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Department of Clinical Nutrition, Sun Yat-sen University of Medical Sciences, Guangzhou, 510080, PR-China
2To whom correspondence should be addressed. E-mail: whling{at}gzsums.edu.cn.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • rice • atherosclerosis • antioxidative status • rabbits
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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,
Breslow 1997
). Major classic risk factors for
cardiovascular diseases include hyperlipidemia, elevated levels of LDL
cholesterol
(LDL-C),3
decreased HDL cholesterol (HDL-C) and smoking. A number of newer,
"nontraditional" cardiovascular risk factors in addition to the
classic risk factors have been identified on the basis of recent
studies of the pathogenesis of atherosclerosis and atherothrombotic
cardiovascular events. Oxidative stress plays a crucial role in the
initiation of atherosclerosis (Oparil and Oberman 1999
).
Reactive oxygen species (ROS) have been implicated in the pathogenesis
of atherosclerosis and hypertension (Liao et al.2000
, McCall and Frei 1999
). Recently, a number of studies indicated that LDL
undergo progressive oxidation, becoming oxidized-LDL (ox-LDL) when
oxidative stress increases in vivo. Several studies have indicated that
ox-LDL play a series of roles in atherosclerotic development by
promoting macrophage foam cell formation and inducing endothelial cell
damage and smooth muscle cell proliferation (Ross 1999
).
A number of studies have shown the importance of antioxidants,
including vitamin E and the antioxidant enzymes such as superoxide
dismutase (SOD), catalase and glutathione peroxidase (GSH-Px), in
protecting animals against the injuries due to oxidative stress, as
well as the effect of an enhanced level of antioxidants in ameliorating
the oxidant tissue injury (Hennekens et al. 1996
,
Stephens et al. 1996
). Elevated levels of ROS or
ox-LDL in vivo could be due to lowered concentrations of
antioxidants and activities of antioxidative enzymes.
The treatment of cardiovascular disease with rice diets was suggested
several decades ago. More than 50 years ago, it was reported that
consumption of white rice decreased blood pressure and lowered
hypercholesterolemia in humans (Genest 1986
,
Kempner 1946
). However, there are different types of
rice. The most common rice consumed by humans (>85%) is white rice;
the rest is colored rice, most of which is red and black rice. Red and
black rice are planted mainly in South Asian and other countries such
as Italy, Greece and the United States. Europeans eat more black rice
than South Asians (Simmons and Williams 1997
). Colored
rice has long been consumed in China and is considered to be a health
food, but there are no studies available concerning the effects of
consumption of red or black rice on atherosclerosis or cardiovascular
diseases.
An early study by our group showed that red rice consumption (30 g/100
g diet) in rats increased the concentration of plasma HDL-C and
activity of blood GSH-Px (Ma et al. 1999
). The
potentially beneficial effect of red and black rice consumption would
be to improve the lipid profile and protect against oxidative stress,
thus retarding atherosclerotic formation and development. The present
study was designed to investigate the influence of natural red or black
rice consumption on atherosclerotic plaque formation or development
induced by high cholesterol diet feeding in rabbits and to explore
possible mechanisms by which colored rice consumption decreases
atherosclerotic plaque formation.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Male New Zealand White rabbits (n = 36) aged 9 wk
and weighing 1.91 kg were obtained from the animal center of Guangzhou,
PR-China. Rabbits were housed individually in standard stainless
steel cages at 24°C with a 12-h light:dark cycle (lights on,
0630–1830 h). Rabbits had free access to food and tap water. All
experiments were performed in accordance with the protocol approved by
the standing committee on animals of Sun Yat-sen University of
Medical Sciences. Preceding the study, all rabbits consumed the same
diet (Harlan Teklad, Madison, WI) for 1 wk. Rabbits were divided into 5
groups and fed one of the following for 10 wk: normal laboratory rabbit
diet (normal group, n = 6); normal diet with high
cholesterol 0.5 g/100 g (HC group, n = 6); HC diet
with 30 g/100 g white rice powder (WR group, n = 8); HC diet with 30 g/100 g red rice powder (RR diet, n
= 8); HC diet with 30 g/100 g black rice powder (BR group,
n = 8). The concentrations of protein, carbohydrate
and fat as well as other constituents of the white, red and black rice
were determined by chemical analysis. The protein levels in the diets
with rice supplements were adjusted to the same level as the normal
diet (18 g/100 g) by adding casein to compensate the protein shortage
from rice powder. The different diets were adjusted to contain 10 g/100
g fat (Table 1
). The raw material of white and colored rice was husked in the same way
(unpolished) so that the rice used underwent the same minimal amount of
grinding. The rabbits were weighed every 2 wk during the experiment. At
the end of experiment, all rabbits were deprived of food overnight and
killed under ether anesthesia. Blood was collected by heart puncture.
Whole blood and serum were prepared for laboratory analysis. The major
organs and aorta of each rabbit were harvested, washed with
ice-cold isotonic saline and weighed. Serum and tissue samples were
stored at -20°C until used for analysis.
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After the rabbits were killed, aorta tissue between its origin and
bifurcation into the iliac arteries was taken gently, free of adhering
tissues. A small part of the arterial specimen at the end of
bifurcation without plaques was dissected and then rinsed with
ice-cold PBS for tissue malondialdehyde (MDA) measurement. The
large part of aorta between its origin and bifurcation into the iliac
arteries was opened longitudinally and prepared for plaque assay.
Atherosclerotic plaque areas were assessed by a previously described
method (Prasad and Kalra 1993
). Briefly, the aortic
strips were immersed in 10% buffered formalin solution for 24 h
and then rinsed in 70% alcohol. The tissue was then immersed in
Herxheimer’s solution containing Sudan IV (5 g), ethyl alcohol 70%
(500 mL) and acetone (500 mL) at room temperature for 15 min and washed
in running water for 1 h. Photographs of the intimal surface of
the aorta were taken and colored slides were made. The slide was
projected on a Caramate Projector Screen with a grid in mm2
and the total atherosclerotic areas of the intimal surface of the aorta
was measured in mm2. The extent of atherosclerosis was
expressed as a percentage of the luminal surface that was covered by
atherosclerotic plaques.
Serum lipid profile.
Serum cholesterol, triglyceride (TG) and HDL-C concentrations were
determined by enzymatic methods using a Hitachi Automatic Analyzer
(Tokyo, Japan) and the kits provided by the First Chemical and
Pharmaceutical Institute of Japan (Tokyo, Japan). Serum TG
concentrations were measured by hydrolyzing the triglycerides and
measuring the released glycerol (Bucolo and David 1973
).
Serum total cholesterol (TC) was determined by using a cholesterol
esterase and cholesterol oxidase assay (Allain et al. 1974
). Serum concentrations of HDL-C were measured by the
same method, as was serum TC after removing LDL-C and VLDL
cholesterol (VLDL-C) with magnesium dextran sulfate. Serum LDL
concentrations were calculated according to Friedewald formula
(Friedewald et al. 1972
), which assumes that circulating
VLDL consist of 80% triglycerides and 20% cholesterol. Apolipoprotein
(apo) B and apo AI were analyzed using commercially available kits
(French Bioerieux Sa, RCS Lyon, France), which use the turbidity
immunoassay method of Ikeda et al. (1991)
.
Preparation of tissue fractions for measurement of ROS and antioxidant enzyme activity.
The methods for preparation of tissue fractions and measurement of ROS
and antioxidant enzymes were as described previously (Prasad et al. 1992
). The tissues (liver or aorta) were removed, cleaned
of gross adventitial tissue, blotted dry and weighed. They were then
homogenized in 5–10 volumes of 50 mmol/L phosphate buffer (pH 7.4) at
4°C for 30 s using a polytron homogenizer. The homogenate was
filtered through cheese cloth and the filtrate was centrifuged at 1500
x g for 10 min. The resulting supernatants were
used for measurement of ROS, total antioxidant capacity (TAC) and
antioxidant enzymes.
Preparation of erythrocyte lysate.
Erythrocyte lysates were prepared by the method of Minami and Yoshikawa (1979)
. Briefly, blood was collected in tubes
containing EDTA and centrifuged (1500 x g) for 15 min at
4°C. The sediment containing the erythrocytes was suspended
in normal saline and recentrifuged. This process was repeated twice.
Sedimented RBC (0.2 mL/L) were added to 0.8 mL of ice-cold
distilled water and mixed thoroughly. This hemolysate was used for
estimation of GSH-Px and SOD activities.
ROS level in the liver.
The ROS in the liver supernatant were measured by using the fluorescent
probe 2',7'-dichlorodihydrofluorescin (DCFH) (Lebel et al. 1992
). Briefly, DCFH was prepared from 2',7'-dichlorofluorescin
(DCFH-DA) by mixing 1.0 mmol/L DCFH-DA (0.5 mL) in methanol with
NaOH (0.1mol/L, 2.0 mL). For assaying ROS formation, the reactions were
performed in 40 mmol/L Tris-HCl, pH 7.4, in a total volume of 0.4
mL that contained DCFH solution (100 µL). The
fluorescence was monitored by a Hitachi F3010 Fluorescence
Spectrophotometer with an excitation wavelength of 488 nm and an
emission wavelength of 525 nm. The results were expressed as the
relative fluorescence intensity (RFI).
TAC in serum and liver.
The TAC of serum and liver supernatants were measured using the ability
of endogenous antioxidants to scavenge the
2,2'-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) radical cation
(Severin et al. 1999
).
SOD and GSH-Px activities.
SOD activity in the liver supernatant or erythrocyte lysate was
measured as described by Oyanagui(1984)
. Briefly,
cytochrome c (10 µmol/L) reduction was measured after
30 s of incubation at 25°C with 50 µmol/L
xanthine and 2.5 µmol/L xanthine oxidase in 50 mmol/L
potassium phosphate buffer (pH7.8). Absorption at 550 nm was recorded
continuously on a Shimazu Multi-Purpose 5000 spectrophotometer
(Shimadzu, Kyoto, Japan). GSH-Px activity in liver supernatant was
measured using 5,5'-dithiobis (2-nitrobenzoate) as described
(Lawrence and Burk 1976
). Briefly, the assay mixture
consisted of 2.0 mL of 75 mmol/L phosphate buffer (pH 7.0), 50
µL of 60 mmol/L GSH, 0.1 mL of 3 x 104 U/L GSH reductase, 0.1 mL of 15 mmol/L
disodium salt of EDTA, 0.1 mL of 3 mmol/L NADPH, various amounts
(50–200 µL) of supernatant (200–500
µg protein) and 0.3 mL of water. The final volume of
the reaction mixture was 3.0 mL. The reaction was started by the
addition of 0.1 mL of 75 mmol/L H2O2.
Conversion of NADPH to NADP was monitored continuously at 340 nm for 4
min.
Determination of MDA.
Serum and aorta (lower part of the aorta without plaque) or liver
supernatants were analyzed for MDA by the thiobarbituric acid reaction
using HPLC with a C-18 column and UV-visible detector (Chen et al. 1998
).
Statistical analysis.
Results are expressed as means ± SD. The differences among the five groups were analyzed by one-way ANOVA. A Student-Newman-Keuls test was used to determine the significance of differences between any two groups. Differences of P < 0.05 were considered significant.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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50% less than that in rabbits fed the HC or white rice diets
(P < 0.05) (Fig. 1
). There were no significant difference in plaque areas of rabbits fed
the HC or WR diets.
|
). The circulating HDL-C and apo AI concentrations in rabbits fed
red or black rice were significantly higher than those in rabbits fed
white rice or HC diets (P < 0.05). The ratio of
LDL-/HDL-C was lower in rabbits fed colored rice than in rabbits fed
the white rice or HC diets.
|
). Although there were no differences in MDA of serum or liver among
rabbits fed HC or rice diets, MDA levels of aorta of rabbits fed the HC
and WR diets were significantly higher than in those fed colored rice
diets (Table 3)
. The liver TAC and erythrocyte SOD in the groups fed
red or black rice were significantly elevated compared with those of
rabbits fed HC or WR diets (P < 0.05) (Table 3)
. Blood
(data not shown) and liver GSH-Px also tended to be greater
(P < 0.07) in rabbits fed colored rice compared with
rabbits fed the HC and WR diets (Table 3)
.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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50% less in
rabbits fed red or black rice compared with those fed white rice or
high cholesterol diets. The basic diet did not differ among the three
rice groups except for the different type of rice supplemented. The
significant reduction in the atherosclerotic plaque from consumption of
colored rice vs. the HC and white rice diets indicated that red rice or
black rice can prevent atherosclerotic plaque formation and
progression. To our knowledge, this is the first finding of a
beneficial effect of red or black rice on prevention of
atherosclerosis.
HDL-C is considered to be "good" cholesterol in the circulation
(Stein and Stein 1999
). It carries the cholesterol or
cholesterol esters from peripheral tissues or cells to the liver where
cholesterol is metabolized into bile acids. This pathway plays a very
important role in reducing the cholesterol level in blood and
peripheral tissues, and in inhibiting the atheroslcerotic plaque
formation in the aorta. White rice consumption has been reported to
lower blood pressure and plasma lipids (Genest 1986
,
Kempner 1946
). In this study, white rice with 0.5%
cholesterol did not significantly affect the lipid profile compared
with rabbits fed 0.5% cholesterol only. However, colored rice
consumption significantly increased (55%, P < 0.05)
serum HDL cholesterol and apo AI concentrations compared with white
rice consumption. This phenomenon suggests that enhanced HDL-C and
apo AI concentrations contributed to the reduction in atherosclerotic
lesion areas of aorta in rabbits fed red or black rice diets compared
with those fed the white rice diet.
The beneficial effect of rice consumption was studied predominantly
from rice bran oil (RBO) or bran fiber. In this study, the
beneficial influence of colored rice appeared not to be due to the
fiber because the fiber content in the rice diets was less than that in
the HC or normal diets. RBO contains oleic, linoleic and linolenic
acids as unsaturated fatty acids, and palmitic and stearic acids as
saturated fatty acids. In addition, RBO contains unsaponifiable
materials including tocopherols, 
-oryzanol, phytosterols,
tocotrienols and squalene (Rukmini and Raghuram 1991
). A
number of studies in humans and animals revealed that RBO consumption
lowers serum total TG, TC and LDL-C, and increases plasma HDL-C
concentrations (Nicolosi et al. 1991
,
Purushothama et al. 1995
, Seetharamaiah and Chandrasekhara 1989
). RBO has hypocholesterolemic activity, and
the enhanced HDL concentration is characterized by a relatively high
content of non-fatty acid components. It was reported that
-oryzanol and tocotrienols of RBO participate in its
hypocholesterolemic effects (Purushothama et al. 1995
,
Sugano et al. 1999
). In this study, there were no
significant differences in serum TC or LDL-C or in apo B
concentrations among rabbits consuming different rice diets, in
agreement with previous reports (Marsono et al. 1993
,
Miyoshi et al. 1986
). Therefore, the
cholesterol-lowering effect of RBO induced by unsaturated fatty
acids or unsaponifiable materials appears to be a minor factor in the
lowering of atherosclerotic plaque formation in rabbits fed colored
rice. However, whether some components in rice bran such as
-oryzanol and tocotrienols are responsible for the enhancement of
serum HDL concentration requires further clarification.
Although a close relationship exists between high blood cholesterol
levels and atherosclerosis, it has been suggested that this
relationship might be dependent on enhanced oxidative stress
(Ohara et al. 1993
). Hypercholesterolemia increases the
levels of ROS in arterial endothelial cells. Elevated ROS can stimulate
the progression of atherosclerotic pathogenesis, in part by promoting
endothelial dysfunction, which is the earliest stage of
atherosclerosis, and damaging vascular smooth muscle cells (Hogg 1998
, Kunsch and Medford 1999
,Liao et
al.2000). To counteract the oxidants, an important endogenous
antioxidant system exists in vivo, which includes antioxidant compounds
such as vitamin E and antioxidant enzymes such as SOD, catalase,
glutathione peroxidase, glutathione reductase, glutathione transferase
and glucose-6-phosphate dehydrogenase (Thomas 1999
). It
has been reported that supplementation of antioxidant substances such
as vitamin E inhibits or retards the development of atherosclerosis in
animals (Jialal and Fuller 1995
, Steinbrecher 1997
). In addition, some minerals such as selenium and zinc may
play very important roles in antioxidation (Neve 1995
,
Oteiza et al. 1995
, Torra et al. 1997
).
ROS and MDA are the most commonly used markers of oxidation. In this
study, supplementation of red or black rice in rabbits significantly
lowered liver ROS and aortic MDA, indicating that colored rice
supplementation decreased oxidative stress in vivo. Simultaneously,
colored rice supplementation increased antioxidant capacity, including
enhanced serum and liver TAC and erythrocyte SOD activity. Because
consumption of red or black rice leads to improved antioxidation and
decreased peroxidation processes, damage from oxidative stress to
artery endothelial or smooth muscle cells will be reduced, with fewer
atheroslerotic plaques formed in the aorta. Although the present study
showed the beneficial effects of red or black rice consumption in
improvement of peroxidation and antioxidant processes in vivo, the
mechanisms involved have not been determined. The vitamin E
concentration in the rice diets was lower than that in the normal and
HC diets; thus, plasma vitamin E concentration may be not related to
the improvement of antioxidative status in rabbits fed colored rice.
But selenium, an antioxidant nutrient, was higher in the colored rice
diets than in the white rice or HC diet. This antioxidant nutrient
might be responsible in part for the enhancement of antioxidant status
in this study. The mechanism by which selenium enhanced the antioxidant
status has not been fully elucidated. Selenium is an integral part of
the antioxidant enzyme glutathione peroxidase (GSH-Px). In the present
study, there were no differences in GSH-Px activities in rabbits
consuming different diets with various concentrations of selenium. This
is in agreement with a previous study reported by Neve (1995)
in which selenium supplementation increased blood
selenium concentration; however, there were no significant differences
in either plasma or erythrocyte GSH-Px activity.
Because tocopherols and tocotrienols rich in RBO may improve the
oxidative state (Rukmini and Raghuram 1991
), these
compounds derived from colored rice may also have contributed to the
improved antioxidant status in rabbits. In addition, other constituents
of colored rice such as amino acids, nicotinic acid, riboflavin and
minerals may contribute in part to antioxidative improvements because
they were higher in colored rice than in white rice.
Alternatively, some special constituents with antioxidative properties such as flavonoids exist in red rice or black rice, but were not identified in the colored rice we used. These constituents may be responsible for the prevention of atherosclerotic plaque formation and improvement in lipid profile as well as antioxidative status. Further studies are required to elucidate the beneficial effect and to identify the constituents responsible for the positive health effect of colored rice consumption.
|
FOOTNOTES |
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3 Abbreviations used: apo, apolipoprotein; C, cholesterol; DCFH, 2',7'-dichlorodihydrofluorescin; DCFH-DA, 2',7'-dichlorofluorescin; GSH-Px, glutathione peroxidase; MDA, malondialdehyde; ox-LDL, oxidized LDL; RFI, relative fluoresence intensity; ROS, reactive oxygen species; SOD, superoxide dismutase; TAC, total antioxidative capacity; TG, triglyceride.
Manuscript received September 21, 2000. Initial review completed October 21, 2000. Revision accepted February 7, 2001.
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REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Allain C. C., Poon L. S., Chan C.S.G., Richmond W., Fu P. C. Enzymatic determination of total serum cholesterol. Clin. Chem. 1974;20:740-745
2.
Braunwald E. Shattuck lecture—cardiovascular medicine at the turn of the millennium: triumphs, concerns, and opportunities. N. Engl. J. Med. 1997;337:1360-1369
3. Breslow J. L. Cardiovascular disease burden increases, NIH funding decreases. Nat. Med. 1997;3:600-601[Medline]
4. Bucolo G., David H. Quantitative determination of serum triglycerides by the use of enzymes. Clin. Chem. 1973;19:476-482[Abstract]
5. Chen C. Y., Huang T., Lin H. Association between oxidative stress and cytokine production in nickel-treated rats. Arch. Biochem. Biophys. 1998;356:127-132[Medline]
6. Friedewald W. T., Levy R. I., Frederickson D. S. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of the preparative ultracentrifuge. Clin. Chem. 1972;18:499-502[Abstract]
7. Genest J. Nutritional management of hypertension: past, present, and future. Can. J. Physiol. Pharmacol. 1986;64:836-839[Medline]
8.
Hennekens C. H., Buring J. E., Manson J. E. Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N. Engl. J. Med. 1996;334:1145-1149
9. Hogg N. Free radicals in disease. Semin. Reprod. Endocrinol. 1998;16:241-248[Medline]
10. Ikeda T., Shibuya Y., Senba U., Sugiuchi H., Araki S., Uji Y., Okabe H. Automated immunoturbidimetric analysis of six serum apolipoproteins: correlation with radial immunodiffusion assays. J. Clin. Lab. Anal. 1991;5:90-95[Medline]
11. Jialal I., Fuller C. J. Effect of vitamin E, vitamin C and beta-carotene on LDL oxidation and atherosclerosis. Can. J. Cardiol. 1995;11(suppl.):97G-103G
12. Kempner W. Some effects of the rice diet treatment of kidney disease and hypertension. Bull. N.Y. Acad. Med. 1946;22:350-370
13.
Kunsch C., Medford R. M. Oxidative stress as a regulator of gene expression in the vasculature. Circ. Res. 1999;85:753-766
14. Lawrence R. A., Burk R. F. Glutathine peroxidase activity in selenium deficient rat liver. Biochem. Biophys. Res. Commun. 1976;71:952-956[Medline]
15. Lebel C. P., Ischiropoulos H., Bondy S. C. Evaluation of the probe 2',7'-dichlorofluorescin as an indicator of reactive oxygen species formation and oxidative stress. Chem. Res. Toxicol. 1992;5:227-231[Medline]
16.
Liao D. F., Jin Z. G., Baas A. S., Daum G., Gygi S. P., Aebersold R., Berk B. C. Purification and identification of secreted oxidative stress-induced factors from vascular smooth muscle cells. J. Biol. Chem. 2000;275:189-196
17. Ma J., Ling W. H., Ge H., Wang T. The effect of supplements of red rice on plasma lipid and antioxidative status in rats. Food Sci. (Chinese) 1999;20:54-55
18. Marsono Y., Illman R. J., Clarke J. M., Trimble R. P., Topping D. L. Plasma lipids and large bowel volatile fatty acids in pigs fed on white rice, brown rice and rice bran. Br. J. Nutr. 1993;70:503-513[Medline]
19. McCall M. R., Frei B. Can antioxidant vitamins materially reduce oxidative damage in humans?. Free Radic. Biol. Med. 1999;26:1034-1053[Medline]
20. Minami M., Yoshikawa H. A simplified assay method of superoxide dismutase activity for clinical use. Clin. Chim. Acta 1979;92:337-343[Medline]
21. Miyoshi H., Okuda T., Oi Y., Koish H. Effects of rice fiber on fecal weight, apparent digestibility of energy, nitrogen and fat, and degradation of neutral detergent fiber in young men. J. Nutr. Sci. Vitaminol. 1986;32:581-589
22. Neve J. Human selenium supplementation as assessed by changes in blood selenium concentration and glutathione peroxidase activity. J. Trace Elem. Med. Biol. 1995;9:65-73[Medline]
23. Nicolosi R. J., Ausman L. M., Hegsted D. M. Rice bran oil lowers serum total and low density lipoprotein cholesterol and apo B levels in nonhuman primates. Atherosclerosis 1991;88:133-142[Medline]
24. Ohara Y., Peterson T. E., Harrison D. G. Hypercholesterolemia increases endothelial superoxide anion production. J. Clin. Invest. 1993;91:2546-2551
25. Oparil S., Oberman A. Nontraditional cardiovascular risk factors. Am. J. Med. Sci. 1999;317:193-207[Medline]
26. Oteiza P. I., Olin K. L., Fraga C. G., Keen C. L. Zinc deficiency causes oxidative damage to proteins, lipids and DNA in rat testes. J. Nutr. 1995;125:823-829
27. Oyanagui Y. Reevaluation of assay methods and establishment of kit for superoxide dismutase activity. Anal. Biochem. 1984;142:290-296[Medline]
28. Prasad K., Kalra J. Oxygen free radicals and hypercholesterolemic atherosclerosis: effect of vitamin E. Am. Heart J. 1993;125:958-973[Medline]
29. Prasad K., Lee P., Mantha S. V., Kalra J., Prasad M., Gupta J. B. Detection of ischemia-reperfusion cardiac injury by cardiac muscle chemiluminescence. Mol. Cell. Biochem. 1992;115:49-58[Medline]
30. Purushothama S., Raina P. L., Hariharan K. Effect of long term feeding of rice bran oil upon lipids and lipoproteins in rats. Mol. Cell. Biochem. 1995;146:63-69[Medline]
31.
Ross R. Atherosclerosis—an inflammatory disease. N. Engl. J. Med. 1999;340:115-126
32. Rukmini C., Raghuram T. C. Nutritional and biochemical aspects of the hypolipidemic action of rice bran oil: a review. J. Am. Coll. Nutr. 1991;10:593-601[Abstract]
33. Seetharamaiah G. S., Chandrasekhara N. Studies on hypocholesterolemic activity of rice bran oil. Atherosclerosis 1989;78:219-223[Medline]
34. Severin E., Nave B., Stander M., Ott R., Traupe H. Total antioxidative capacity is normal in sera from psoriasis patients despite elevated bilirubin, tocopherol and urate levels. Dermatology 1999;198:336-339[Medline]
35. Simmons D., Williams R. Dietary practices among Europeans and different South Asian groups in coventry. Br. J. Nutr. 1997;78:5-14[Medline]
36. Stein O., Stein Y. Atheroprotective mechanisms of HDL. Atherosclerosis 1999;144:285-301[Medline]
37. Steinbrecher U. P. Dietary antioxidants and cardioprotection—fact or fallacy. Can. J. Physiol. Pharmacol. 1997;75:228-233[Medline]
38. Stephens N. G., Parson A., Schofield P. M., Kelly K., Cheeseman M. J., Mitchinson M. J. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study. Lancet 1996;347:781-786[Medline]
39. Sugano M., Koba K., Tsuji E. Health benefits of rice bran oil. Anticancer Res 1999;19:3651-3657[Medline]
40. Thomas J. A. Oxidative stress and oxidant defense. Shils M. E. Olson J. A. Shihe M. Ross A. C. eds. Modern Nutrition in Health and Disease 9th ed. 1999:751-760 Williams & Wilkins Baltimore, MD.
41. Torra M., Rodamilans M., Montero F., Corbella J. Serum selenium concentration of a healthy northwest Spanish population. Biol. Trace Elem. Res. 1997;58:127-133[Medline]
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