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Role of Cuminum cyminum on Ethanol and Preheated Sunflower Oil

Induced Lipid Peroxidation
K. Arunaa; R. Rukkumania; P. Suresh Varmaa; Venugopal P. Menona
a
Department of Biochemistry, Faculty of Science, Annamalai University, Annamalainagar, Tamil
Nadu, India

To cite this Article Aruna, K. , Rukkumani, R. , Varma, P. Suresh and Menon, Venugopal P.(2006) 'Role of Cuminum
cyminum on Ethanol and Preheated Sunflower Oil Induced Lipid Peroxidation', Journal of Herbs, Spices & Medicinal
Plants, 11: 4, 103 — 114
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 Role of Cuminum cyminum on Ethanol
and Preheated Sunflower Oil Induced
Lipid Peroxidation
K. Aruna
R. Rukkumani
P. Suresh Varma
Venugopal P. Menon
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ABSTRACT. Alcohol is a neurotoxin associated with significant mor-

tality and morbidity. Ethanol is found to induce a dose-dependent in-
crease in lipid peroxidation. The elevation in lipid peroxidative products
and the loss of antioxidant defense potential are enhanced when alcohol
is consumed along with polyunsaturated fatty acids. The present study
evaluated the effect of Cuminum cyminum on lipid peroxidation induced
by ethanol and preheated (to oxidize) sunflower oil. Hepatotoxicity, as-
sessed by the activities of plasma aspartate transaminase (AST), alkaline
phosphatase (ALP), and ␥-glutamyl transferase (GGT), was apparent in
rats fed alcohol and preheated oil as compared with control rats on a
normal diet. The toxicity was associated with lipid peroxidation and a dis-
ruption in the antioxidant defense mechanism, as evidenced by increased
levels of thiobarbituric acid reactive substances (TBARS), hydroperoxides,
and free fatty acids (FFA) in the liver; decreased levels of glutathione, vita-
min C, and vitamin E in the liver and kidney; and decreased activities of
superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) in
the liver. Treatment with cumin significantly reversed the metabolic

K. Aruna, R. Rukkumani, P. Suresh Varma, and Venugopal P. Menon are affiliated

with the Department of Biochemistry, Faculty of Science, Annamalai University,
Annamalainagar 608 002, Tamil Nadu, India.
Address correspondence to: Venugopal P. Menon at the above address (E-mail:
cmrana@sify.com).
Journal of Herbs, Spices & Medicinal Plants, Vol. 11(4) 2005
Available online at http://www.haworthpress.com/web/JHSMP
© 2005 by The Haworth Press, Inc. All rights reserved.
doi:10.1300/J044v11n04_11 103
 104 JOURNAL OF HERBS, SPICES & MEDICINAL PLANTS

trends associated with alcohol and preheated sunflower oil, bringing

liver and kidney activities close to normal levels, indicating antioxidant
properties of cumin. [Article copies available for a fee from The Haworth Doc-
ument Delivery Service: 1-800-HAWORTH. E-mail address: <docdelivery@
haworthpress.com> Website: <http://www. HaworthPress. com> © 2005 by The
Haworth Press, Inc. All rights reserved.]

KEYWORDS. Ethanol, lipid peroxidation, antioxidants, heated sun-

flower oil, n-6 PUFA, Cuminum cyminum
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INTRODUCTION

Alcoholic patients and experimental animals exposed to ethanol usu-

ally display biochemical signs of oxidative damage. In the body, the pri-
mary pathway for the oxidation of ethanol to acetaldehyde is via alcohol
dehydrogenase in the liver, although ethanol can also be reduced by an
inducible microsomal ethanol oxidizing system (21). Induction of the
microsomal system results in enhanced acetaldehyde production, which
in turn impairs defense systems against oxidative stress. The liver
cytochrome P450 form CYP2E1, a major component of the microsomal
ethanol oxidizing system, has been implicated in hepatotoxicity due to
ethanol (16).
In recent years, an increased focus on replacing some of the individ-
ual fat intake with unsaturated fat has arisen. Current data, however, in-
dicates that the newer, heart friendly oils, such as sunflower oil, posses a
high polyunsaturated fatty acid (PUFA) n-6 content and high n-6/n-3
ratio that are detrimental to health (34). 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 prod-
ucts are produced, some of which are toxic, depending on the level of
intake (1).
Ayurveda, the ancient form of Indian medicine that deals with plants
and plant products, uses active ingredients in plants for treating diseases
(26). Indeed, several spices and herbs are claimed to possess medicinal
properties (35) and, because they are plant products, are considered to
have less or be free from side effects when compared with synthetic
medicines (38). Among the spices used by traditional healers, the
consumption of cumin, Cuminum cyminum L. (Apiaceae), in India is
relatively large. Cumin is widely used in ayurvedic medicine for the
 Aruna et al. 105

treatment of dyspepsia, diarrhea, and jaundice and has stomachic, di-

uretic, carminative, emmanogogic and antispasmodic properties (12).
This study investigated the antioxidative effect of cumin seeds on
heated oil and ethanol induced oxidative stress.

MATERIALS AND METHODS

Plant material. Cumin, Cuminum cyminum L., seeds purchased from

a local market in Chidambaram, Tamil Nadu, India, were used in this
study. The seed, positively identified by a Botanist, in the Department
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of Botany, Annamalai University, Annamalinagar, India, were cleaned

of extraneous matter, dried in shade for 4 to 5 h and then finely pow-
dered in a mechanical mixer. The resulting cumin powder was dissol-
ved in water just before use.
Experimental animals. Male albino rats, Wistar strain bred and raised
in the Central Animal House, Rajah Muthiah Medical College,
Annamalai University, were used as test animals in this study. The rats,
weighing 140 to 160 g, were housed in plastic cages with filter tops un-
der semi-natural light-dark conditions at room temperature and fed a
pellet diet (Hindustan Lever, Ltd., Mumbai. India) with water given ad
libitum.
Chemicals. Ethanol was purchased from E. Merck, Co., Dermstadt,
Germany. Sunflower oil, marketed by Gold Winner (Chennai, India),
was purchased from a local market in Chidambaram, India. The sun-
flower oil was subjected to two frying cycles of 30 min each at 180⬚C to
produce preheated oil that would simulate oil after use in cooking. All
other chemicals and biochemicals used for the experiments were of
analytical grade.
Experiment. The experimental animals were randomly divided
among the treatment groups for experimental treatment (Table 1). At
the end of the 45-day experimental treatment period, the animals were
anesthetized with ketamin hydrochloride at 30 mg/kg body weight and
then sacrificed, after an overnight fast, by decapitation. Blood was col-
lected in heparinized tubes for separation of the plasma into fractions
for analysis. The liver and kidneys were then removed from the animals,
freed of blood, and placed in ice-cold holders containing 0.9 percent
NaCl until used in analyses. The project was approved by the institu-
tional ethical committee (Reg. No. 160/1999/CPSEA).
 106 JOURNAL OF HERBS, SPICES & MEDICINAL PLANTS

TABLE 1. Experimental treatments.

Treatment Animal diet1

Control Standard diet
Cumin Standard diet ⫹cumin
Alcohol Standard diet ⫹ ethanol
Alcohol ⫹ cumin Standard diet ⫹ ethanol ⫹ cumin
Preheated oil Standard diet ⫹ pre-heated sunflower oil
Preheated oil ⫹ cumin Standard diet ⫹ pre-heated sunflower oil and
cumin
Alcohol ⫹ preheated oil Standard diet + ethanol and preheated sun-
flower oil
Alcohol ⫹ preheated oil ⫹ cumin Standard diet plus ethanol ⫹ preheated sun-
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flower oil ⫹ cumin

1 All test animals received the standard pellet diet or the standard pellet diet supplemented with a 20% solu-
tion of ethanol (23), with preheated (to oxidize) sunflower oil (15%), with cumin (given by intragastric tube,
0.25 g/kg body weight in distilled water), or a combination of alcohol, preheated sunflower oil, and/or cumin
at the above levels.

Plasma ␥-glutamyl transferase (E.C.2.3.2.2) was assayed by the

method of Fiala et al. (9), activity of plasma aspartate transaminase
(E.C.2.6.1.1) was assayed by the method of Reitman and Frankel (27),
and activity of alkaline phosphatase (E.C.3.1.3.1) was assayed (using a
reagent kit) by the method of King and Armstrong (14). The concentra-
tion of thiobarbituric acid reactive substances (TBARS) in liver and
kidney tissues was estimated by the method of Yagi (40), hydro-
peroxides were determined by the method of Jiang et al. (11), and the
level of free fatty acids determined by the method of Falholt et al. (8).
Glutathione (GSH) content of tissues was determined by the method of
Ellman (7), while tissue ascorbic acid was estimated by the method of
Roe and Kuether (28) and vitamin E was determined by the method of
Baker and Frank (4). The activity of glutathione peroxidase (E.C.1.11.
1.9) was assayed by the method of Rotruck et al. (29), the activity of
superoxide dismutase (E.C.1.15.1.1) by the method of Kakkar et al. (13)
and the activity of catalase (E.C.1.11.1.6) by the method of Sinha (33).
Statistical analysis. Statistical analysis was done using analysis of
variance (ANOVA) followed by Duncan’s Multiple Range Test
(DMRT) at P < 0.05 level.

RESULTS

The average weight gain by alcohol and preheated sunflower oil fed
rats was significantly reduced when compared with normal control rats
 Aruna et al. 107

(Table 2). Animals given cumin along with the preheated oil and alco-
hol, however, had nearly normal patterns of weight gain. The activity of
plasma ␥-glutamyl transferase (GGT), aspartate transferase (AST), and
alkaline phosphatase (ALP) increased significantly in animals in test
groups given preheated oil, alcohol, or alcohol ⫹ preheated oil as com-
pared with animals in the control group fed a normal diet (Table 3). The
administration of cumin along with the preheated oil and alcohol
showed a marked reduction in the activity of the liver enzymes GGT,
AST, and ALP. Changes in the level of tissue TBARS, hydroperoxides,
and free fatty acids (FFA) were increased significantly in animals fed
preheated oil, alcohol, and alcohol ⫹ preheated oil as compared with
the control animals on a normal diet (Table 4). The administration of
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along with the preheated oil, alcohol, and alcohol ⫹ preheated oil
decreased the noted increase in TBARS, hydroperoxides, and FFA lev-
els. The levels of GSH, vitamin C and E decreased significantly in ani-
mals fed the preheated oil, alcohol, and alcohol ⫹ preheated oil as
compared with the control group of animals (Table 5). Administration

TABLE 2. Changes in body weight.

Treatments Body weight

Initial Final Change
(g) (g) (g)
Control 137.29 213.30 76.01
⫾ 6.13 ⫾ 7.51 ⫾ 6.73acfgh
Cumin 148.79 224.46 75.67
⫾ 3.79 ⫾ 5.23 ⫾ 2.54cfgh
Alcohol 150.25 202.92 52.66
⫾ 5.29 ⫾ 4.73 ⫾ 3.98b
Alcohol ⫹ cumin 141.27 211.69 70.42
⫾ 2.39 ⫾ 6.25 ⫾ 4.54gh
Preheated oil 140.38 205.55 65.18
⫾ 4.39 ⫾ 8.39 ⫾ 3.41deh
Preheated oil ⫹ cumin 139.83 215.15 73.88
⫾ 4.61 ⫾ 3.79 ⫾ 5.98fgh
Alcohol ⫹Preheated oil 151.23 211.47 60.24
⫾3.27 ⫾ 7.43 ⫾ 5.28e
Alcohol ⫹ Preheated oil ⫹ 145.71 214.81 69.10
cumin ⫾ 5.62 ⫾ 2.79 ⫾ 4.51h
1 Means ± S.D. from six test animals per treatment; values within a column with the same superscript letter
are not significantly different at P < 0.05 by Duncan’s Multiple Range Test.
 108 JOURNAL OF HERBS, SPICES & MEDICINAL PLANTS

TABLE 3. The effect of cumin on activity of GGT, AST, and ALP.

Treatment GGT ALP AST

(IU/liter) (IU/liter) (IU/liter)
Control 0.60 ⫾ 0.04acfgh 79.20 ⫾ 4.87acfgh 83.95 ⫾ 4.19acfg
Cumin 0.60 ⫾ 0.05cfgh 77.34 ⫾ 4.23cfg 84.91 ⫾ 4.89 cfg
Alcohol 1.25 ⫾ 0.13b 147.09 ⫾ 7.73b 140.26 ⫾ 8.20 b
Alcohol ⫹ cumin 0.62 ⫾ 0.04gh 83.16 ⫾ 5.17gh 92.92 ⫾ 5.45gh
Preheated oil 0.79 ⫾0.05d 123.72 ⫾8.71d 120.81 ⫾5.64d
Preheated oil ⫹ cumin 0.61 ⫾ 0.02fgh 83.00 ⫾ 1.98fgh 88.50 ⫾ 2.13fgh
Alcohol ⫹ preheated oil 1.42 ⫾0.07e 171.89 ⫾10.35e 181.45 ⫾13.07e
Alcohol ⫹ preheated oil 0.64 ⫾ 0.06h 85.35 ⫾ 5.16 h 95.90 ⫾ 5.65 h
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⫹ cumin
1 Means ± S.D. from six test animals per treatment; values within a column with the same superscript letter
are not significantly different at P < 0.05 by Duncan’s Multiple Range Test.

TABLE 4. The effect of cumin on level of tissue TBARS, hydroperoxides, and

free fatty acids.

TBARS1 Hydroperoxides1 Free fatty acids1

Treatment Liver Kidney Liver Kidney Liver Kidney
(mmoles/100 g) (mmoles/100 g) (mg/100 g)
Control 0.55 0.76 87.78 79.65 625.58 410.38
⫾ 0.02acfg ⫾0.04acfgh ⫾ 4.18acfg ⫾ 4.04acf ⫾ 47.66acfg ⫾ 28.48acfg
Cumin 0.57 0.76 85.80 75.76 628.25 420.74
⫾ 0.03cfgh ⫾ 0.03cfgh ⫾ 3.51c ⫾ 4.11c ⫾ 31.53 cf ⫾ 25.84cfg
Alcohol 1.66 1.64 148.77 121.95 879.57 678.94
⫾ 0.10b ⫾ 0.09b ⫾ 10.10b ⫾ 7.33b ⫾ 59.15 b ⫾ 37.51b
Alcohol ⫹ 0.60 0.81 93.98 85.37 647.11 437.05
cumin ⫾ 002gh ⫾ 0.04gh ⫾ 5.07gh ⫾ 3.26gh ⫾ 44.95gh ⫾ 27.72gh
Pre-heated oil 0.83 0.91 110.25 110.71 753.21 569.21
⫾ 0.05d ⫾ 0.07d ⫾ 5.76d ⫾ 5.90d ⫾ 47.29d ⫾ 27.89d
Pre-heated oil 0.57 0.77 90.16 82.71 643.66 423.86
⫹ cumin ⫾ 0.01fgh ⫾ 0.02fgh ⫾ 3.56fg ⫾ 3.34fg ⫾ 28.2fgh ⫾ 15.3fg
Alcohol ⫹ 2.01 1.92 171.31 167.74 995.29 810.3
pre-heated oil ⫾ 0.15e ⫾ 0.14e ⫾ 10.59e ⫾ 10.39e ⫾ 61.34e ⫾ 93.89e
Alcohol ⫹ 0.62 0.82 97.26 90.25 655.29 443.58
pre-heated oil ⫾ 0.03h ⫾ 0.03h ⫾ 6.10h ⫾ 4.67h ⫾ 630.16 h ⫾ 29.00h
⫹ cumin
1 Means ± S.D. from six test animals per treatment; values within a column with the same superscript letter
are not significantly different at P < 0.05 by Duncan’s Multiple Range Test.
 Aruna et al. 109

TABLE 5. The effect of cumin on the level of tissue GSH, and vitamins C and E.

Treatment GSH1 Vitamin C1 Vitamin E1

Liver Kidney Liver Kidney Liver Kidney
(mg /100 g tissue) (mg /100 g tissue) (mg /100 g tissue)
Control 136.11 117.97 1.24 1.08 0.82 0.53
⫾ 7.78acfg ⫾ 5.84acfgh ⫾ 0.08acfg ⫾ 0.08acfgh ⫾ 0.05acfgh ⫾ 0.03acfg
Cumin 138.30 118.29 1.27 1.07 0.82 0.52
⫾ 8.19cf ⫾ 7.47cfgh ⫾ 0.05cfg ⫾ 0.04cfgh ⫾ 0.04cfgh ⫾ 0.04cfg
Alcohol 85.86 93.92 0.84 0.88 0.60 0.39
⫾ 4.70b ⫾ 4.32b ⫾ 0.07b ⫾ 0.07bd ⫾ 0.03b ⫾ 0.02b
Alcohol ⫹ 130.71 112.98 1.12 1.01 0.78 0.49
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cumin ⫾ 5.66gh ⫾ 5.56gh ⫾ 0.07gh ⫾ 0.06gh ⫾ 0.04gh ⫾ 0.03gh

Preheated oil 97.39 70.39 0.97 0.81 0.61 0.40
⫾ 6.48d ⫾ 5.12d ⫾ 0.05d ⫾ 0.04d ⫾ 0.04d ⫾ 0.03d
Preheated oil 132.10 115.40 1.20 1.03 0.79 0.49
⫹ cumin ⫾ 3.9fg ⫾ 6.00fgh ⫾ 0.03fgh ⫾ 0.07fgh ⫾ 0.03fgh ⫾ 0.02fg
Alcohol ⫹ 61.51 53.27 0.51 0.61 0.41 0.31
preheated oil ⫾ 5.39e ⫾ 2.17e ⫾ 0.03e ⫾ 0.02e ⫾ 0.02e ⫾ 0.00e
Alcohol ⫹ 127.80 109.96 1.14 0.99 0.77 0.48
preheated oil ⫾ 5.0h ⫾ 7.96h ⫾ 0.08h ⫾ 0.07h ⫾ 0.05h ⫾ 0.03h
⫹ cumin
1 Means ± S.D. from six test animals per treatment; values within a column with the same superscript letter
are not significantly different at P < 0.05 by Duncan’s Multiple Range Test.

of cumin along with the preheated oil, alcohol, and alcohol ⫹ preheated
oil kept the levels of GSH, vitamin C, and E near those of control ani-
mals, but were still reduced as compared with animals in the control
group.
The activities of SOD, GPx and catalase in the liver of animals re-
ceiving preheated oil, alcohol, and alcohol ⫹ preheated oil were de-
creased significantly when compared with control animals not treated
with oil or alcohol (Table 6). The activities of these enzymes in the oil
and alcohol treated animals increased significantly if cumin was admin-
istered at the same time.

DISCUSSION

Alcohol affects almost all organs of the body due to its water and fat
soluble properties that allow the ethanol to permeate all tissues. In our
 110 JOURNAL OF HERBS, SPICES & MEDICINAL PLANTS

TABLE 6. The effect of cumin on liver enzymes.

Treatment SOD1 GPx1 Catalase1

(U enzyme)2 (␮M glutathione)3 (␮M H2O2)4
Control 10.40 14.41 82.65
⫾ 0.65acfg ⫾ 0.71acfg ⫾ 5.25acfgh
Cumin 11.03 14.83 81.25
⫾ 0.52cfg ⫾ 0.89cf ⫾ 4.93cfgh
Alcohol 6.43 8.21 58.76
⫾ 0.05b ⫾ 0.49b ⫾ 4.20bd
Alcohol ⫹ cumin 9.56 13.59 78.17
⫾ 0.57gh ⫾ 0.87gh ⫾ 5.16gh
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Preheated oil 7.13 9.31 61.39

⫾ 0.61d ⫾ 0.62d ⫾ 4.12d
Preheated oil ⫹ cumin 10.21 14.07 80.62
⫾ 0.49fgh ⫾ 0.63fgh ⫾ 3.41fgh
Alcohol ⫹ preheated oil 5.31 5.21 43.27
⫾ 0.32e ⫾ 0.31e ⫾ 2.79e
Alcohol ⫹ preheated oil 9.25 12.99 75.13
⫹ cumin ⫾ 0.70 h ⫾ 0.69h ⫾ 6.23h
1 Means ± S.D. from six test animals per treatment; values within a column with the same superscript letter
are not significantly different at P < 0.05 by Duncan’s Multiple Range Test.
2 Units of enzyme required for 50% inhibition of NBT reduction/min/mg protein.
3 Glutathione utilized in µM ⫻ min⫺1 ⫻ mg⫺1 protein.
4 H O utilized in µM ⫻ min⫺1 ⫻ mg⫺1 protein.
2 2

study, the average weight gain by rats during experimental period was
significantly reduced by alcohol and by preheated sunflower oil fed rats
as compared with normal control rats not given alcohol or sunflower oil.
Rajakrishnan et al. (25) have also observed a decrease in weight gain in
rats treated with alcohol and such a decrease in the body weight could
be due to the toxic effects of ethanol (39). The animals fed alcohol and
treated with cumin, however, had weight gains similar to the controls,
showing the protective effect of cumin.
Damage to the liver after ethanol ingestion is a well-known phenom-
enon and hepatic injury from the alcohol is signaled by the leakage of
cellular enzymes into plasma (5). Our study indicated increased plasma
activity of GGT, AST, and ALP in rats given alcohol and preheated sun-
flower oil. Earlier reports have shown that exposure of hepatocytes to
ethanol perturbs the membrane structure and function thereby increasing
the leakage of AST (24). Ethanol also causes structural and functional
changes in the mitochondria and increases membrane permeability, lead-
ing to the leakage of mitochondrial enzymes into the circulation (6).
 Aruna et al. 111

Serum GGT is widely used as a laboratory test for the hepatobiliary dis-
eases especially of alcoholic liver disease and alcohol induced liver
damage (19).
Susceptibility to alcohol may be related to the consumption of differ-
ent types of dietary fat (20). Ethanol induction of CYP 4502E1 has been
observed to be related to the concentration of PUFA in the diet (2). The
increased activities of GGT, AST and ALP in test animals treated with
preheated oil and with alcohol ⫹ preheated oil may be due to increased
volatile and other toxic agents produced during thermal oxidation of oil.
Previous reports have shown increased activities of plasma AST and
ALP in rats fed thermally oxidized oil as compared with control rats
(10,31). Earlier studies in our laboratory also demonstrated increased ac-
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tivity of plasma AST and ALP in alcohol ⫹ preheated sunflower oil fed
rats (3). The observed decrease in the activity of hepatic marker enzymes
after cumin administration are consistent with cumin preserving struc-
tural integrity of the liver from the toxic effects of alcohol and heated oil.
Significantly increased levels of lipid peroxidation indices for
thiobarbituric acid reactive substances (TBARS), hydroperoxides, and
free fatty acids were noted in the liver and kidney of animals given alco-
hol as compared with control animals not given alcohol. The cyto-
chrome P450 2E1 containing microsomal ethanol oxidizing system is
strikingly inducible by chronic ethanol consumption, which results not
only in an increased production of acetaldehyde, but also in the genera-
tion of substantial amounts of superoxide, as well as hydroxy and other
free radicals (17). Our results also demonstrated increased levels of
TBARS, hydroperoxides and free fatty acids in animals treated with
preheated oil and the alcohol ⫹ preheated oil fed rats when compared
with normal control rats.
Susceptibility to lipid peroxidation is reported to be a function of
fatty acid unsaturation and increased intake of PUFA increases oxida-
tive tissue damage (15). Turpeinen et al. (37) have observed a small but
significant increase in TBARS and hydroperoxides in vitro after sun-
flower oil diet. Increased level of TBARS and hydroperoxides in the an-
imals fed preheated oil and alcohol ⫹ preheated oil in our study may be
due to increased susceptibility of the tissues to the combined effect of
toxic metabolites formed from the ethanol and preheated oil.
Increased levels of FFA in alcohol fed animals may be due to increased
formation of acetate, which in turn forms FFA. The increased NADH/
NAD⫹ ratio formed during ethanol metabolism also favors fatty acid syn-
thesis (30). The increased FFA in preheated sunflower oil and alcohol ⫹
preheated sunflower oil fed animals is most likely due to increased intake
 112 JOURNAL OF HERBS, SPICES & MEDICINAL PLANTS

of oil rich in PUFA that may eventually increase the level of FFA. The
significant reduction in the level of TBARS, hydroperoxides, and FFA
noted in animals having alcohol ⫹ preheated oil treated with cumin may
be due to cumin scavenging or neutralizing free radicals, interacting with
the oxidative cascade, quenching oxygen, inhibiting oxidative enzymes
like cytochrome P450, and/or chelating metal ions (such as Fe2⫹), inhib-
its the lipid peroxidation and thus reduces TBARS, hydroperoxides, and
free fatty acids. In this context, Mortinez-Tome et al.(18) have also
shown that cumin inhibits lipid peroxidation.
Our results also demonstrated decreased levels of the non-enzymatic
antioxidants (GSH and vitamins C and E) in the liver and kidney and de-
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creased activity of enzymatic antioxidants (SOD, GPx, and catalase) in

the liver of animals fed alcohol, preheated sunflower oil, or alcohol ⫹
preheated oil as compared with normal control rats. Induction of CYP
2E1 by ethanol results in enhanced acetaldehyde production which in
turn impairs defense system against oxidative stress (22). The antioxi-
dant status was found to be near normal when cumin was administered
along with alcohol and preheated oil. This may be due cumin strength-
ening the detoxification system in addition to the antioxidant properties
of the spice, enhancing the detoxification capacity by effectively scav-
enging oxygen radicals. The antioxidant activity of culinary herbs and
spices suggests that in addition to imparting flavor to food, they possess
potential health benefits by inhibiting lipid peroxidation (32).
We conclude that the antioxidant properties of cumin can reduce the
adverse effects produced by alcohol and preheated sunflower oil.

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