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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 METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • rice • atherosclerosis • oxidative status • lipids • rabbits.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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). Few effective measures exist to prevent and treat the disease due to its pathological complexity. Research in the last two decades has shown that human atherosclerosis has many characteristics of an inflammatory disorder and does not result simply from the accumulation of lipids. The pathology of atherosclerosis comprises a complex interaction among lipids, the endothelium, circulating and tissue inflammatory cells, platelets and vascular smooth muscle cells (2
). Although hypercholesterolemia is important in 
50% of patients with cardiovascular disease, other factors such as increased oxidative stress and serum homocysteine must be considered (3
). Modification of these harmful components of inflammation in the arteries would be beneficial in creating new avenues for management of the disease in the 50% of patients who do not have hypercholesterolemia (4
).
Oxidative stress plays an important role in the initiation and progression of atherosclerosis (5
). Reactive oxygen species (ROS)3
are ubiquitous and occur naturally in all aerobic species, arising from both exogenous and endogenous sources. They are quite reactive and readily damage biological molecules, including DNA, protein, carbohydrate and lipids (6
). It has been reported that there are many oxidative stress indicators in tissues or blood such as 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), 4-hydroxynonenal (4-HNE) and lipid peroxides (LPO) (7
). Excessive production of ROS is implicated in the development of atherosclerosis or coronary heart disease (CHD) at different stages, including vascular endothelial cell damage, foam cell formation, vascular smooth muscle cell proliferation, gene expression, impaired vasomotor reactivity and plaque instability (8
,9
). Many in vitro and some in vivo studies have suggested that oxidative modification of LDL is involved in the onset of atherosclerosis and exacerbates its clinical manifestations (4
). Hence, the hypothesis was formulated that antioxidants may at least in part prevent atherosclerosis and cardiovascular disease. Dietary antioxidants, such as vitamins E and C have received considerable attention in this regard (10
).
As research progresses and epidemiologic and clinical trials of antioxidants are being reported, an apparent contradiction emerges, i.e., supplementation studies with individual antioxidants are yielding primarily negative results (11
). There are large population studies showing that natural foods rich in antioxidants are associated with a low incidence of cardiovascular diseases. For example, the Mediterranean and Japanese diets have shown these cardioprotective aspects (12
–14
). There is growing evidence that classic risk factors for CHD do not differ greatly in populations of southern Europe and Japan, compared with other Western countries (15
,16
). This suggests that other unexplored risk factors are favorably affected by these diets. Food composition studies have shown that both the Mediterranean and Japanese diets are rich in antioxidants derived from fruits, tea, red wine and olive oil and in (n-3) fatty acids, derived from fish, nuts and certain seed oils.
China is a country with a low incidence of atherosclerosis or CHD, which might be largely attributable to the Chinese diet. About 60% of the energy intake of the Chinese people is from carbohydrate, which is derived mainly from rice. The cardioprotective effect of rice diets was suggested several decades ago (17
,18
). There are different kinds of rice including white rice and colored rice. We recently found that supplementation of black rice, compared with white rice significantly reduced atherosclerotic plaque formation induced by hypercholesterolemia in rabbits, and the mechanism of this action was related to improvement of antioxidant status (19
). Most of antioxidants, complex carbohydrates and phytochemicals of rice including proteins, lipids, vitamins, minerals and flavonoids exist in the bran and germ. The endosperm contains primarily large amounts of starch. It is postulated that the beneficial effects of black rice in reducing atherosclerotic plaque formation may be due to the enriched nutrients and phytochemicals in the bran.
The present study was designed to investigate the influence of supplementation of the outer layer of black rice on atherosclerotic plaque formation induced by hypercholesterolemia in rabbits, and to explore the possible mechanisms by which this fraction inhibits atherosclerotic plaque formation.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Male New Zealand white rabbits (n = 32) aged 9 wk and weighing 2.16 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 for 1 wk. They were then divided into four groups and fed one of the following for 60 d: nonpurified rabbit diet (normal group, n = 8); normal diet with high cholesterol (0.5 g/100 g) and lard 3.5 g/100 g (HC group, n = 8); the HC diet with 5 g/100 g of the white rice out layer fraction (WRF group, n = 8); the HC diet with 5 g/100 g of the black rice outer layer fraction (BRF group, n = 8). The raw material of white and black rice was husked, and the outer layer fractions (bran) of white and black rice (10% of whole grain) were further ground. The compositions of the rice outer layer fraction and experimental diets were analyzed chemically (Table 1
). The protein and energy in the different diets were adjusted to the same levels by adding casein and cornstarch (Table 2
). The rabbits were weighed every week. At the end of experiment, all rabbits were deprived of food overnight and killed under diethyl ether anesthesia. Blood was collected, and 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. The serum samples were stored at -80°C, and aorta samples were stored in liquid nitrogen until analyzed.
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Protein was determined by the classic Kjeldahl nitrogen analysis, and fat was assayed by Soxhlet extraction. The carbohydrate, crude fiber, moisture and ash contents were measured according to Osborne and Voogt (20
); iron, zinc, and selenium were assayed using an atomic absorption spectrophotometer (SpectrAA40, Varian, Mulgrave, Victoria, Australia). Thiamin was determined on a fluorospectrophotometer (Hitachi F3010, Tokyo, Japan); vitamin E was measured by using a HPLC system (Bio-Rad Model 1706, Hercules, CA); the flavonoids were analyzed by using UV-spectrophotometer (Shimadzu Multi-Purpose 5000 spectrophotometer, Kyoto, Japan) (20
).
Processing of aorta fragments.
Immediately after the aorta fragment was taken between its origin and bifurcation into the iliac arteries, it was washed with ice-cold sterile physiologic saline to remove debris and blood residues. The proximal ascending aortic arch was dissected from each rabbit and divided into three 3-mm cross sections. The three sections were immersion-fixed in 4% formaldehyde solution for 24 h for morphological analyses. The remaining aorta was opened longitudinally and its adventitial coat was removed, and the tunica media and tunica intima were stored in liquid nitrogen for biochemical analyses.
Assessment of atherosclerotic plaques.
The excised samples were embedded in paraffin and sliced 4 µm thick. Hematoxylin, eosin and elastica-van Gomori staining were performed. The cross sections with elastica-van Gomori staining were recorded by a three-chip CCD video camera (JVCky-F 30B, Tokyo, Japan). The area within the internal elastic lamina (IEL, as the indicator of artery size) and lumen area (as the area for blood flow) were measured in the three sections using a digital image analyzer (Kontron IBAS2.5, Eching, Germany). The plaque size was calculated with the following formula: [(IEL - lumen area)/IEL] x 100. The arithmetic mean was calculated and used for further statistical analyses of the plaque size in the proximal ascending aortic arch (21
,22
).
Serum lipid profile.
Serum triglyceride (TG), total cholesterol (TC), LDL cholesterol (LDL-C), HDL-C, apoprotein (apo)AI and apoB were measured using a Hitachi Automatic Analyzer (Tokyo, Japan). Serum TG concentrations were assayed by hydrolyzing the triglycerides and measuring the released glycerol (23
). Serum TC was determined by using a cholesterol esterase and cholesterol oxidase assay (24
). Serum concentrations of HDL-C were assayed by the same method, as was serum TC after the removal of LDL-C and VLDL-C with magnesium dextran sulfate. Serum LDL concentrations were calculated according to the Friedwald formula (25
), which assumes that circulating VLDL consist of 80% triglycerides and 20% cholesterol. ApoAI and apoB were determined by the turbidity immunoassay method (26
).
Fatty acids level in serum.
The levels of serum fatty acids were determined by capillary gas phase chromatography after extraction by methanol and phenol (4:1, v/v) and transesterification directly in a one-step reaction (27
). The relative amount of each fatty acid (g/100 g) was quantified. Serum saturated fatty acids (SFA), monounsaturated fatty acids (MUFA), and polyunsaturated fatty acids (PUFA) were calculated by summing the four SFA acids, three MUFA and ten PUFA measured, respectively. The PUFA/SFA ratio (P:S) and (n-3) PUFA were also calculated.
8-OHdG level in aorta.
Aortic segments were homogenized in a Polytron apparatus (Glas-Col Homogenizer, Jet-Pak, Terre Haute, IN) in 250 mmol/L sucrose and 50 mmol/L Tris HCl (pH7.4, ice-cold). A 50 g/L homogenate was centrifuged at 1500 x g for 15 min; the resulting supernatants were used for measurement of MDA and superoxide dismutase (SOD). The pellet containing nuclei was dispersed in 8 volumes of 10 mmol/L Tris-HCl, 0.1mol/L EDTA, 20 mg/L RNase, 0.5%SDS (pH 8.0), incubated for 1 h at 37°C and then lysed at 37°C for 8 h in the presence of 100 mg/L proteinase K. The suspension was extracted twice with phenol/water/chloroform and twice with chloroform alone. DNA was precipitated from the aqueous phase with 2 volumes of anhydrous alcohol and 0.2 volume sodium caproate. Collected DNA was further washed with ice-cold 70% ethanol.
DNA was suspended in 200 µL of 20 mmol/L sodium acetate buffer (pH4.8) and digested with 20 µg nuclease P1 at 37°C for 30 min. The solution was neutralized with 20 µL of 1.0 mol/L Tris-HCl, pH7.4, before the addition of 1.3 U Escherichia coli alkaline phosphatase. The reaction was incubated at 37°C for 1 h, after which the digest was passed through a 30,000 MWCO filter (Millipore, Bedford, PA) (28
).
Analysis of DNA hydrolysates was performed with a Bio-Rad (Hercules, CA) model 700 HPLC system. An aliquot was injected onto a Supelcosil LC-18-DB deactivated reversed-phase column (4 mm x 30 cm, 10-µm particle size; Millipore) with a 2-cm guard cell. Nucleosides were separated using a mobile phase consisting of 12.5 mmol/L citric acid, 25 mmol/L sodium acetate, 30 mmol/L NaOH and 10 mmol/L acetic acid, pH 5.1, at a flow rate of 1 mL/min. Detection of 8-OHdG was performed using a model 1049A electrochemical detector (Hewlett-Packard, Waldronn, Germany) with the applied potential set to 0.6 V. UV detection of 2-deoxyguanosine was performed using a model 1706 UV detector (Bio-Rad) with UV absorption at 254 nm (29
).
Determination of MDA.
MDA in the serum and aorta supernatants was measured by the thiobarbituric acid reaction using HPLC with a C18 column and UV-visible detector (30
); tetraethoxypropane was used as standard.
Vitamin E level in serum.
The vitamin E in the serum was determined by HPLC analysis using benzo(a)pyrene as the standard after extraction with ethanol (100 µL) and n-hexane (0.7 mL) as described elsewhere (31
). The column used was a Spherisorb C18 column (4.6mm x 10cm, 3-µm particle size; Millipore) protected by a 2-cm guard column. The absorption of 
-tocopherol is affected by serum lipid, and carried in serum lipoproteins; thus, -tocopherol analysis should take account of serum lipid concentrations. Serum level of -tocopherol was expressed relative to serum total cholesterol and triglyceride contents as its lipid-normalized concentrations (32
,33
).
SOD activity.
Erythrocyte and aorta supernatants were analyzed for SOD activity by using the xanthine oxidase method (34
). 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 (pH 7.8). Absorption at 550 nm was recorded continuously on a Shimazu Multi-Purpose 5000 spectrophotometer (Shimadzu).
Statistical analysis.
Results are expressed as means ± SD, and the differences were determined by one-way ANOVA coupled with the Student-Newman-Keuls multiple comparison test. Differences with P < 0.05 were considered significant.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The rabbits fed the different diets did not differ in body weight throughout the experiment (data not shown).
Atherosclerotic plaque formation.
There were no visible atherosclerotic plaques in aortae of rabbits fed the normal diet, but atherosclerotic plaques of various degrees were visible in aortae of rabbits fed the HC, WRF and BRF diets. Plaque formation was much more severe in rabbits fed the HC or WRF diets than in those fed the BRF diet. Typical atherosclerotic plaques of aortae of rabbits fed HC, WRF or BRF diets showed injury to endothelial cells, infiltration of inflamed cells, assembling foam cells, cellular necrosis and proliferation of fibroblasts and smooth muscle cells (Fig. 1
). The plaque area in rabbits fed the BRF diet was lower than in the HC- (66%) or WRF- (75%) fed rabbits (P < 0.001) which did not differ from one another (Fig. 2
and 3).
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Serum TG, TC, LDL-C/HDL-C and apoAI/apoB in rabbits fed the normal diet differed from other groups (P < 0.05). However, there were no differences in serum lipids among the groups fed the HC, WRF and BRF diets (data not shown). Similarly, serum total SFA, MUFA, PUFA, (n-3) fatty acids and the P/S ratio in rabbits fed the normal diet were lower than those in rabbits fed the WRF and BRF diets (P < 0.05), but they did not differ among the HC, WRF and BRF groups (Table 3
). The serum concentration of most individual fatty acids except 18:1 did not differ between the WRF and BRF dietary groups.
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Although HC, WRF and BRF diets lowered the SOD activity of erythrocytes and aorta, and the level of serum -tocophecol compared with the normal diet in rabbits (P < 0.05) (Table 4
), there were no differences in these variables among the groups fed the three diets.
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. There were no differences in the 8-OHdG levels of aorta between the rabbits fed the HC and WRF diets or between the rabbits fed the normal and BRF diets.
The BRF diet significantly (P < 0.05) decreased the MDA levels of serum (-37%) and aorta (-50%) compared with the WRF diet (Table 4)
. MDA levels in serum and aorta in the groups fed the BRF diet were still higher than those of rabbits fed the normal diet. The levels of 8-OHdG and MDA in aorta were significantly correlated with the atherosclerotic plaque area (r = 0.719 and 0.605, P < 0.01), respectively.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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).We speculated that inhibition of atheroslerotic plaque formation by BRF might be mediated by its improvement of antioxidation status, lipid metabolism and the anti-inflammation response.
Currently, MDA and 8-OHdG are among the most valuable makers of lipid peroxidation and DNA oxidative products, respectively (7
). In the present study, the BRF diet decreased aortic 8-OHdG and serum and aortic MDA significantly (Table 4)
. This indicated that supplementation of the black rice outer layer fraction decreased oxidative stress. Because oxidative stress plays a large role in the development of atherosclerosis, the decreased peroxidation processes and DNA oxidative damage by supplementation of the BRF reduced the damage of oxidative stress to artery endothelial or smooth muscle cells, contributing to the inhibition of atheroslerotic plaque formation in aorta.
Consumption of fruits and vegetables, olive oil, red wine and tea is inversely correlated with the rates of heart disease (8
). These foods are particularly rich in natural antioxidants, including ascorbate (vitamin C), the tocopherols (vitamin E) and carotenoids. A sufficient supply of dietary antioxidants might help prevent or delay the occurrence of pathological changes associated with oxidative stress. To explore the mechanism by which supplementation of BRF decreased the aortic oxidative stress, vitamin E concentration of serum was measured because it is considered to be a potent antioxidant compound in vivo and in vitro and may improve oxidative stability (35
). In this study, the serum vitamin E concentration did not differ between the BRF and WRF groups, indicating that it might not be the primary antioxidant contributing to the lowering of oxidative status in aortic tissue by the BRF diet.
In the present study, antioxidant status in blood was not improved as efficiently as aortic tissue in rabbits fed BRF diet because blood and erythrocyte SOD activities did not differ among the HC, WRF and BRF groups. A number of studies have shown that oxidative stress is increased by high blood lipid levels (36
). The elevated oxidative capacity induced by high blood lipids might be too strong to be reduced, and antioxidant status in the circulatory system is improved little by supplementation of BRF. This may explain in part why serum SOD was not significantly improved in rabbits fed the BRF compared with rabbits fed the WRF diets. There is increasing evidence indicating that oxidized LDL play an important role in the development of atherosclerosis. The oxidation of LDL is thought to take place in the arterial intima when the particles have become isolated from circulating water-soluble antioxidants (37
). The facts that the BRF diet lowered atherosclerotic plaque and decreased aortic MDA levels suggest that the antioxidants in this diet act efficiently in the artery intima, thereby inhibiting athersclerotic formation.
Epidemiologic studies have shown dietary flavonoid intake to be inversely associated with mortality from CHD (38
). Flavonoids are potent antioxidants and can protect against the oxidation of LDL, a process implicated in atherogenesis. Flavonoids also show antilipoperoxidant and anti-inflammation properties (39
). Because the amount of flavonoids in the black rice outer layer fraction was 5.4 times as much as that of white rice outer layer fraction (Table 1)
, the antiatherogenic effect of the BRF diet in rabbits might be related to the antioxidative properties of flavonoid-like compounds.
Several studies have suggested that some elements such as zinc and selenium may in part be antiatherogenic by inhibiting oxidative stress-responsive events in endothelial cell dysfunction (40
–42
). The BRF diet contained higher levels of zinc than did the WRF diet, which might also contribute to inhibition of atherosclerosis formation in rabbits fed BRF. In addition, other levels of constituents such as riboflavin and minerals are higher in the BRF than in the WRF diet, which may contribute in part to oxidative improvement.
Epidemiologic studies have shown that the level of dietary fat intake is positively correlated with the average serum cholesterol value and mortality from CHD (43
). A number of different investigators have demonstrated that in addition to total fat, the fatty acid composition of diets influences serum TC in humans. In general, SFA elevate serum cholesterol concentration, and unsaturated fatty acids decrease it. Rice bran oil (RBO) is composed mainly of unsaturated fatty acids, including oleic, linoleic and linolenic acids. In addition, RBO contains unsaponifiable materials including tocopherols, 
-oryzanol, phytosterols, tocotrienols and squalene (34
). The beneficial effects of rice consumption were reported to derive from the RBO or bran fiber. In the present study, the beneficial influence of the rice outer layer fraction appeared not to be due to the fiber because the fiber content of the two rice diets was virtually the same. A number of studies in humans and animals have revealed that RBO consumption lowered serum total TG, TC and LDL-C, and increased plasma HDL-C concentrations (44
–46
). In the present study, serum lipids and apo B concentrations did not differ among the HC, WRF and BRF groups. Also the serum concentration of most fatty acids except 18:1 did not differ between the WRF and BRF groups. Therefore, RBO did not appear to be responsible for lowering atherosclerotic plaque formation in rabbits fed the BRF diet.
The atherogenic process is largely a fibroproliferative inflammatory response involving macrophages and T lymphocytes, which are present in the arterial intima at all stages in the development of atherosclerotic lesions. It has been reported that flavonoids and anthocyanidin or anthocyanin have anti-inflammatory properties. A series of studies (47
–49
) found that flavonoid derivatives possess anti-inflammatory activity in vitro and in vivo. Flavonoid derivatives including prenylated compounds such as morusin, kuwanon C and sanggenon D and biflavonoids such as bilobetin and ginkgetin inhibited nitric oxide (NO) production from lipopolysaccharide (LPS). Inhibition of NO production was mediated by suppression of inducible nitric oxide synthase (iNOS), but not by direct inhibition of iNOS enzyme activity. Because NO produced by iNOS plays an important role in inflammatory disorders, inhibition of NO production by these flavonoids may contribute at least in part to their anti-inflammatory and immunoregulating potentials in vivo. In addition to antioxidation, flavonoid- and anthocyanidin-like compounds in the BRF diet may be antiatherogenic through their anti-inflammatory action, and thereby inhibit the development of atherosclerotic plaques.
Prostaglandins (PG) are present in a wide variety of tissues and play a central role in inflammation. It has been reported that PGE2 contributes to the pathogenesis of cardiovascular disease through proinflammatory activities. The inflammatory PG is converted from arachidonic acid in membrane phospholipids through the function of the enzyme cyclooxygenase (COX). At least two forms of the enzyme COX exist, a constitutive (COX-1) form and an inducible (COX-2) form. COX-1 is mainly responsible for the biosynthesis of PG involved in homeostatic regulation, whereas the second isoform, COX-2, is primarily involved in producing PG in response to a wide spectrum of environmental insults and internal stimuli. COX-2 may participate in the initiation and pathogenesis of atherosclerosis via a rapid and excessive production of prostanoids, which has a proatherosclerotic effect (50
). Certain flavonoids are potent inhibitors of PG production and COX-2 expression in a concentration-dependent manner (48
,51
). Inhibition of COX-2 expression by flavonoids may be one of the mechanisms responsible for their anti-inflammatory effect (48
). In the present study, inhibition of COX-2 expression and PG production or release by the higher flavonoid contents in the BRF diet could be another mechanism by which it inhibited atherosclerotic plaque formation in rabbits. However, the anti-inflammatory action and antiatherogenic properties of the BRF diet warrant further elucidation.
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FOOTNOTES |
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3 Abbreviations used: apo, apoprotein; BRF, black rice outer layer fraction; CHD, coronary heart disease; COX, cyclooxygenase; HC, high cholesterol diet; HDL-C, HDL cholesterol; 4-HNE, hydroxynonenal; IEL, internal elastic lamina; iNOS, inducible nitric oxide synthase; LDL-C, LDL cholesterol; LPO, lipid peroxides; LPS, lipopolysaccharide; MDA, malondialdehyde; MUFA, monounsaturated fatty acids; 8-OHdG, 8-hydroxydeoxyguanosine; PG, prostagladins; PUFA, polyunsaturated fatty acids; RBO, rice bran oil; ROS, reactive oxygen species; SFA, saturated fatty acids; SOD, superoxide dismutase; TC, total cholesterol; TG, triglycerides; WRH, white rice outer layer fraction.
Manuscript received 24 July 2001. Initial review completed 24 August 2001. Revision accepted 1 October 2001.
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