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Laboratory of Food and Biodynamics, Nagoya University Graduate School of Bioagricultural Sciences and * Department of Geriatrics, Nagoya University Graduate School of Medical Sciences, Nagoya 464-8601, Japan
1To whom correspondence should be addressed.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • cholesterol • lipid peroxidation • oxidative stress • NZW rabbits • sesaminol glucosides
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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,
Rice-Evans et al. 1996
, Sugiyama et al. 1996
, Tsuda et al. 1996
and 1998
). Flavonoids,
which are phenolic compounds present in fruits, vegetables, beverages
and grains, and possess antioxidative properties, may act alone or in
combination with other compounds such as the glucosinolates, indoles,
dithiolthiones, and isothiocyanates to contribute to the
anticarcinogenic and antiatherogenic activities. The most abundant
lignans in sesame seeds (Sesamum indicum Linn, Pedaliaceae),
sesamin and sesamolin, are reported to lack any appreciable in vitro
antioxidative activity. Rather, the high antioxidative properties of
sesame seed appear to be related to lignans, such as sesamol
(Budowski 1950
), sesamolinol, pinoresinol, p1
(Fukuda et al. 1985
and 1986
) and sesaminol (Kang et al. 1998a
and 1998b
). These compounds also have inhibitory
effects on membrane lipid peroxidation, the microsome peroxidation
induced by ADP-Fe3+/NADPH (Kang et al. 1998b
) and the oxidation of LDL induced by copper ions
(Kang et al. 1999
) or 2,2'-azobis
(2,4-dimethylvaleronitrile)
(AMVN)2
(Kang et al. 1998b
), and show synergistic effects in
elevating the levels of vitamin E in rat liver and plasma
(Kamal-Eldin et al. 1995
, Yamashita et al. 1995
). We recently found that sesaminol acts as an antioxidant
by scavenging peroxyl radicals (Kang et al. 1998a
).
The hypocholesterolemic properties of sesamin have been attributed to
its ability to decrease hydroxymethylglutaryl-CoA-reductase activity,
to reduce cholesterol absorption in the intestinal tract and to
increase the excretion of cholesterol into the bile (Hirose et al. 1991
, Sugano et al. 1990
).;1> Sesame
seed contains large quantities of lignan glucosides (Ryu et al. 1998
), including pinoresinol glucosides (Katsuzaki et al. 1992
);2> and sesaminol glucosides (Katsuzaki et al. 1994
), each of which possesses a lower peroxyl radical
scavenging activity than the corresponding aglycone. However, these
glucosides act as precursors of lipid-soluble antioxidative lignans
(Osawa et al. 1995
). In the rat gastrointestinal tract,
the glucosides are hydrolyzed by ß-glucosidase to yield glucose plus
the aglycone (Osawa et al. 1995
).
Flavonoids are present as glucosides in human plasma (Paganga and Rice-Evans 1996). The physiologic potentials of these
compounds have attracted much interest due to their antioxidative
properties and their possible roles in intracellular and extracellular
defense against oxygen radicals. In addition, the formation of lipid
radicals and hence of lipid peroxidation products in response to
oxidative stress can be influenced by antioxidant feeding (Slim et al. 1996
).
We previously described the isolation of three sesaminol glucosides
from sesame seed as follows:
sesaminol-2'-O-ß-D-glucopyranosyl
(1
2)-ß-D-glucopyranoside;
sesaminol-2'-O-ß-D-glucopyranoside; and
sesaminol-
2'-O-ß-D-glucopyranosyl(12)-[ß-D-glucopyranosyl
(16)]-ß-D-glucopyranoside (Fig. 1
) (Katsuzaki et al. 1994
). To determine their actions in
vivo, wefed rabbits diets containing cholesterol with or
without defatted sesame flour (DSF) and evaluated their sesaminol
metabolism and blood lipid levels. We also evaluated the effect of the
oxidative stress induced by 2,2'-azobis (2-amidinopropane)
dihydrochloride (AAPH) ex vivo.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The protocols for animal experiments were approved by the Laboratory
Animal Care Advisory Committee of Nagoya University. Male New Zealand
White (NZW) rabbits (2.3–2.7 kg; Kitayama, Japan) were housed
individually at 24 ± 1°C with a 12-h light:dark cycle. They
were allowed free access to water and commercial rabbit nonpurified
diet for 14 d to enable them to adapt to the new environment.
Rabbits were then assigned to one of four groups (Table 1
) and were fed control or experimental diets containing DSF (Table 2
). DSF was prepared by extraction with n-hexane to remove
oil and lipid-soluble antioxidants (Katsuzaki et al. 1994
). Its general composition is given in Table 3
. All of the diet ingredients were products of Clea Japan (Tokyo,
Japan). Food intake of each rabbit was restricted to 120 g/d.
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Biochemical analyses.
Serum triglyceride (TG), total cholesterol (TC), phospholipid (PL) and HDL cholesterol (HDL-C) concentrations were determined enzymatically using a commercial kit (Nippon Shoji, Osaka, Japan). To determine TC and TG levels in liver, the liver was weighed, homogenized and extracted with chloroform/methanol (2:1, v/v) to isolate total lipid. TC and TG levels in liver were determined enzymatically using the commercial kit. Protein concentrations were determined with a bicinchonic acid protein assay kit (Pierce, Rockford, IL), using bovine serum albumin as the standard.
Measurement of oxidative susceptibility and free radical trapping capacity.
The extent of lipid peroxidation was determined as 2-thiobarbituric
acid (TBA) reactive substances (TBARS) in serum (Kang et al. 1998b
) and liver (Ohkawa et al. 1979
). Briefly,
each reaction mixture contained a 0.1-mL sample, 0.2 mL of 0.28 mmol/L
SDS (Wako, Osaka, Japan), 1.5 mL of 3.3 mol/L acetic acid solution (pH
5.0) and 1.5 mL of 56 mmol/L aqueous solution of TBA (Merck, Darmstadt,
Germany), made up to 4.0 mL with distilled water. The samples were
boiled at 95°C for 60 min, cooled on ice, extracted with 4.0 mL
n-butanol/pyridine (15:1, v/v), and centrifuged at 800
x g for 10 min. The absorbance of the upper layer
at 532 nm was measured, and TBARS were calculated as malondialdehyde
equivalents using freshly diluted malondialdehyde bis (dimethyl acetal)
1,1,3,3-tetraethoxypropane (Aldrich Chemical, Milwaukee, WI) and
hydrolyzed with 1 mol/L HCl (Philpot 1963
) as the
standard.
Oxidative stability was determined by treating the liver homogenates with AAPH (Wako). Briefly, AAPH was added to the liver homogenate that contained 1 mg protein; the final volume was adjusted to 1 mL with PBS (pH 7.4). The mixture was incubated at 37°C, with 20 µL of 0.18 mmol/L BHT (Wako), and TBARS were measured as above.
Tocopherol determination.
The concentrations of 
- and 
-tocopherol in the serum and liver
were analyzed by HPLC (Ueda and Igarashi 1987
). Serum
(200 µL) was added to a 10-mL screw-capped tube
together with 3 mL n-hexane, 0.8 mL H2O and
1 mL ethanol. The samples were mixed and centrifuged for 15 min at 800
x g. Tissue samples were homogenized for 15 s
in 5 vol of buffer with a Brinkman homogenizer;3> equipped with a
PT20ST probe generator (Hitachi, Tokyo, Japan); 0.4 mL of each was
added to a screw-capped tube as above. To each were added 1 mL of
0.48 mmol/L ethanolic pyrogallol (Wako) and 1 mg/L of ethanolic
2,2,5,7,8-pentamethyl-6-chromanol (PMC), (Eisai, Tokyo, Japan) as an
internal standard. A 0.02-mL aliquot of 0.01 mol/L KOH was added to
each and the samples were incubated at 70°C for 30 min. To each was
added 4.5 mL of 5.8 mol/L NaCl, and the samples were extracted with 3
mL 10% ethyl acetate in n-hexane. Each hexane layer was
transferred to a microfuge tube, evaporated in vacuo under
N2, then resuspended in 200 µL
n-hexane containing 1 mg PMC/L. HPLC was performed by
autoinjecting 40 µL onto a Develosil ODS
NH2-Column (4.6 i.d. x 250 mm, Nomura Chemical, Aichi,
Japan) using n-hexane/isopropanol (98:2, v/v) as a
mobile phase. The fluorescence detector was set to excitation at 295 nm
and emission at 325 nm, essentially as described by Burton et al. (1983)
, except that the column was at room temperature and
the flow rate was 1.0 mL/min. Standard stock solutions contained 1 mg
of - or -tocopherol (Eisai) in 1 mL of n-hexane.
Each was quantified by a peak ratio method using PMC as an internal
standard.
Sesaminol determination.
Serum (200 µL) was vortexed with 1.4 mL ethyl acetate
and centrifuged at 750 x g for 15 min. One
milliliter of the ethyl acetate layer was transferred to a microfuge
tube, evaporated in vacuo and resuspended in 50 µL
MeOH. Electrochemical detection (ECD) was performed by injecting each
20-µL sample onto a Develosil ODS-Column (4.6 i.d.
x 250 mm, Nomura), using 30 mmol/L lithium-acetate
methanol/H2O (6:4, v/v) as the mobile phase, and operated
at a flow of 0.8 mL/min at ambient temperature. ECD was performed at
500 mV. Sesaminol was isolated by preparative reversed-phase HPLC
from crude sesame flour digested with 5000 U/g
ß-glucosidase (Sigma Chemical, St. Louis, MO; Fukuda et al. 1985
), and its purity confirmed by proton nuclear magnetic
resonance. Sesaminol concentration was calculated from peak area
responses using a standard curve prepared by ECD chromatography of
known amounts of pure sesaminol, and calculated by linear regression
(r2 = 0.9982). The relationship of peak
area to the weight of standard sesaminol under these conditions was
linear from 0.000372 to 0.372 µg/injection.
Sesaminol glucoside determination.
Serum (1 mL) was deproteinized with 4 vol of methanol and centrifuged at 800 x g for 10 min. The methanol was removed from the supernatant by rotary evaporation under vacuum at 35°C. Each dried sample was resuspended in 50 µL MeOH, and HPLC (Jasco, Tokyo, Japan) was performed by injecting a 20-µL sample onto a Develosil ODS-Column (4.6 i.d. x 250 mm, Nomura). HPLC was performed at ambient temperature, using 0.8 mL/min MeOH/H2O (1:1, v/v) as the mobile phase, and monitored at 280 nm.
Statistical analysis.
Results are presented as means ± SD. The data were tested by ANOVA, followed by Fisher's test to identify significant difference. All analyses were performed using StatView software version 5.0J (Abacus Concepts, Berkeley, CA). A level of P < 0.05 was considered significant.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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) (P < 0.05). Before the experiment began, serum TC,
TG, PL and HDL-C concentrations did not differ among the groups
(Fig. 3
). However, all four lipid concentrations in serum were greater in the
two groups fed cholesterol after 45 and 90 d. At 45 d, serum
HDL-C concentration in rabbits fed Chol + DSF was greater than in
those fed cholesterol alone. Rabbits fed Chol + DSF had lower hepatic
TC and TG concentrations than did those fed Chol alone (P
< 0.05), but rabbits fed control and DSF diets did not differ
(Table 4
).
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). When the liver homogenate was subjected in vitro to AAPH-induced
oxidation, TBARS levels were significantly lower in rabbits fed Chol +
DSF than in those fed Chol, but rabbits fed control and DSF diets did
not differ (Fig. 5
).
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- and -tocopherol concentrations were higher in
the Chol and Chol + DSF groups than in the other two groups, and there
were no significant differences in serum of rabbits fed DSF compared
with those fed the control diet. However, - and -tocopherol
concentrations in liver were significantly higher in rabbits fed DSF
than in the controls (P < 0.05). Sesaminol was
detectable in both the serum and liver of rabbits fed Chol + DSF with
the concentration greater in those fed DSF alone (Table 5
). Sesaminol glucosides were not detected in serum or liver from any
group (data not shown).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, Lokesh et al. 1981
). Recent studies have demonstrated a direct
relationship between hypercholesterolemia and mortality from coronary
heart disease (Efendy et al. 1997
, Xu et al. 1998
). During its metabolism, dietary cholesterol is delivered
to the liver cells, where substantial amounts of reactive oxygen
species are generated (Erdincler et al. 1997
,
Konecka and Jezierski 1997
, Prasad and Kalra 1993
). This process generates highly toxic products, including
such lipid peroxides as aldehydes, epoxides and carbonyls, as well as
the rapid consumption of antioxidants such as tocopherol or vitamin C
(Erdincler et al. 1997
, Esterbauer et al. 1992
).
Many studies have shown that dietary phenolic phytochemicals can
effectively scavenge free radicals (Efendy et al. 1997
,
Kang et al. 1998b
, Silva et al. 1998
,
Xu et al. 1998
). Sesaminol, a phenolic lignan-type
compound contained in sesame seed, is one of the most potent free
radical scavengers (Kang et al. 1998a
). The substitution
of phenolic groups with glucose in sesaminol decreases its
antioxidative activity (Osawa et al. 1995
). Flavonoids,
phloretin and quercetin have been reported to be absorbed from the diet
as glucosides, but studies of sesaminol glucosides have not yet been
done. Dietary sesaminol glucosides could not be detected in serum or
liver because sesaminol glucosides are highly water soluble and
gradually hydrolyzed by ß-glucosidase in the gut. Sesaminol was
detected in abundant quantities in the serum and liver of rabbits fed
sesaminol glucosides, indicating that sesaminol is the principal
metabolite of sesaminol glucosides.
Our observation that sesaminol glucosides had no effect on liver weight
differs from reports showing that the lipid-soluble sesame lignans
increase liver weight (Hirose et al. 1991
, Kang et al. 1998b
, Yamashita et al. 1995
). Sesamin
has been shown to possess hypocholesterolmic activity by inhibiting
both the absorption and synthesis of cholesterol (Hirata et al. 1996
,;4> Hirose et al. 1991
), and to
protect the liver against injury induced by the continuous inhalation
of ethanol or the intraperitoneal administration of carbon
tetrachloride (Akimoto et al. 1993
).;5> The
difference in our results may arise because sesaminol glucosides were
not accumulated in liver because of their high water solubility.
In rabbits fed a diet containing 10% DSF plus 1% cholesterol, serum
levels of TC, HDL-C, TG, and PL were not significantly different
than in those fed cholesterol alone except HDL-C in serum was
greater in Chol + DSF than in Chol at 45 d. Tovar-Palacio et al. (1998)
;6> suggested that high levels of HLD-C
and apolipoprotein A-I are associated with the reduction of
coronary heart disease, but our findings suggest that an elevation of
HDL-C is insufficient to explain the antiatherogenic effect of DSF.
The concentration of lipid peroxidation products, as well as the
alteration of antioxidative variables in the liver, may reflect the
oxidative stress injury induced by dietary cholesterol. We found higher
serum and liver TBARS levels in cholesterol-fed rabbits than in
those fed cholesterol plus DSF, indicating that formation of lipid
peroxidation products was reduced by feeding sesaminol glucosides. We
recently found that sesaminol inhibits the oxidation of LDL induced by
AAPH or copper ion (Kang et al. 1999
) or AMVN
(Kang et al. 1998a
), indicating that this compound acts
as an antioxidant.
Several reports have suggested that tocopherol and sesame lignans act
synergistically as antioxidants (Kamal-Eldin et al. 1995
, Yamashita et al. 1995
). For example,
Yamashita and Namiki (1994)
found that long-term
feeding of sesame seed suppressed the advancement of senescence. In
addition, it has been shown that the binding activity of tocopherol
isomers with tocopherol-binding protein is strongly enhanced by
sesame lignans (Yamashita et al. 1995
). However, we
observed that rabbits fed DSF had concentrations of - and
-tocopherol in serum that were not different from those fed a
control diet, whereas concentrations of - and -tocopherol in the
liver of DSF-fed rabbits were significantly higher than in rabbits
fed the control diet (P < 0.05). The levels of
- and -tocopherol were higher in the liver and serum of rabbits
fed cholesterol than in those not fed cholesterol. The increase in
tocopherol levels due to cholesterol feeding may be explained by the
increase of solubility of tocopherol.
Our results suggest a mechanism for the antioxidative effects of sesame
seed lignans. Ingested sesaminol glucosides are hydrolyzed to sesaminol
in the gut (Osawa et al. 1995
), which is transported to
organs through the blood stream and strongly inhibits lipid
peroxidation. In addition to the antioxidative properties of sesaminol,
our findings suggest that this compound may protect against lipid
peroxidation induced by oxidative stress.
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FOOTNOTES |
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Manuscript received October 16, 1998. Initial review completed November 5, 1998. Revision accepted July 4, 1999.
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