
The increased levels of PL may be due to the increased
availability of FFA. Since PUFA is a component of PL,
the increased PUFA intake may increase the levels of
PL in plasma.
The free fatty acid levels are enhanced in alcohol fed
group, which may be attributed to the increased forma-
tion of acetate, which in turn forms FFA. The increased
NADH/NAD+ ratio due to ethanol ingestion also fav-
ours fatty acid synthesis. Increased FFA in alcohol +
PUFA (raw + heated) may also be due to increased
lipid breakdown and increased dietary PUFA, also may
eventually increase the FFA levels.
Curcumin by scavenging or neutralizing free radicals
(Soudamini et al., 1992), interacting with oxidative
cascade (Unnikrishnan and Rao, 1992), quenching
oxygen, inhibiting oxidative enzymes like cytochrome
P450 (Soudamini et al., 1992), and by chelating metal
Copyright © 2003 John Wiley & Sons, Ltd.
ions like Fe2+ (Sreejavan and Rao, 1994), inhibits lipid
peroxidation and thus reduces TBARS and HP, sta-
bilizes membrane and thus prevents the hike of ALP
and GGT. Its effective antioxidant property decreases
the utilization of Vitamin C and Vitamin E and thus
maintains their levels.
The decrease in cholesterol level by curcumin is due
to the induction of 7α -hydroxylase activity by curcumin,
which facilitates biliary excretion of cholesterol (Babu
and Srinivasan, 1997). The spices are known to affect
bile acid excretion and thus curcumin also influence
other lipid levels. The decreased levels of PL and TG
may also be due to the decreased FFA synthesis by
curcumin, which may suppress the enzymes involved in
FFA synthesis.
In our study, IC was found to be more effective
than curcumin in protecting the membrane against
lipid peroxidation and improving antioxidant status.
Flavonoids and monophenolic compounds have been
well described over recent years for their properties as
antioxidants and scavengers of reactive oxygen species
and nitrogen species (Bourne et al., 2000). Ferulic acid
is a flavonoid and both ferulic acid and vanillin are
monophenolics and thus both are effective antioxidants.
Reports show that ferulic acid is effective on lipid
peroxidative systems induced by Fe2+ [Uchinda et al.,
1996]. UV absorption of ferulic acid catalyses stable
phenoxy radical formation and thereby potentiates
its ability to terminate free radical chain reaction. By
virtue of effectively scavenging deleterious radicals
and suppressing oxidative reactions, FA is shown as an
important antioxidant (Graf, 1992). Reports have shown
that FA is absorbed as Ferulic acid β -glucuronide, and
the antioxidant property of ferulic acid is not only due
to the hydrophobic FA but also due to the hydrophilic
sugar moiety (Ohta et al., 1997). Thus FA is proved to
be an effective antioxidant.
Reports say that the supplementation of phenolic
compounds leads to increased antioxidant activity in
plasma and a significant increase in Vitamin E content
(Carbonneau et al., 1997). The presence of phenolic
group in vanillin may contribute to the antioxidant
property. It has been proposed that hydroxy and
hydroperoxy radicals initiate hydrogen abstraction from
a free phenolic substrate to form a phenoxy radical
that can rearrange to a quinone methide radical inter-
mediate (Pan et al., 1999) and thus reduce free radicals.
Thus the combined effects of FA and vanillin in IC
effectively decrease the TBARS and HP and effectively
modulate the antioxidant status.
The levels of lipids were significantly reduced in
photo-irradiated curcumin treatment groups compared
to curcumin. The vanillin and ferulic acid, the compon-
ents of IC, due to their effective antioxidant property,
protects membrane and prevents FFA release. FFA
being a substrate for other lipids, its decrease may re-
flect on the levels of lipids. Recent reports show that γ -
oryzanol, a mixture of ferulic acid, can lower cholesterol
level in blood and lower the incidence of coronary heart
disease. In Japan it has been used as a natural anti-
oxidant in foods, beverages and cosmetics (Scavariello
and Ardlano, 1998). Thus, the vanillin and ferulic acid
effectively reduce lipids by an unknown mechanism.
We therefore conclude from our results that IC is
more effective in controlling lipid peroxidation and lipid
levels in circulation than curcumin.
Phytother. Res. 17, 925–929 (2003)
 EFFECTS OF CURCUMIN AND IC ON CIRCULATORY LIPIDS AND LPO
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