original papers - Advances in Clinical and Experimental Medicine

ORIGINAL PAPERS
Adv Clin Exp Med 2008, 17, 3, 293–305
ISSN 1230−025X
© Copyright by Silesian Piasts
University of Medicine in Wrocław
BOŻENA REGULSKA−ILOW1, RAFAŁ ILOW1, PRZEMYSŁAW KOWALSKI2
The Influence of Quercetin on Plasma Lipid Profile
of Laboratory Rats Fed Fresh and Oxidized Fats
Wpływ kwercetyny na profil lipidowy osocza szczurów
doświadczalnych na diecie z tłuszczem świeżym i utlenionym
1
2
Department of Food Science and Nutrition, Silesian Piasts University of Medicine in Wrocław, Poland
Department of Pathological Anatomy, Silesian Piasts University of Medicine in Wrocław, Poland
Abstract
Background. Lipids contained in the diet affect the composition of cell membranes in organs and organelles and
influence their permeability, which may condition the bioactivity of quercetin.
Objectives. The aim of the study was to evaluate the effect of quercetin on plasma lipid profile of experimental
rats under conditions of oxidative stress caused by oxidized dietary fats.
Material and Methods. Using rats fed a diet with an 8% fat content, the influence of quercetin on total lipid (TL),
triglyceride (TG), total cholesterol (TCH), HDL−cholesterol (HDL−CH), and phospholipid concentrations in the
plasma were assessed. The atherogenic index was calculated according to the formula (TCH – HDL−CH)/HDL−
CH. The source of pro−oxidants in the rats’ diet was either oxidized sunflower oil or oxidized lard. The four−week
experiment involved 80 male Buffalo rats, of which 40 received 0.075% quercetin as a supplement to their diet (60
quercetin per mg/kg of the rat’s body mass).
Results. Increased levels of TG were observed in the plasma of the rats fed a diet with quercetin and fresh oil
(141.4 ± 11.3 vs. 62.4 ± 17.4 mg/dl) and quercetin and oxidized oil (112.0 ± 12.1 vs. 55.8 ± 11.8 mg/dl) compared
with the respective controls. The mean plasma TL level increased from 2.5 ± 0.6 to 3.5 ± 0.3 g/l in the rats fed
quercetin and fresh oil compared with the control animals. Rats fed a diet with quercetin and fresh oil revealed
a decreased HDL cholesterol level (34.3 ± 6.3 vs. 27.1 ± 3.0 mg/dl), while the level increased in the rats fed a diet
including fresh lard and quercetin (27.4 ± 2.7 vs. 35.1 ± 3.8 mg/dl) compared with the groups on diets without
quercetin. Decreased plasma HDL cholesterol levels were observed in the rats fed oxidized fats and quercetin,
i.e. oil (38.1 ± 8.0 vs. 30.6 ± 3.7 mg/dl) or lard (33.2 ± 3.3 vs. 27.9 ± 3.1 mg/dl), compared with the groups on diets
without quercetin. Rats on a diet with oxidized oil had increased atherogenic index after quercetin addition
(1.12 ± 0.2 vs. 0.59 ± 0.3). Quercetin did not affect the plasma levels of TCH and phospholipids in either of the
investigated groups. Compared with those of controls, the livers of the animals fed a diet with quercetin and fresh
oil revealed accumulation of lipids, which was manifested by increased values of lipid metabolism parameters and
confirmed by histopathological evaluation of liver samples.
Conclusions. Under the experimental conditions, quercetin did not show any beneficial effect on plasma lipid pro−
file in animals fed diets with oxidized fats (oil and lard). The addition of quercetin to the diet resulted in a number
of unfavorable effects of oxidized fat consumption in the animals which were not observed in the rats fed diets
without quercetin (Adv Clin Exp Med 2008, 17, 3, 293–305).
Key words: rats, quercetin, oxidized fats, lipids profile, histopathology.
Streszczenie
Wprowadzenie. Tłuszcze zawarte w diecie, warunkując skład błon komórkowych narządów i organelli, wpływa−
ją na ich przepuszczalność, co może być czynnikiem, od którego zależy aktywność biologiczna kwercetyny.
Cel pracy. Ocena wpływu kwercetyny na profil lipidowy osocza szczurów doświadczalnych w warunkach stresu
oksydacyjnego wywołanego utlenionymi tłuszczami pokarmowymi.
Materiał i metody. Podawano szczurom diety z 8% zawartością tłuszczu i 0,5% dodatkiem cholesterolu i ocenia−
no wpływ kwercetyny na stężenie lipidów ogólnych (TL), triglicerydów (TG), cholesterolu całkowitego (TCH),
HDL−cholesterolu (HDL−CH) i fosfolipidów w osoczu. Źródłem prooksydantów w diecie szczurów były utlenio−
ne: olej słonecznikowy i smalec. Czterotygodniowe doświadczenie żywieniowe przeprowadzono z udziałem 80
294
B. REGULSKA−ILOW, R. ILOW, P. KOWALSKI
szczurów, samców, rasy Buffalo, których 40 otrzymywało 0,075% dodatek kwercetyny jako suplement diety (60
mg kwercetyny/kg masy ciała).
Wyniki. Obserwowano wzrost stężenia TG w osoczu szczurów na diecie z kwercetyną i olejem świeżym (141,4 ± 11,3
vs 62,4 ± 17,7 mg/dl) oraz kwercetyną i olejem utlenionym (112,0 ± 12,1 vs 55,8 ± 11,8 mg/dl) w stosunku do od−
powiedniej grupy kontrolnej. Wzrosło średnie stężenie TL, z 2,5 ± 0,6 do 3,5 ± 0,3 g/l, w osoczu szczurów na die−
cie z kwercetyną i świeżym olejem w porównaniu do grupy kontrolnej. W osoczu szczurów na diecie z kwercety−
ną i świeżym olejem nastąpił spadek stężenia frakcji HDL cholesterolu (34,3 ± 6,3 vs 27.1 ± 3.0 mg/dl), a w oso−
czu szczurów na diecie ze świeżym smalcem i kwercetyną wzrost stężenia frakcji HDL cholesterolu (27,4 ± 2,7 vs
35,1 ± 3,8 mg/dl) w stosunku do grup na diecie bez kwercetyny. Obserwowano obniżenie stężenia frakcji HDL
cholesterolu w osoczu szczurów karmionych utlenionymi tłuszczami i kwercetyną, olejem (38,1 ± 8,0 vs 30,6 ±
± 3,7 mg/dl) lub smalcem (33,2 ± 3,3 vs 27,9 ± 3,1) w stosunku do grup na diecie bez kwercetyny. Nastąpił wzrost
współczynnika aterogenności w grupie szczurów na diecie z utlenionym olejem (1,12 ± 0,2 vs 0,59 ± 0,3). Kwer−
cetyna nie wpływała na stężenia TCH i fosfolipidów w osoczu szczurów doświadczalnych w żadnej z badanych
grup. W wątrobach zwierząt na diecie z kwercetyną i świeżym olejem w porównaniu z grupą kontrolną obserwo−
wano kumulację lipidów wyrażoną wzrostem wartości wskaźników przemian lipidowych i potwierdzonych wyni−
kami badania histopatologicznego wycinków wątrobowych.
Wnioski. W warunkach doświadczenia kwercetyna nie wykazywała działania korzystnego na profil lipidowy
w osoczu zwierząt na diecie z utlenionymi tłuszczami (olejem i smalcem). Dodatek kwercetyny do diet spowodo−
wał wystąpienie u zwierząt niekorzystnych skutków spożywania tłuszczów utlenionych, których nie stwierdzono
u szczurów na diecie bez kwercetyny (Adv Clin Exp Med 2008, 17, 3, 293–305).
Słowa kluczowe: szczury, kwercetyna, profil lipidowy, histopatologia.
Quercetin is a commonly and abundantly con−
sumed flavonoid [1, 2]. Its daily intake is associated
with the alimentary habits of a given population and
ranges from several to several dozen milligrams per
day [3]. The main source of quercetin in Denmark,
Holland, and Japan is tea [1, 4, 5], in Finland,
Greece, and Yugoslavia onions and apples [3], in the
USA tea and citrus fruit [5], and in Italy and France
red wine [6]. Large amounts of this compound are
found in red wine, onion, chives, savoy cabbage,
cranberries, and apples [7, 8]. This dietary compo−
nent exerts a diversified biological effect, which has
been widely described in the literature [2, 8, 9]. It
reveals anti−oxidative properties and is a strong
“sweeper” of free radicals [10]. It also affects the
activity of many enzymes, e.g. cyclo− and lipoxyge−
nase, elongase, and desaturase, thus affecting fatty−
acid metabolism and leukotriene and prostaglandin
synthesis [11, 12]. An inverse correlation has been
observed between flavonoid intake and ischemic
heart disease and cancers [1, 3, 13].
Experimental studies suggest that plasma lipid
profile and the composition of fatty acids in the cell−
membrane phospholipids undergo modification
under the influence of diet and reflect their content
in consumed fats [14, 15]. An adequate level of
polyunsaturated fatty acids in the lipids of the cell
membrane conditions its fluidity, permeability, and
the transport of dietary components to the
cell’s cytosol [16, 17]. Fats subjected to oxidation
differ in the amount of fatty acids and polar fraction
content from their fresh counterparts. Results of
studies on the effect of oxidized fats on lipid metab−
olism are contradictory [18–20]. According to some
authors they are risk factors of ischemic heart dis−
ease due to their hypercholesterolemic and oxida−
tive stress−evoking activities [20, 21]. However,
other experiments did not confirm their atherogenic
effect [19, 22, 23]. According to some authors,
quercetin decreases the level of plasma lipid com−
ponents [24–26], while others maintain that
flavonoids exert a hypercholesterolemic effect [26].
The lack of studies on the effect of dietary
components that could modify the effect of
quercetin prompted the present experiment. It was
assumed that the factors that may affect the activ−
ity of querectin include the kind (plant or animal)
and quality (fresh or oxidized) of consumed fat.
The quality of oxidized fat in the diet, evaluated on
the basis of peroxide and anisidine indices and the
content of the polar fraction, corresponded to the
quality of frying oil in fast−food restaurants. The
content of quercetin corresponded to the amount
consumed in the human diet.
Material and Methods
Experimental Design
The study was carried out on eighty male
Buffalo rats with an initial mean body mass of 147 ±
± 28.3 g and a final body mass of 226.0 ± 28.4 g.
For the four weeks of the experiment the rats were
kept in appropriate conditions (room temperature,
12 hour light−dark rhythm). All the procedures for
the animal experiments were approved by the local
authorities. The animals were divided into eight
groups with 10 animals per group. Half of the rats
(n = 40) were given a diet with an 8% sunflower
oil content, while the other half (n = 40) were
given a diet with an 8% pork lard content. Within
these two supergroups receiving sunflower oil or
Influence of Quercetin on Lipid Profile of Rats Fed Fresh and Oxidized Fats
295
Table 1. Ingredients of the diets used in the experiments, containing 8% fat
Tabela 1. Skład diety doświadczalnej zawierającej 8% tłuszczu
Diet ingredients
(Składniki diety)
Amount in g/kg diet
(Zawartość w g/kg diety)
Casein
Fat (oil or lard)
Grain starch
Potato starch
Sucrose
Vitamin supplement (solid)
Vitamin supplement (liquid)
Mineral supplement
Vitamin E
Cholesterol
Distilled water
252
80
100
50
380.7
5
5*
50
0.3*
5
100*
Components of the mineral supplement:
(Skład mieszanki mineralnej:)
NaH2PO4 · 2 H2O
Mg SO4
NaCl
KCl
FeSO4 · 7 H2O
CuSO4 · 5 H2O
MnSO4 · 1 H2O
ZnCO3
Na2MoO4 · 2 H2O
KJO3
CaCO3
25.16
2.95
1.27
3.43
0.62
0.31
0.15
0.50
0.00648
0.0003
17.5
Components of the solid vitamin supplement:
(Skład mieszanki witaminowej stałej:)
inositol
p−aminobenzoic acid
Nicotinic acid (vitamin PP)
Riboflavin (vitamin B2)
Pyridoxal (vitamin B6)
Folic acid
D−calcium pantothenate
Thiamin (vitamin B1)
Vitamin K
Grain starch
amount in g/60 kg diet
(zawartość w g/60 kg diety)
6.60
6.60
6.60
1.32
1.32
0.12
4.08
1.32
0.60
complete to 300 g
Components of the liquid vitamin supplement:
(Skład mieszanki witaminowej płynnej:)
Vitamin A
Vitamin D3
Vitamin B12
Distilled water
amount in U/60 kg diet
(zawartość U/60 kg diety)
1 200 000
132 000
1.8 mg
complete to 300 cm3
* Amount in cm3.
* Zawartość w cm3.
lard, half (n = 20) had a diet with oxidized sun−
flower oil or lard and the other half with fresh fat.
Half of the rats (n = 10) eating a diet with fresh fat
and half of the rats eating a diet with oxidized fat
also had the bioflavonoid quercetin. The supple−
ment came to 0.75 g per kilo of diet (60 quercetin
per mg/kg rat body mass). The experiment was
performed using Quercetin dihydrate reagent
(Fluka, cat. no. 83370). The rats had unlimited
access to the fodder and to water. Their consump−
tion of fodder and water was checked every two
days and their body mass measured once per week.
The diet was prepared according to the method
described in [27] (Table 1).
Preparation of Oxidized Fat
for Use as an Ingredient
of the Diet
Two equal portions of pork lard and two of
refined sunflower oil were prepared. One portion of
each was kept fresh, while the other was subjected
296
B. REGULSKA−ILOW, R. ILOW, P. KOWALSKI
• TCH, HDL−CH, and TG levels using the
Biosystems enzymatic diagnostic tests TCH (cat.
no. 11539), HDL−CH (cat. no. 11523), and TG
(cat. no. 11529);
• phospholipid concentration by the enzy−
matic method using the bioMerieux Inc. diagnos−
tic test (cat. no. 61491);
• total lipid content by the enzymatic method
using the Lachema diagnostic tests (cat. no. 1135801);
• histopathology examination: for light
microscopy the liver samples were fixed in
buffered 10% formalin and embedded in paraffin.
All cytoplasmic vesicular lesions visible micro−
scopically in H−E (hematoxylin−eosin)−stained
liver slides were considered to be fat changes. The
intensity of fatty changes in hepatocytes was esti−
mated semi−quantitatively. To confirm the pres−
ence of fats, frozen liver samples were stained
with oil red and Sudan III;
• the percentage of fat droplet volume inside
hepatocytes was assessed in ten random high−
power views;
• the total number of fat−storing hepatocytes
was calculated as the percentage of total cells;
• the atherogenic index was calculated
according to the formula (CHC – HDL choles−
terol)/ HDL cholesterol [21].
to thermal oxidation. The oxidation process was
carried out by heating the fat under a quartz lamp
for 65 hours. A 2.5−cm−thick layer of fat was placed
in a porcelain dish, 21 × 29 cm. The quartz lamp
was 14 cm from the surface of the fat. The initial
temperature of the fat was 50ºC and its final temperature was no higher than 75ºC. The oxidation
conditions were established based on the report of
Ziemlański et al. [28]. In the fresh and oxidized fats,
the content of the polar fraction was determined and
the fatty acid component and the content of prima−
ry and secondary products of oxidation were mea−
sured as the peroxide and anisidine values (Table 2).
Preparation of the Biological
Material for Analysis
After completion of the feeding stage of the
experiment, the rats underwent light ether anesthe−
sia and blood was taken directly from their hearts
into test tubes containing heparin. After the rats
had been sacrificed, their livers were prepared.
The livers were rinsed in a physiological salt solu−
tion, blotted dry, and weighed.
Parameters Determined
from the Biological Material
The following parameters were determined
from analyses of the biological material:
Table 2. Changes in quality parameters of fresh and oxidized fats
Tabela 2. Zmiany wskaźników jakości tłuszczów świeżych i utlenionych
Kind of fat/Quality parameter
(Rodzaj tłuszczu/wskaźniki jakości)
Superoxide number:
(Liczba nadtlenkowa:)
meq O2/kg
mg O2/100g
Fresh lard
(Świeży smalec)
Oxidized lard
(Utleniony
smalec)
Fresh
sunflower oil
(Świeży olej
słonecznikowy)
Oxidized
sunflower oil
(Utleniony olej
słonecznikowy)
1.5 ± 0.0
0.05
169.3 ± 0.2
5.3
3.4 ± 0.0
0.11
666.7 ± 0.0
20.8
Anisidine number
(Liczba anizydynowa)
0.5 ± 0.2
39.1 ± 0.4
4.5 ± 0.0
68.8 ± 0.8
Polar fraction %
(Frakcja polarna) %
1.3
16.9
2.1
36.5
43.3
43.6
8.6
24.5
45.1
45.5
22.3
30.6
10.7
9.8
68.2
42.9
0.9
1.1
0.9
2.0
Fatty acid type: %
(Suma kwasów tłuszczowych: %)
saturated
(nasycone)
monounsaturated
(jednonienasycone)
polyunsaturated
(wielonienasycone)
unidentified
(niezidentyfikowane)
Influence of Quercetin on Lipid Profile of Rats Fed Fresh and Oxidized Fats
Statistical Assessment
of the Results
The normality of the distributions in the exam−
ined groups were assessed by Shapiro−
Wilk’s W test. In case of lack of a normal distrib−
ution, logarithmic transformation was applied. The
significance of the differences between the aver−
age values in the examined groups was assessed
using one−way analysis of variance (p < 0.05).
Data were tested for homogeneity of variances by
Levene’s test. To assess the influence of differ−
ences on the analysis of variance (the average
comparison post hoc), Tukey’s Honest Significant
Difference test (HSD) was applied. Cochrane−
−Cox’s test was used in case of a normal distribu−
tion of variables but lack of homogeneity of the
variance. The nonparametric Kruskal−Wallis test
was used for comparisons in case of lack of a nor−
mal distribution as well as a lack of homogeneity
of the variance of variables. All the statistical cal−
culations were done with the STATISTICA 6.0 PL
(StatSoft. Inc., USA).
Results
Fat Added to Fodder
The polar fraction content, oxidation parame−
ters, and fatty acid content in the fats added to the
rats’ fodder are presented in Table 2. The peroxide
index of the sunflower oil increased after oxida−
tion 196 times and that of lard 113 times.
Oxidation also increased the anisidine index,
which was 15 times higher in oil and 78 times
higher in lard. The oxidation conditions used in the
experiment resulted in a significant decomposition
of the polyunsaturated fatty acids in the sunflower
oil. Their content in the oxidized oil was 37%
lower. On the other hand, the content of monoun−
saturated acids in the oxidized oil increased by
37% and that of saturated fatty acids by 185%. The
composition of fatty acids in the oxidized lard
underwent a slight change in comparison to its
fresh counterpart. The polar fraction content in the
fats increased by factors of 13 in lard and 17 in oil
after oxidation.
The Effect of Quercetin
on Plasma Lipid Profile
In the rats which were given quercetin in their
diet, plasma TG levels increased statistically signifi−
cantly only when the dietary source of the fat includ−
ed fresh oil (141.4 ± 11.3 vs. 62.4 ± 17.4 mg/dl) or
oxidized oil (112.0 ± 12.1 vs. 55.8 ± 11.8 mg/dl).
297
The results are presented in Table 3. The addition
of quercetin resulted in a significant increase in the
total lipid level, from 2.5 ± 0.6 to 3.5 ± 0.3 g/l, in
the plasma of rats on a diet with fresh oil. No
changes in this parameter were observed in the
remaining groups compared with the controls. The
plasma levels of the HDL fraction revealed reverse
changes in the rats fed quercetin and fresh fats, oil
or lard, compared with the respective controls. The
plasma levels of HDL cholesterol in the rats given
fresh oil decreased (34.3 ± 6.3 vs. 27.1 ± 3.0
mg/dl) and in the rats fed fresh lard increased
(27.4 ± 2.7 vs. 35.1 ± 3.8 mg/dl). The addition of
quercetin produced similar changes, i.e. a decrease
in plasma HDL cholesterol levels in the rats fed
oxidized fats (oil: 38.1 ± 8.0 vs. 30.6 ± 3.7 mg/dl,
lard: 33.2 ± 3.3 vs. 27.9 ± 3.1 mg/dl). Quercetin
produced a significant increase in the atherogenic
index in the the group of rats fed oxidized oil
(1.12 ± 0.2 vs. 0.59 ± 0.3). The addition of
querectin did not have any effect on the plasma
levels of total cholesterol and phospholipids in
either of the experimental groups.
The Effect of the Kind
and Quality of Dietary Fat
on Plasma Lipid Profile
Oil vs. Lard
Compared with the control group fed oil
(Diet 1), the control group of rats fed lard (Diet 2)
revealed significantly higher levels of plasma lipid
components, such as triglycerides, total choles−
terol, and total lipids, which were, respectively,
2.25, 1.22, and 1.44 times higher. The atherogenic
index also increased by 93%. On the other hand,
HDL cholesterol level was significantly lower, by
20%. The findings are presented in Table 3. Rats
fed oxidized lard (Diet 6) had significantly higher
plasma triglycerides levels (2 times) and athero−
genic index (59%) than the rats fed oxidized oil
(Diet 5), while the phospholipid level was signifi−
cantly lower (23%).
Fresh vs. Oxidized Fat
Rats receiving a diet with oxidized oil (Diet 5)
demonstrated significantly lower total cholesterol
levels (1.32 times) and atherogenic index (56%)
than the control animals fed fresh oil (Diet 1). In
comparison with the control group given fresh lard
(Diet 2), rats fed oxidized lard (Diet 6) had signif−
icantly lower levels of lipid components, with the
exception of HDL cholesterol. The atherogenic
index was also significantly lower, by 64%. The
triglyceride, total cholesterol, and phospholipid
levels decreased, respectively, 1.25, 1.52, and
140.4 ± 20.7 b e
97.0 ± 9.2 b e
27.4 ± 2.7 a b e
1.3 ± 0.1 b
3.6 ± 0.5 e
2.59 ± 0.6 b e
62.4 ± 17.4 a e
79.2 ± 9.6 b e
34.3 ± 6.3 a e
1.2 ± 0.1
2.5 ± 0.6 a e
1.34 ± 0.3 b e
Triglycerides mg/dl
(Triglicerydy mg/dl)
Total cholesterol mg/dl
(Cholesterol całk. mg/dl)
HDL−cholesterol mg/dl
(HDL−cholesterol mg/dl)
1.60 ± 0.5
3.5 ± 0.3 a c
1.1 ± 0.1
27.1 ± 3.0 a
69.4 ± 9.8
141.4 ± 11.3 a c
Sunflower oil
+ quercetin
(Olej słoneczniko−
wy + kwercetyna)
diet 3
(dieta 3)
1.77 ± 0.3 c
4.1 ± 0.7 c
1.3 ± 0.1
35.1 ± 3.8 a c
96.6 ± 6.1 c
143.1 ± 14.9 c
Lard + quercetin
(Smalec +
kwercetyna)
diet 4
(dieta 4)
a – statystyczna różnica między 1 i 3 lub 2 i 4.
b – statystyczna różnica między 1 i 5 lub 2 i 6.
c – statystyczna różnica między 3 i 7 lub 4 i 8.
d – statystyczna różnica między 5 i 7 lub 6 i 8.
e – statystyczna różnica między 1 i 2 lub 5 i 6.
* wskaźnik aterogenności = (cholesterol całkowity – HDL−cholesterol)/HDL−cholesterol [21].
x ± SD – średnia ± odchylenie standardowe.
a – statistically significant difference between 1 and 3 and 2 and 4.
b – statistically significant difference between 1 and 5 and 2 and 6.
c – statistically significant difference between 3 and 7 and 4 and 8.
d – statistically significant difference between 5 and 7 and 6 and 8.
e – statistically significant difference between 1 and 2 and 5 and 6.
* atherogenic index = (total cholesterol – HDL cholesterol)/HDL cholesterol [21]
X ± SD – mean ± standard deviation
Atherogenic index*
(Aterogenny indeks*)
Total lipids g/l
(Lipidy całkowite g/l)
Phospholipids g/l
(Fosfolipidy g/l)
Control – lard
(Grupa kontrol−
na – smalec)
diet 2
(dieta 2)
Control
– sunflower oil
(Grupa kontrol−
na – olej sło−
necznikowy)
diet 1
(dieta 1)
Variable
(Zmienne)
X ± SD
Tabela 3. Wpływ różnych diet na profil lipidowy w surowicy szczurów doświadczalnych
Table 3. The influence of the type of diet on the lipid profile of the plasma of the laboratory rats
0.59 ± 0.3 b d e
3.0 ± 0.5
1.3 ± 0.1 e
38.1 ± 8.0
59.7 ± 10.2 b
55.8 ± 11.8 d e
Oxidized
sunflower oil
(Utleniony olej
słonecznikowy)
diet 5
(dieta 5)
0.94 ± 0.3 b e
3.1 ± 0.6
1.0 ± 0.2 b e
33.2 ± 3.3 b
64.0 ± 9.0 b
112.4 ± 29.4 b e
Oxidized – lard
(Utleniony
smalec)
diet 6
(dieta 6)
1.12 ± 0.2 d
2.7 ± 0.6 c
1.2 ± 0.1
30.6 ± 3.7
64.5 ± 8.3
112.0 ± 12.1 c d
Oxidized sunflower
oil + quercetin
(Utleniony olej
słonecznikowy
+ kwercetyna)
diet 7
(dieta 7)
0.99 ± 0.4 c
2.9 ± 0.2 c
1.1 ± 0.1
27.9 ± 3.1 c
54.8 ± 7.9 c
113.4 ± 17.1c
Oxidized lard
+ quercetin
(Utleniony smalec
+ kwercetyna)
diet 8
(dieta 8)
298
B. REGULSKA−ILOW, R. ILOW, P. KOWALSKI
68.0 ± 0.0 e
30.0± 6.2 eb
43.5 ± 16.2 e
40.0 ± 0.0 abe
5.0 ± 0.0 a e
1.0 ± 0.0 ae
Total lipids mg/g
(Lipidy całkowite)
52.5 ± 15.5 a
33.5 ± 7.8 a
63.0 ± 22.3
28.0 ± 6.7
67.0 ± 0.1
3.5 ± 0.5
12.3 ± 2.3
Lard + quercetin
(Smalec +
kwercetyna)
diet 4
(dieta 4)
a – statystyczna różnica między 1 i 3 lub 2 i 4.
b – statystyczna różnica między 1 i 5 lub 2 i 6.
c – statystyczna różnica między 3 i 7 lub 4 i 8.
d – statystyczna różnica między 5 i 7 lub 6 i 8.
e – statystyczna różnica między 1 i 2 lub 5 i 6.
* wskaźnik aterogenności = (cholesterol całkowity – HDL−cholesterol)/HDL−cholesterol [21].
x ± SD – średnia ± odchylenie standardowe.
a – statistically significant difference between 1 and 3 and 2 and 4.
b – statistically significant difference between 1 and 5 and 2 and 6.
c – statistically significant difference between 3 and 7 and 4 and 8.
d – statistically significant difference between 5 and 7 and 6 and 8.
e – statistically significant difference between 1 and 2 and 5 and 6.
* atherogenic index = (total cholesterol – HDL cholesterol)/HDL cholesterol [21]
X ± SD – mean ± standard deviation
Number of liver cells
accumulating fat %
(Liczba komórek wątroby
gromadząca tłuszcz)
Volume of liver cells
occupied by fat [%]
(Objętość komórki wątroby
zajęta przez tłuszcz)
3.6 ± 0.3 a
3.7 ± 0.5
1.7 ± 0.1 a
Total cholesterol
(Cholesterol całk.) mg/g
73.0 ± 0.0 a
18.9 ± 4.0 a c
9.6 ± 1.1 e b
4.1 ± 0.5 a e
Triglycerides mg/g
(Triglicerydy)
Sunflower oil
+ quercetin
(Olej słoneczniko−
wy + kwercetyna)
diet 3
(dieta 3)
Control – lard
(Grupa kontrol−
na – smalec)
diet 2
(dieta 2)
Control
– sunflower oil
(Grupa kontrol−
na – olej sło−
necznikowy)
diet 1
(dieta 1)
Variable
(Zmienne)
X ± SD
1.4 ± 1.3
3.8 ± 1.9
46.0 ± 0.0 d b
1.9 ± 0.2
3.9 ± 0.4 e
Oxidized
sunflower oil
(Utleniony olej
słonecznikowy)
diet 5
(dieta 5)
Tabela 4. Wpływ różnych diet na profil lipidowy w wątrobie i wyniki badań histopatologicznych wątrób szczurów doświadczalnych
8.7 ± 6.4
13.5 ± 5.8 b
68.0 ± 0.0 d
3.0 ± 0.3
15.3 ± 2.3 b e
Oxidized – lard
(Utleniony
smalec)
diet 6
(dieta 6)
Table 4. The influence of the type of diet on the lipid profile of the livers and histopathological examination of the livers of laboratory rats
1.4 ± 1.3
5.5 ± 1.6
50.0 ± 0.0 d
2.2 ± 0.2
5.5 ± 0.9 c
Oxidized sunflower
oil + quercetin
(Utleniony olej
słonecznikowy
+ kwercetyna)
diet 7
(dieta 7)
16.0 ± 5.2
18.0 ± 2.6
79.0 ± 0.0 d
3.7 ± 0.7
17.8 ± 2.7
Oxidized lard
+ quercetin
(Utleniony smalec
+ kwercetyna)
diet 8
(dieta 8)
Influence of Quercetin on Lipid Profile of Rats Fed Fresh and Oxidized Fats
299
300
B. REGULSKA−ILOW, R. ILOW, P. KOWALSKI
1.3 times, while the level of HDL cholesterol
increased significantly, 1.2 times.
extracts. Analysis of the histopathological prepa−
rations confirmed these observations.
The Effect of Quercetin
on Lipid Profile in the Livers
of the Experimental Animals
Histopathological Assessments
Compared with those of the control group
(Diet 1), the livers of the animals fed a diet with
quercetin and fresh oil (Diet 3) revealed an accu−
mulation of lipids in the form of a 4.6−fold
increase in triglyceride level, a 2.1−fold increase in
total cholesterol level, and a 1.8−fold increase in
total lipid level (Table 4). The histopathological
evaluation of the liver sections revealed a 6.7−fold
increase in the volume of the liver cells occupied
by fat and 52.5−fold increase in liver cells accu−
mulating fats (Table 4). Quercetin did not have any
effect on the accumulation of lipids in the livers of
the rats fed a diet with lard, as evaluated by the
levels of TG, TCH, and total lipids in the liver
Histopathological sections of the liver revealed
the presence of steatosis only in the form of fat
storage in the hepatocytes (Table 4, Fig. 1–8).
Changes associated with steatosis degenerativa
were not observed; there was no degradation of
cytoplasmic structures, lysis of cells in the steatot−
ic tissues, fibrosis around the steatotic cells, or the
formation of fat pseudocysts. The accumulation of
fat was mainly of the microvesicular type.
Depending on the size of the steatosis, small
droplets initially collected around the circumfer−
ence of the cell and then, as the steatosis pro−
gressed, the size of the droplets increased and they
began to occupy the area approximate to the nucle−
us, or even filled the entire cell. However, no
coarse−droplet steatosis was observed and there
were no single large drops forcing the nuclei to the
Fig. 1. Oil – control
Fig. 3. Oil + quercetin
Ryc. 1. Olej – badanie kontrolne
Ryc. 3. Olej + kwercetyna
Fig. 2. Lard – control
Fig. 4. Lard + quercetin
Ryc. 2. Smalec – badanie kontrolne
Ryc. 4. Smalec + kwercetyna
Influence of Quercetin on Lipid Profile of Rats Fed Fresh and Oxidized Fats
301
Fig. 5. Oxidized oil
Fig. 7. Oxidized oil + quercetin
Ryc. 5. Olej utleniony
Ryc. 7. Olej utleniony + kwercetyna
Fig. 6. Oxidized lard
Fig. 8. Oxidized lard + quercetin
Ryc. 6. Smalec utleniony
Ryc. 8. Smalec utleniony + kwercetyna
edges of the cells. Besides this, there were single
cases of very scant changes in the liver in the form
of minimal proliferations of the membranes of indi−
vidual bile canals and very scant fibrosis around
the blood vessels. Inflammatory infiltration was
also visible and widespread. In the majority of the
samples, this consisted of single or at most several
scattered cells of chronic inflammatory infiltration.
However, they were nonspecific and were found on
a few occasions to be more widespread in the con−
trol rats than in the rats of the other groups.
tract, but the products of their metabolism, i.e.
aldehydes and ketones, are easily absorbed from
the digestive tract and are toxic. It is worth noting
that in oxidized lard, the secondary products of
oxidation are prevalent in the total content of oxi−
dation products, i.e. in the polar fraction. The polar
fraction content in the oxidized oil, and also in the
oxidized lard, disqualified these fats from being
consumable, as their allowable level should not
exceed 24% [30]. The unfavorable effect of satu−
rated fatty acids on the lipid profile is well under−
stood and well documented in a number of studies
[31–34]. The reference information on the effect
of oxidized fat on the level of plasma lipid com−
ponents is contradictory. The results of our exper−
iment demonstrated that the oxidized fats, both oil
and lard, had a more beneficial effect on the plas−
ma lipid profile than their fresh counterparts. This
seemingly paradoxical effect may be explained by
the decreased assimilability of oxidatively altered
fats. Similar results were obtained by Lo and Lu
[19], but opposite results by Ziemlański et al. [28].
Discussion
The fat added to the diets, either sunflower oil
and lard, oxidized according to the procedure
described by Ziemlański [28], was characterized
by oxidation parameters which are observed in
fast−food restaurants after five days of frying [29].
Peroxides are hardly absorbed from the alimentary
302
B. REGULSKA−ILOW, R. ILOW, P. KOWALSKI
According to numerous reports [23, 24, 33],
quercetin exerts a beneficial effect on the lipid pro−
file. Studies performed by Hayek at al. [35], evalu−
ating the effect of flavonoids in mice with athero−
sclerotic changes, did not demonstrate any signifi−
cant improvement in the plasma content of lipid
fractions, but confirmed a decreased size of the ath−
erosclerotic plaque in the aorta. Reports on the
influence of flavonoids on the direction of plasma
lipid profile changes in rats on diets including fresh
fats demonstrate that their effect depends on the
dose and kinds of dietary bioflavonoids as well as
on the amount of dietary fat [26, 36, 37]. Zduńczyk
et al. [36] investigated the effect of bioflavonoids
from chokeberry, skullcap, broad bean, and tea on
lipid metabolism and confirmed that the range of
changes in the level of plasma lipids correlated
with the kinds of flavonoids in the diet.
Supplementation of diet with flavonoid extracts
from skullcap, anthocyanins from chokeberry, and
condensed tannin extracts from faba beans did not
decrease total cholesterol and its LDL fraction.
Skullcap extract, however, decreased triglyceride
and HDL cholesterol content.
The Effect of Quercetin
on Plasma Lipid Profile
The results of the present study confirmed that
quercetin affects lipid metabolism in the plasma of
experimental animals. In this experiment, lipid
metabolism was evaluated on the basis of the lev−
els of TG, HDL cholesterol, TCH, and TL as well
as the atherogenic index. Under the experimental
conditions, quercetin was shown to modify the
plasma lipid profile in rats at a rate depending on
the kind and amount of fat in the diet. The levels of
the above parameters of plasma lipid metabolism
in the rats fed a diet with fresh lard were statisti−
cally significantly higher, except for phospholipids,
than the same parameters in the rats fed fresh oil.
Quercetin added to a diet including oil and
lard affected the direction of changes in the lipid
metabolism, which depended on the kind of the
dietary fat. Quercetin exerted an unfavorable
effect on the plasma lipid profile in rats fed sun−
flower oil. The unfavorable effects were more pro−
nounced in the plasma of rats on fresh oil than in
those on oxidized oil. The unfavorable effect of
quercetin on plasma lipid profile in rats fed fresh
oil was manifested by a significant increase in the
total lipid level and in the level of their compo−
nent, i.e. triglycerides, as well as by a significant
decrease in HDL cholesterol level, which was not
accompanied by changes in the total cholesterol
level compared with the control group.
The consequences of the effect of quercetin on
total cholesterol and HDL cholesterol levels
included an insignificant increase in the athero−
genic index. Quercetin added to the diet including
sunflower oil (Diet 3) resulted in an increase in
triglyceride and total lipid levels to those observed
in the rats fed lard (Diet 2). The investigated para−
meters of the lipid profile in the plasma of rats in
both groups had similar magnitudes. Moreover,
similar levels of lipid metabolism parameters were
found in the plasma of rats fed oxidized lard (Diet
6) and oxidized oil with addition of quercetin (Diet
7). Quercetin elevated the investigated parameters
to the levels observed in rats fed a diet with oxi−
dized lard.
The most beneficial lipid profile was observed
in the plasma of rats fed a diet which included
fresh (Diet 1) or oxidized (Diet 5) oil. After the
addition of quercetin to the diet with oil, fresh or
oxidized, it appeared that quercetin unfavorably
modified the plasma lipid profile. The parameters
of lipid metabolism approached the values of the
parameters observed in fresh (Diet 2) and oxidized
(Diet 6) lard. The diet became more atherogenic.
A significant increase in the atherogenic index as
a consequence of the effect of quercetin on total
cholesterol and HDL cholesterol levels was
observed in the rats fed a diet with oxidized fat.
Moreover, the rats in this group revealed a signifi−
cant increase in the level of triglycerides.
Quercetin added to a diet including lard affect−
ed only one of the investigated parameters, i.e. the
plasma HDL cholesterol level. The directions of
changes in the HDL cholesterol level were opposite
in the plasma of rats fed fresh lard compared with
oxidized lard. Quercetin added to the fresh lard diet
caused an elevation of HDL cholesterol level
which was not accompanied by changes in the
level of total cholesterol compared with the con−
trols. This resulted in an insignificant decrease in
the atherogenic index in this group. The remaining
parameters of lipid metabolism remained unaffect−
ed by quercetin. In the group of rats fed a diet with
oxidized lard, quercetin lowered the HDL choles−
terol level and this was an unfavorable effect.
The quality of dietary lard and sunflower oil
had an effect on the atherogenic index. Its value
was lower in the groups of rats fed oxidized fats.
This seemingly paradoxical effect may be
explained by reduced assimilability of the ther−
mally altered fats. It seems that oxidized fats are
not used as a source of energy as intensively as
their fresh counterparts, probably due to the poly−
merization of fatty acids, which is more intense in
sunflower oil and less intense in lard.
The effect of fat on the organism was more ben−
eficial the lower the observed atherogenic index.
Influence of Quercetin on Lipid Profile of Rats Fed Fresh and Oxidized Fats
Consistent with expectations, the sunflower oil had
a more favorable effect on the lipid fractions in the
blood plasma; a lower atherogenic index was calcu−
lated in the rats fed fodder including oil.
The Effect of Quercetin
on Lipid Fraction Content
in Rats Fed Diets
with Oxidized Fats
The effect of flavonoids on lipid metabolism
in animals fed oxidized fats is poorly understood
and has not been frequently analyzed by other
authors [39]. The results obtained in the present
experiment showed that the effect of quercetin on
plasma lipid components depends on the kind of
oxidized fat. No differences in the composition of
the plasma lipid fraction between animals fed oxi−
dized lard (Diet 6) and oxidized lard and quercitin
(Diet 8) were demonstrated. However, an unfavor−
able, 100% higher triglyceride concentration and
a 90% higher atherogenic index were observed in
the group fed fodder containing oxidized oil and
quercetin (Diet 7) compared with rats fed oxidized
oil (Diet 5).
Flavonoids possess anti−atherosclerotic prop−
erties, mainly as a result of their protection of LDL
particles against oxidation. Accumulation of cho−
lesterol on the arterial wall precedes the formation
of foam cells formed from oxidized LDL [38].
Thus the presence of antioxidants in the diet
should have a favorable effect on the lipid profile;
however, the findings of the present study proved
otherwise. The cholagogic effect of quercetin
probably caused a higher absorption of fat, which
was observed only in those animals which were
fed fodder with oil. The plasma level of triglyc−
erides was increased, similarly to animals fed fod−
der containing fresh oil and the flavonoid.
Available data on the effect of quercetin on the
components of plasma lipids in the presence of
various toxic factors are contradictory. The effect
of flavonoids depends on the applied dose and the
kind of toxic factor. An experiment on rats [39] fed
303
oxidized oil and a 0.4% addition of grapefruit
extract, which investigated the effect of quercetin
on lipid metabolism in rats subjected to the pro−
longed effect of ammonium fluoride vapors,
demonstrated a decreased content of total choles−
terol and triglycerides as well as a hepatoprotec−
tive effect of the flavonoid. In this experiment, the
dose of quercetin was 89 and 22 times lower than
in the present experiment.
The authors concluded that under the experi−
mental conditions, querectin did not appear to
have a favorable effect on plasma lipid profile in
animals fed a diet with oxidized fat. The addition
of quercetin to the diet resulted in a number of
unfavorable effects of oxidized fat consumption in
the animals which was not observed in the rats
which were on diets without quercetin. Quercetin
probably enhanced the production of bile by the
liver, which facilitated the digestion of oxidized
fats and the absorption of toxic products of oxida−
tion from the polar fraction. Under the experimen−
tal conditions, unfavorable effects of quercetin on
the plasma lipid profile were observed. Their man−
ifestation included first of all an unfavorable
increase in the atherogenic index as well as
increased levels of certain lipid components of the
plasma. Quercetin revealed a positive effect (it
increased plasma HDL cholesterol level, while the
total cholesterol level remained unchanged) only
in the rats on a diet with fresh lard. In the remain−
ing groups of animals, this positive effect was
lacking. A more beneficial composition of the lipid
fraction was observed in the groups of rats on diets
with oxidized fats compared with those fed their
fresh counterparts. This probably resulted from the
fact that the oxidized food mass added to the fod−
der included the polar fraction, which is not
absorbable from the digestive systems of the
experimental animals. Comparison of the plasma
lipid profiles of animals fed fodder containing oxi−
dized fats and quercetin and of animals receiving
fresh fats and quercetin showed a beneficial reduc−
tion in the plasma lipid components, which result−
ed from the failure to absorb part of the oxidized
fat and not from the action of quercetin.
References
[1] Hertog MG, Freskens EJ, Hollman PC, Katan MB, Kromhout D: Dietary flavonoids and cancer risk in the
Zuphten Elderly Study. Nutr Cancer 1994, 22, 175–184.
[2] Peterson J, Dwyer J: Flavonoids: dietary occurrence and biochemical activity. Nutr Res 1998, 18, 1995–2018.
[3] Hertog MGL, Kromhout D, Aravanis C, Blackburn H, Buzina R, Fidanza F, Giampaoli S: Flavonoid intake
and long−term risk of coronary heart disease and cancer in the Seven Countries Study. Arch Intern Med 1995, 155,
381–386.
[4] Arai Y, Watanabe S, Kimira M, Shimoi K, Mochizuki R, Kinae N: Dietary intakes of flavonols, flavones and
izoflavones by Japanese women and the inverse correlation between quercetin intake and plasma LDL cholesterol
concentration. J Nutr 2000, 130, 2243–2250.
304
B. REGULSKA−ILOW, R. ILOW, P. KOWALSKI
[5] Chun OK, Chung SJ, Song WO: Estimated dietary flavonoid intake and major food sources of U.S. adults.
J Nutr 2007, 137, 1244–1252.
[6] Balestrieri ML, Schiano C, Felice F, Casamassimi A, Balestrieri A, Milone L, Servillo L, Napoli C: Effect of
low doses of red wine and pure resveratrol on circulating endothelial progenitor cells. J Biochem 2008, 143, 179–186.
[7] Aherne SA, O`Brien N: Dietary flavonoids: Chemistry, food content, and metabolism. Nutrition 2002, 18, 75–81.
[8] Erlund I: Review of the flavonoids quercetin, hesperetin, and naringenin. Dietary sources, bioactivities, bioavail−
ability, and epidemiology. Nutr Res 2004, 24, 851–874.
[9] Formica JV, Regelson W: Review of the biology of quercetin and related bioflavonoids. Food ChemToxic 1995,
33, 1061–1080.
[10] Lee SY, Munerol B, Pollard S, Youdim KA, Pannala AS, Kuhnle GG, Debnam ES, Rice−Evans C, Spencer JP:
The reaction of flavanols with nitrous acid protects against N−nitrosamine formation and leads to the formation of
nitroso derivatives which inhibit cancer cell growth. Free Rad Biol Med 2006, 40, 323–334.
[11] Jenkins KJ, Atwal AS: Flavonoids increase tissue essential fatty acids in vitamin E−deficient chicks. J Nutr
Biochem 1995, 6, 97–103.
[12] Ruiz−Gutierrez V, Muriana FJG: Effect of ingestion of thermally oxidized frying oil on desaturase activities and
fluidity in rat−liver microsomes. J Nutr Biochem 1992, 3, 75–79.
[13] Hertog MG, Feskens EJ, Hollman PC, Katan MB, Kromhout D: Dietary antioxidant flavonoids and risk of
coronary heart disease: the Zutphen Elderly Study. Lancet 1993, 342, 1007–1011.
[14] Barzanti V, Pregnolato P, Maranesi M, Bosi I, Baracca A, Solaini G, Turchetto E: Effect of dietary oils con−
taining graded amounts of 18:3 n−6 and 18:4 n−3 on cell plasma membranes. J Nutr Biochem 1995, 6, 21–26.
[15] Kotkat HM, Rady AA, Nemcsok J: Effect of dietary fish oil (active EPA−30) on liver phospholipids in young
and aged rats. Comp Biochem Physiol Part A Mol Integr Physiol 1999, 122, 283–289.
[16] Cohen LA, Rose DP, Wynder EL: A rationale for dietary intervention in postmenopausal breast cancer patients:
an update. Nutr Cancer 1993, 19, 1–10.
[17] Hayam I, Cogan U, Mokady S: Dietary oxidized oil enhances the activity of (Na+K+)ATPase and acetylo−
cholinesterase and lowers the fluidity of rat erythrocyte membrane. J Nutr Biochem 1993, 4, 563–586.
[18] Hochgraf E, Cogan U, Mokady S: Dietary oxidized linoleic acids enhances liver cholesterol biosynthesis and
secretion in rats. J Nutr Biochem 2000, 11, 176–180.
[19] Lu YF, Lo YCh: Effect of deep frying oil given with and without dietary cholesterol on lipid metabolism in rats.
Nutr Res 1995, 15, 1783–1792.
[20] Williams MJ, Sutherland WH, McCormick MP, de Jong SA, Walker RJ, Wilkins GT: Impaired endothelial
function following a meal rich in used cooking fat. J Am Coll Cardiol 1999, 33, 1050–1055.
[21] Ammu K, Raghunath MR, Sankar TV, Lalitha KV, Devadasan K: Repeated use of oil for frying fish. Effects
of feeding the fried fish to rats. Nahrung 2000, 5, 368–372.
[22] Eder K: The effects of a dietary oxidized oil on lipid metabolism in rats. Lipids 1999, 14, 717–724.
[23] Lee SH, Jeong TS, Park YB, Kwon YK, Choi MS, Bok SH: Hypocholesterolemic effect of hesperetin mediat−
ed by inhibition of 3−hydroxy−3 methylglutaryl coenzyme A reductase and acyl coenzyme A: cholesterol acyl−
transferase in rats fed high−cholesterol diet. Nutr Res 1999, 19, 1245–1258.
[24] Park SY, Bok SH, Jeon SM, Park YB, Lee SJ, Jeong TS, Choi MS et al.: Effects of rutin and tannic acids sup−
plements on cholesterol metabolism in rats. Nutr Res 2002, 22, 283–295.
[25] Czerny B, Put A, Myśliwiec Z, Juzyszyn Z: The influence of quercetin on some parameters of lipid metabolism
in rats chronically exposed to ammonium fluoride. Fluoride 2000, 33, 27–32.
[26] Fremont L, Gozzelino MT, Franchi MP, Linard A: Dietary flavonoids reduce lipid peroxidation in rats fed
polyunsaturated or monounsaturated fat diets. J Nutr 1998, 128, 1495–1502.
[27] Reeves PG, Nielsen FH, Fahey GC: AIN−93 purified diets for laboratory rodents: final report of the American
Institute of Nutrition ad hoc writing committee on the reformulation of the AIN−76A rodent diet. J Nutr 1993, 123,
1939–1951.
[28] Ziemlański Ś, Panczenko−Kresowska B, Budzyńska−Topolewska J, Żelazkiewicz K, Kołakowska A: Effect
of variously oxidized marine fish fat on guinea pig organism. Acta Aliment Polon 1992, 17/31, 159–169.
[29] Daniewski M, Pawlicka M, Filipek A, Jacórzyński B, Mielniczuk E, Balas J, Domina P: Assessment of qual−
ity control tests for frying fat of french fries. Pol J Human Nutr Metab 2001, 28, 132–139.
[30] Firestone D: Worldwide regulation of frying fats and oils. INFORM 1993, 4, 1366–1371.
[31] Roche H M: Unsaturated fatty acids. Proc Nutr Soc 1999, 58, 397–401.
[32] Salter M, Mangiapane EH, Bennet AJ, Bruce JS, Billett MA, Anderton KL, Marenah ChB, Lawson N,
White DA: The effect of different dietary fatty acids on lipoprotein metabolism: concentration−dependent effects
of diets enriched in oleic, myristic, palmitic and stearic acids. Br J Nutr 1998, 79, 195–202.
[33] Allan FJ, Thompson KG, James KAC, Manktelow BW, Koolaard JP, Johnson RN, McNutt PV: Serum
lipoprotein cholesterol and triglyceride concentrations in pigs fed diets containing fish oil, milkfat, olive oil and
coconut oil. Nutr Res 2001, 21, 785–795.
[34] Chi MS, Ray RL, Williams DC, Tuig MV, Galbreath K: Effects of dietary fat on blood pressure and plasma
lipids in spontaneously hypertensive rats. Nutr Res 1999, 19, 917–925.
[35] Hayek T, Fuhrman B, Vaya J, Rosenblat M, Belinky P, Coleman R, Elis A, Aviram M: Reduced progression
of atherosclerosis in apolipoprotein E−deficient mice following consumption of red wine, or its polyphenols
quercetin or catechin, is associated with reduced susceptibility of LDL to oxidation and aggregation. Arterioscler
Thromb Vasc Biol 1997, 17, 2744–2749.
Influence of Quercetin on Lipid Profile of Rats Fed Fresh and Oxidized Fats
305
[36] Zduńczyk Z, Freinagel S, Wróblewska M, Juśkiewicz J, Oszmiański J, Estrella I: Biological activity of
polyphenol extracts from different plant sources. Food Res Int 2002, 35, 183–186.
[37] Bok SH, Shin YW, Bae KH, Jeong TS, Kwon YK, Park YB, Choi MS: Effects of naringin and lovastatin on
plasma and hepatic lipids in high−fat and high−cholesterol fed rats. Nutr Res 2000, 20, 1007–1015.
[38] Meyer AS, Heinonen M, Frankel EN: Antioxidant interactions of catechin, cyanidin, caffeic acid, quercetin, and
ellagic acid on human LDL oxidation. Food Chem 1998, 61, 71–75.
[39] Juśkiewicz J, Zduńczyk J, Wróblewska M, Oszmiański J, Hernandez T: The response of rats to feeding with
diets containing grapefruit flavonoid extract. Food Res Int 2002, 35, 201–205.
Address for correspondence:
Bożena Regulska−Ilow
Department of Food Science and Nutrition
Silesian Piasts University of Medicine
pl. Nankiera 1
50−140 Wrocław
Poland
Tel.: +48 71 784 02 09
E−mail: [email protected]
Conflict of interest: None declared
Received: 11.01.2008
Revised: 6.03.2008
Accepted: 29.05.2008