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- and 
-Tocotrienol Concentrations in Skin and Adipose Tissue of Rats Fed the Tocotrienol-Rich Fraction Extracted from Palm Oil1
Department of Food and Nutrition, School of Life Studies, Sugiyama Jogakuen University, Nagoya, Japan
2To whom correspondence should be addressed. E-mail: kanaey{at}food.sugiyama-u.ac.jp
ABSTRACT
The metabolism of tocotrienol remains unclear. We studied the
distribution of tocotrienol in rats fed the tocotrienol-rich
fraction extracted from palm oil. We have previously shown that dietary
sesame seeds markedly elevate the tocopherol concentration in rats. In
this study, we also examined the effect of dietary sesame seeds on the
tocotrienol concentration. In experiment 1, rats (4-wk-old) were fed
the diet with 
-tocopherol alone or with - and 
-tocotrienols.
In experiment 2, the effect of dietary sesame seeds on tocopherol and
tocotrienol concentrations in rats fed the diet with tocopherol and
tocotrienol was studied. The rats were fed the experimental diet for 8
wk in both experiments. - and -Tocotrienols accumulated in the
adipose tissue and skin, but not in plasma or other tissues, of the
rats fed tocotrienols. Dietary sesame seeds elevated (P
< 0.05) tocotrienol concentrations in the adipose tissue and
skin, but did not affect their concentrations in other tissues or in
plasma. The -tocopherol concentration in all tissues and plasma of
rats fed -tocopherol was extremely low but was elevated
(P < 0.05) in many tissues by feeding sesame
seeds. These data suggest that the transport and tissue uptake of
vitamin E isoforms are different. Dietary sesame seeds elevate the
concentrations of both tocopherols and tocotrienols.
KEY WORDS: • adipose tissue • sesame seeds • skin • tocotrienol • vitamin E • rats
Vitamin E is a potent fat-soluble antioxidant that inhibits lipid
peroxidation in biological membranes. In nature, compounds with vitamin
E activity are -, ß-, - or 
-tocopherols and -, ß-, -
or -tocotrienols. The chemical properties of these vitamin E
isoforms include antioxidative activities. The antioxidative activities
of -tocotrienol, which inhibit lipid peroxidation in rat microsome
and mitochondria, and the oxidation of dioleoylphosphatidylcholine
liposomes are higher than those of -tocopherol (1
–3
).
However, the antioxidative activities of vitamin E isoforms in vitro
are poorly correlated with their biological activities. -Tocopherol
has the highest biological activity among the vitamin E isoforms
because the levels of the other isoforms are lower than that of
-tocopherol.
Dietary vitamin E isoforms are absorbed in the intestine and carried to
the liver as a result of the uptake of chylomicron remnants
(4
). There is no discrimination between -tocopherol and
other isoforms during the absorption and chylomicron secretion by the
intestine (5
, 6
). -Tocopherol transfer protein
(-TTP)3
catalyzes -tocopherol secretion by a novel non–Golgi-mediated
pathway in liver cells, and -tocopherol is incorporated into VLDL
and transported to the various tissues by lipoproteins
(7
). The other isoforms of vitamin E such as tocotrienols
and -tocopherol are excreted because their affinity for -TTP is
low. Hosomi et al. (8
) have reported that the relative
affinity of tocopherol isoforms or -tocotrienol for -TTP
correlate well with their biological activity. In addition, patients
who have ataxia with vitamin E deficiency also have an extremely low
vitamin E concentration in plasma due to mutations in the -TTP gene
(9
). Thus, the affinity of vitamin E isoforms for -TTP
is a critical determinant of their biological activities, and the low
biological activities of -tocopherol and tocotrienols may be due to
their low affinity for -TTP.
However, the presence of an -TTP–independent vitamin E transport
pathway has been suggested (4
). It was reported that
lipoprotein lipase (EC 3.1.1.34) has the transfer activity of vitamin E
in vitro (10
) and in vivo (11
). Vitamin E
isoforms may be transferred from chylomicrons to some tissues by
lipoprotein lipase before the discrimination by -TTP in the liver.
Some reports have recently suggested the accumulation of
-tocotrienol or tocotrienols in adipose tissue and skin. Burton et
al. (12
) have shown that a large amount of -tocopherol
was present in the adipose tissue and skin of elective surgery
patients. Hayes et al. (13
) have shown that large amounts
of - and -tocotrienol are present in the adipose tissue of
hamsters fed diet containing - and -tocotrienols. Podda et al.
(14
) have shown that large amounts of - and
-tocotrienols are present in the skin of hairless mice fed a
commercial diet containing a small amount of tocotrienols. We have also
shown that substantial amounts of - and -tocotrienols are
detected in the skin of rats, nude mice and hairless mice
(15
). Thus, -tocopherol and tocotrienols may be
transferred to some tissues, such as the adipose tissue and skin, by
lipoprotein lipase. In this study, we determined the tissue
distribution of dietary tocotrienol in rats.
Sesame seeds contain -tocopherol and negligible amounts of
-tocopherol. We have previously shown that dietary sesame seeds
markedly elevate -tocopherol concentrations in the liver, kidney and
plasma of rats fed a diet without -tocopherol (16
).
Recently, Lemcke-Norojärvi et al. (17
) reported that
dietary sesame oil elevated the -tocopherol concentration in the
serum of Swedish women. We have also shown that dietary sesame seeds
elevate the -tocopherol concentrations in the liver, kidney and
plasma of the rats fed a diet with -tocopherol (18
).
The purpose of this study was to determine whether dietary sesame seeds
elevate the tocotrienol concentration in rats. Here we show the
tissue-specific accumulation of tocotrienol and its elevation by
dietary sesame seeds.
MATERIALS AND METHODS
Materials.
The tocotrienol-rich fraction (TRF) extracted from palm oil was
kindly provided by Lion (Tokyo, Japan). The TRF used in expt. 1
consists of 227 mg/g -tocopherol, 353 mg/g -tocotrienol and 497
mg/g -tocotrienol. The TRF used in expt. 2 consists of 166 mg/g
-tocopherol, 319 mg/g -tocotrienol and 482 mg/g -tocotrienol.
-and -Tocotrienols used as standards were purchased from Merck
(Tokyo, Japan). -and -Tocopherols were donated by Eisai (Tokyo,
Japan). Roasted white sesame seeds were a gift of Shinsei (Aichi,
Japan).
Animals and diets.
Male Wistar rats (3 wk old) were purchased from Japan SLC (Shizuoka,
Japan). Rats were maintained at 24.5°C with a 12-h light cycle
(lights on from 0800 to 2000) and allowed free access to water and
food. The rats were fed a commercial diet (CE-2, Japan Clea, Tokyo,
Japan) for 7 d before the start of the experiment and then fed the
experimental diet for 8 wk. The composition of the experimental diet is
shown in Table 1
. The rats were killed between 1000 and 1300 h, and all procedures
were performed in accordance with the Animal Experimentation Guidelines
of Nagoya University.
|
The rats were fed the diet without vitamin E (the deficient group,
n = 6), the diet containing 50 mg -tocopherol/kg
diet (the -Toc group, n = 6) or the diet
containing 220 mg TRF/kg diet (the TRF group, n = 6) for 8 wk. After 24 h food deprivation, the rats were anesthetized
with sodium pentobarbital and blood was drawn from the heart using a
heparinized needle and syringe. Liver, brain, kidney, perirenal adipose
tissue, epididymal fat and dorsal skin were taken and stored at
-80°C until use for the determination of tocopherol and tocotrienol
concentrations.
Experiment 2.
The rats were fed the diet without vitamin E (the deficient group,
n = 6), the diet containing 50 mg -tocopherol/kg
diet and 50 mg -tocopherol/kg diet (the -Toc+-Toc group,
n = 6), the diet containing 50 mg -tocopherol/kg
diet and 200 g sesame/kg diet (the -Toc + sesame group,
n = 6), the diet containing 302 mg TRF/kg diet and
50 mg -tocopherol/kg diet (the TRF+-Toc group, n
= 6) or the diet containing 302 mg TRF/kg diet and 200 g
sesame/kg diet (the TRF + sesame group, n = 6) for
8 wk. Two hundred grams of sesame seeds contain 50 mg -tocopherol.
Blood and tissues (including heart, lung and muscle in expt. 2) were
sampled and handled as described for expt. 1.
Determination of tocopherol and tocotrienol concentrations.
The experimental diet or the commercial diet (0.2 g) was put in a
centrifuge tube, and 0.2 mL of 20 g/L sodium chloride, 2 mL of ethanol
containing 60 g/L pyrogallol and 2.7 µg of
2,2,5,7,8-pentamethyl-6-chroman as an internal standard were added.
Then, 0.4 mL of 600 g/L potassium hydroxide was added and saponified at
70°C for 30 min. After adding 9 mL of 20 g/L sodium chloride,
tocopherol and tocotrienol were extracted with 6 mL of hexane
containing 10% (v/v) ethylacetate. Tocopherol and tocotrienol in the
tissues and plasma were extracted as described previously
(20
). Concentrations of tocopherols and tocotrienols were
determined by HPLC (21
). Instrumentation used for HPLC was
a Shimadzu LC-10AS (Shimadzu, Kyoto, Japan) with a Shimadzu RF-10AXL
fluorescence detector (excitation 298 nm, emission 325 nm). The
analytical column used was a Develosil 60–5 (4.6 x 250 mm,
Nomura Chemical, Aichi, Japan). The mobile phase was hexane containing
1% (v/v) dioxane and 0.2% (v/v) isopropylalcohol, and the flow rate
was 1 mL/min.
Determination of thiobarbituric acid reactive substance concentrations.
Thiobarbituric acid reactive substance (TBARS) concentrations in plasma
were determined by the method of Yagi (22
), and those in
tissues were determined by the method of Ohkawa et al.
(23
). The TBARS concentrations are presented as nmol
malondialdehyde (MDA), using tetraethoxypropane as an external
standard.
Statistical analysis.
Data are presented as means ± SEM, n
= 6. They were analyzed by one-way ANOVA with Fisher’s
posthoc test. Mean values of - and -tocotrienol concentrations of
the TRF+-Toc and TRF + sesame groups in expt. 2 were compared using
Student’s t test. Differences with a P
value < 0.05 were regarded as significant.
RESULTS
Vitamin E concentration in the experimental and the commercial diets.
In expt. 1, the -tocopherol concentration in the diets of the
-Toc and the TRF groups was 
50 mg/kg diet (Table 2
). A small amount of -tocopherol derived from stripped corn oil was
detected in all diets. - and -tocotrienols were detected only in
the diet of the TRF group. In expt. 2, the -tocopherol concentration
in the diets of the -Toc+-Toc, -Toc + sesame, TRF+-Toc and
TRF + sesame groups was about 50 mg/kg diet. A small amount of
-tocopherol derived from stripped corn oil was detected in the diet
of the deficient group. The -tocopherol detected in the diet of both
the -Toc + sesame and the TRF + sesame groups was derived from
sesame seeds. - and -Tocotrienols were detected in the diets of
both the TRF+-Toc and the TRF + sesame groups. The commercial diet
(CE-2) contained - and -tocopherols and - and
-tocotrienols, and the -tocopherol concentration was the highest
of these isoforms (Table 2)
.
|
At the start of the experiments, -tocopherol was detected in all
tissues and plasma, and -tocopherol concentration was extremely low
(Fig. 1
). - and -Tocotrienols were detected in perirenal adipose tissue,
epididymal fat and skin, although their concentrations were <5 nmol/g.
The -tocotrienol concentration was less than the -tocopherol
concentration in the CE-2 (Table 2)
, but the -tocotrienol
concentrations were higher than the -tocopherol concentrations in
the adipose tissues and skin.
|
Dietary vitamin E did not affect the food intake, growth or liver
weight of rats (Table 3
). Negligible amounts of -tocopherol were detected in the tissues
(except brain) of the deficient group because of feeding them the
-tocopherol–free diet for 8 wk (Fig. 2
). -Tocopherol was detected in all tissues and plasma of both the
-Toc and TRF groups. In the liver, brain, perirenal adipose tissue,
epididymal fat, skin and plasma, the -tocopherol concentrations in
both the -Toc and TRF groups did not differ. In kidney, the
concentration was greater in the TRF group. Both - and
-tocotrienols were detected in perirenal adipose tissue, epididymal
fat and skin.
|
|
Dietary vitamin E did not affect the food intake, growth or liver
weight of rats (Table 3)
. Negligible amounts of -tocopherol were
detected in the tissues (except brain) of the deficient group because
of feeding them the -tocopherol–free diet for 8 wk (Fig. 3
). -Tocopherol was detected in all tissues and plasma of the
-Toc+-Toc, the -Toc + sesame, the TRF+-Toc and the TRF +
sesame groups. The -tocopherol concentrations in the liver, kidney,
brain and epididymal fat of the -Toc + sesame group were
significantly higher (P < 0.05) than those of the
-Toc+-Toc group, and the -tocopherol concentrations in all
tissues and plasma of the TRF + sesame group were significantly higher
(P < 0.05) than those of the TRF+-Toc group.
-Tocopherol was not detected in any tissue or plasma of the
deficient group, and negligible amounts of -tocopherol were detected
in all tissues and plasma of the -Toc+-Toc and the TRF+-Toc
groups. Dietary sesame seeds elevated (P < 0.05) the
-tocopherol concentrations in all tissues except the liver, although
the concentrations were lower than the -tocopherol concentrations in
those tissues. However, tocotrienols were not detected in any tissues
or plasma of the deficient, -Toc+-Toc, and -Toc + sesame
groups, and only negligible levels of tocotrienols were detected in the
liver, kidney, heart, lung, brain, muscle and plasma of the TRF+-Toc
and the TRF + sesame groups. Both - and -tocotrienols were
detected in perirenal adipose tissue, epididymal fat and skin of the
TRF+-Toc and the TRF + sesame groups. The - and -tocotrienol
concentrations in perirenal adipose tissue, epididymal fat and skin of
the TRF + sesame group were significantly higher (P < 0.05) than those of the TRF+-Toc group.
|
). The TBARS concentrations in perirenal adipose tissue and skin of the
TRF+-Toc group were lower (P < 0.05) than those of
the -Toc+-Toc groups. Moreover, dietary sesame seeds tended to
lower (0.05 < P < 0.1) the TBARS concentrations
in perirenal adipose tissue, epididymal fat and skin of the rats fed
TRF and -tocopherol.
|
DISCUSSION
We have previously shown that dietary tocotrienols are present in
the skin of rats and mice fed a diet containing TRF (15
).
We studied the distribution of tocotrienol and the effect of dietary
sesame seeds on their concentrations in the tissues of rats. We found
that dietary tocotrienol had accumulated in the adipose tissue (Figs. 2
and 3)
. The rats were fed a commercial diet (CE-2) containing - and
-tocotrienols for 7 d before each experiment, and the - and
-tocotrienol concentrations in the adipose tissue of the rats at the
start of the experiment were <5 and 2 nmol/g, respectively (Fig. 1)
.
However, those at the end of the experiment were >20 nmol/g (Figs. 2
and 3)
. Feeding TRF for 8 wk also elevated the - and -tocotrienol
concentrations in the skin. On the other hand, neither - nor
-tocotrienol was detected in the tissues (except for adipose tissues
and skin) and plasma of the rats at the start of the experiment, while
- and -tocotrienol concentrations were below 1 nmol/g in those
tissues and plasma at the end of the experiment. Therefore, dietary
tocotrienols were taken up and accumulated in adipose tissue and skin.
Feeding -tocopherol lowers the -tocopherol concentration in rats
(24
). Supplementation of -tocopherol in the diet
containing sesame seeds inhibits elevation of the -tocopherol
concentration by sesame seeds, as described previously
(18
). In this study, the -tocopherol concentrations in
the tissues and plasma of the rats fed sesame seeds were low (Fig. 3)
because the diets of all groups except the deficient group contained
the same amounts of -tocopherol. Dietary sesame seeds significantly
elevated the -tocopherol concentration in kidney, heart, lung,
brain, muscle, adipose tissues and skin of the rats fed the diet with
or without tocotrienols. However, negligible amounts of - and
-tocotrienols were detected in the tissues (except adipose tissues
and skin) of the rats fed the diet containing TRF and sesame seeds, in
spite of the large amount of tocotrienol in that diet. Dietary sesame
seeds elevated - and -tocotrienol concentrations in both the
adipose tissue and skin but did not affect their concentrations in
other tissues or plasma. These data suggest that the transport, tissue
uptake or stability of -tocopherol and tocotrienols are different.
As mentioned in the introduction, vitamin E isoforms may be transferred
from chylomicrons to the adipose tissue and skin by lipoprotein lipase
before discrimination by -TTP in the liver. However, a negligible
amount of -tocopherol and larger amounts of tocotrienols were
detected in the adipose tissue and skin of rats fed TRF and
-tocopherol (Fig. 3)
. It is unclear why there is the difference
between -tocopherol and tocotrienols. The unsaturated phytyl tail of
tocotrienols might enhance their transfer from chylomicrons to tissues
and might modulate their stability in the lipid due to the fluidity of
phytyl tail.
Dietary sesame seeds elevated not only the tocopherol concentration but
also the tocotrienol concentration in adipose tissue and skin. However,
the precise mechanism of the elevation of those concentrations by
sesame seeds or sesame lignan is unknown. Parker et al.
(25
) have recently reported that the oxidative catabolism
of tocopherols to carboxychromans is catalyzed by cytochrome
P450 3A in HepG2 cells, a well-differentiated
human hepatoblastoma line derived from a hepatocellular carcinoma, and
rat primary hepatocytes. They have also shown that sesamin strongly
inhibits -tocopherol metabolism by HepG2. Carboxychromans are
metabolites of tocopherols and tocotrienols (26
, 27
).
Sesame lignan may inhibit cytochrome P450
3A–dependent catabolism of tocopherol and tocotrienol in rats,
although whether cytochrome P450 3A also
catalyzes tocotrienol catabolism is unknown. We are studying the effect
of dietary sesame seeds on the excretion of carboxychroman in rats fed
tocopherols and tocotrienols.
The antioxidative activity of -tocotrienol to inhibit lipid
peroxidation in vitro is higher than that of -tocopherol
(1
–3
). Adipose tissues contain large amounts of lipid,
and skin is the tissue most directly exposed to ultraviolet rays and
oxygen. We examined the effect of tocotrienol in the adipose tissue and
skin on TBARS concentrations (Fig. 4)
. These tissues’ TBARS
concentrations were higher than those in other tissues and plasma, and
dietary tocotrienol tended to decrease their TBARS concentrations.
Tocotrienol in tissues which can take up tocotrienol, such as adipose
tissue and skin, may act as an antioxidant. Recently, several
biological functions of tocotrienol have been reported
(28
). More studies are needed for a better understanding
of the metabolism of vitamin E isoforms.
FOOTNOTES
1 Supported in part by a Grant-in-Aid for
Scientific Research 11780097 from the Japan Society for the Promotion
of Science, Japan. 
3 Abbreviations used: MDA, malondialdehyde; TBARS,
thiobarbituric acid reactive substance; TRF, tocotrienol-rich
fraction; -TTP, -tocopherol transfer protein.
Manuscript received 1 May 2001. Initial review completed 6 June 2001. Revision accepted 14 August 2001.
LITERATURE CITED
1. Kamat, J. P., Sarma, H. D., Devasagayam, T.P.A., Nesaretnam, K. & Basiron, Y. (1997) Tocotrienols from palm oil as effective inhibitors of protein oxidation and lipid peroxidation in rat liver microsomes. Mol. Cell. Biochem. 170:131-138.[Medline]
2. Kamat, J. P. & Devasagayam, T.P.A. (1995) Tocotrienols from palm oil as potent inhibitors of lipid peroxidation and protein oxidation in rat brain mitochondria. Neurosci. Lett. 195:179-182.[Medline]
3. Serbinova, E. A. & Packer, L. (1994) Antioxidant properties of -tocopherol and -tocotrienol. Methods Enzymol 234:354-366.[Medline]
4. Traber, M. G. & Sie, H. (1996) Vitamin E in humans: demand and delivery. Annu. Rev. Nutr. 16:321-347.[Medline]
5. Kayden, H. J. & Traber, M. G. (1993) Absorption, lipoprotein transport, and regulation of plasma concentrations of vitamin E in humans. J. Lipid Res. 34:343-358.[Medline]
6. Ikeda, I., Imasato, Y., Sasaki, E. & Sugano, M. (1996) Lymphatic transport of -, - and -tocotrienols and -tocopherol in rats. Internat. J. Vit. Nutr. Res. 66:217-221.
7. Traber, M. G. & Arai, H. (1999) Molecular mechanisms of vitamin E transport. Annu. Rev. Nutr. 19:343-355.[Medline]
8. Hosomi, A., Arita, M., Sato, Y., Kiyose, C., Ueda, T., Igarashi, O., Arai, H. & Inoue, K. (1997) Affinity for -tocopherol transfer protein as a determinant of the biological activities of vitamin E analogs. FEBS Lett 409:105-108.[Medline]
9. Ouahchi, K., Arita, M., Kayden, H., Hentati, F., Ben Hamida, M., Sokol, R., Arai, H., Inoue, K., Mandel, J. L. & Koenig, M. (1995) Ataxia with isolated vitamin E deficiency is caused by mutations in the -tocopherol transfer protein. Nat. Genet. 9:141-145.[Medline]
10. Traber, M. G., Olivecrona, T. & Kayden, J. (1985) Bovine milk lipoprotein lipase transfers tocopherol to human fibroblasts during triglyceride hydrolysis in vitro. J. Clin. Invest. 75:1729-1734.
11. Sattler, W., Levak-Frank, S., Radner, H., Kostner, G. M. & Zechner, R. (1996) Muscle-specific overexpression of lipoprotein lipase in transgenic mice results in increased -tocopherol levels in skeletal muscle. Biochem. J. 318:15-19.
12. Burton, G. W., Traber, M. G., Acuff, R. V., Walters, D. N., Kayden, H., Hughes, L. & Ingold, K. U. (1998) Human plasma and tissue -tocopherol concentrations in response to supplementation with deuterated natural and synthetic vitamin E. Am. J. Clin. Nutr. 67:669-684.[Abstract]
13. Hayes, K. C., Pronczuk, A. & Liang, J. S. (1993) Differences in the plasma transport and tissue concentrations of tocopherols and tocotrienols: observations in humans and hamsters. Proc. Soc. Exp. Biol. Med. 202:353-359.[Abstract]
14. Podda, M., Weber, C., Traber, M. G. & Packer, L. (1996) Simultaneous determination of tissue tocopherols, tocotrienols, ubiquinols, and ubiquinones. J. Lipid Res. 37:893-901.[Abstract]
15. Ikeda, S., Niwa, T. & Yamashita, K. (2000) Selective uptake of dietary tocotrienols into rat skin. J. Nutr. Sci. Vitaminol. 46:141-143.
16. Yamashita, K., Nohara, Y., Katayama, K. & Namiki, M. (1992) Sesame seed lignans and -tocopherol act synergistically to produce vitamin E activity in rats. J. Nutr. 122:2440-2446.
17. Lemcke-Norojärvi, M., Kamal-Eldin, A., Appelqvist, L.-Å., Dimberg, L. H., Öhrvall, M. & Vessby, B. (2001) Corn and sesame oils increase serum -tocopherol concentrations in healthy Swedish women. J. Nutr. 131:1195-1201.
18. Yamashita, K., Iizuka, Y., Imai, T. & Namiki, M. (1995) Sesame seed and its lignans produce marked enhancement of vitamin E activity in rats fed a low -tocopherol diet. Lipids 30:1019-1028.[Medline]
19. American Institute of Nutrition (1993) 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. 123:1939-1951.
20. Yamashita, K., Takeda, N. & Ikeda, S. (2000) Effects of various tocopherol-containing diets on tocopherol secretion into bile. Lipids 35:163-170.[Medline]
21. Ueda, T. & Igarashi, O. (1987) New solvent system for extraction of tocopherols from biological specimens for HPLC determination and the evaluation of 2,2,5,7,8-pentamethyl-6-chromanol as an internal standard. J. Micronutr. Anal. 3:185-198.
22. Yagi, K. (1976) A simple fluorometric assay for lipoperoxide in blood plasma. Biochem. Med. 15:212-216.[Medline]
23. Ohkawa, H., Ohishi, N. & Yagi, K. (1979) Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal. Biochem. 95:351-358.[Medline]
24. Behrens, W. A. & Madere, R. (1987) Mechanisms of absorption, transport and tissue uptake of RRR--tocopherol and d--tocopherol in the white rat. J. Nutr. 117:1562-1569.
25. Parker, R. S., Sontag, T. J. & Swanson, J. E. (2000) Cytochrome P4503A-dependent metabolism of tocopherols and inhibition by sesamin. Biochem. Biophys. Res. Commun. 277:531-534.[Medline]
26. Hattori, A., Fukushima, T., Yoshimura, H., Abe, K. & Imai, K. (2000) Production of LLU- following an oral administration of -tocotrienol or -tocopherol to rats. Biol. Pharm. Bull. 23:1395-1397.[Medline]
27. Lodge, J. K., Ridlington, J., Leonard, S., Vaule, H. & Traber, M. G. (2001) - and -Tocotrienols are metabolized to carboxyethyl-hydroxychroman derivatives and excreted in human urine. Lipids 36:43-48.[Medline]
28. Packer, L., Weber, S. U. & Rimbach, G. (2001) Molecular aspects of -tocotrienol antioxidant action and cell signalling. J. Nutr. 131:369S-373S.
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