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© 2004 The American Society for Nutritional Sciences J. Nutr. 134:506-510, March 2004

Biochemical and Molecular Actions of Nutrients

Cereal Alkylresorcinols Elevate {gamma}-Tocopherol Levels in Rats and Inhibit {gamma}-Tocopherol Metabolism In Vitro

Alastair B. Ross1, Yan Chen2, Jan Frank, Joy E. Swanson*, Robert S. Parker*, Arkadiusz Kozubek{dagger}, Torbjörn Lundh**, Bengt Vessby{ddagger}, Per Åman and Afaf Kamal-Eldin

Department of Food Science, Swedish University of Agricultural Sciences (SLU), S-750 07 Uppsala, Sweden; * Division of Nutritional Sciences, Cornell University, Ithaca, NY; {dagger} Department of Lipids and Liposomes, Institute of Biochemistry and Molecular Biology, University of Wroclaw, Przybyszewskiego 63/77, 51–148 Wroclaw, Poland; ** Department of Animal Nutrition and Management, Swedish University of Agricultural Sciences (SLU), S-750 07 Uppsala, Sweden; and {ddagger} Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, S-751 25 Uppsala, Sweden

1To whom correspondence should be addressed. E-mail: Alastair.Ross{at}lmv.slu.se.


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 LITERATURE CITED
 
Alkylresorcinols (AR) are a class of amphiphilic phenolic lipids present in high amounts in wheat and rye bran. They have been reported to be both growth retarding and innocuous when fed to rats, and to have a broad range of bioactivities in vitro, suggested to be related to their ability to bind to proteins and modify membranes. This study was designed to test the effects of AR (purified from rye bran) on growth, tocopherol levels, and cholesterol levels in rats. Rats were fed 1 of 4 different levels of AR for 4 wk: 0 (control), 1 , 2, and 4 g/kg diet. AR did not affect final body, liver, or lung weights. The AR diets increased the levels of {gamma}-tocopherol in liver and lungs (P < 0.05). To investigate whether AR could have increased {gamma}-tocopherol levels via inhibition of tocopherol-{omega}-hydroxylase, HepG2 cells were incubated with AR and the metabolism of {gamma}-tocopherol measured. AR significantly inhibited the conversion of {gamma}-tocopherol to its water-soluble hydroxychroman metabolite in vitro, indicating that AR may increase {gamma}-tocopherol levels via inhibition of tocopherol metabolism in vivo. The 4 g AR/kg diet decreased liver cholesterol (P < 0.001), but did not affect plasma lipids. AR were detected in the perirenal adipose tissue samples of rats fed AR, indicating that they can accumulate in the fatty tissues of rats. High levels of dietary AR moderately affect {gamma}-tocopherol, possibly via inhibition of tocopherol metabolism, and decrease liver cholesterol in rats.

KEY WORDS: • alkylresorcinols • cholesterol • cytochrome P450 • {gamma}-tocopherol • tocopherol-{omega}-hydroxylase

Epidemiologic studies have associated the consumption of whole-grain cereals with decreased incidence of many degenerative "Western" diseases, including diabetes (1), coronary heart disease (2), and some cancers (3). The mechanism(s) of the protective effect of whole-grain cereals have not been fully elucidated, but are suggested to be due to the high amount of fiber, minerals, vitamins, and phenolic compounds associated with the dietary fiber complex (4). One of the main groups of phenolic compounds in whole-grain wheat and rye is a class of phenolic lipids, the alkylresorcinols (AR).3

AR are 1,3 dihydroxy-5-alkylbenzene derivatives present in whole-grain wheat (Triticum aestivum) and rye (Secale cereale) at levels of 320-1430 and 360-3200 µg/g, respectively [(5) and references therein]. AR are located in the outer layers of these cereals, and are therefore concentrated in bran, but are not present in refined flour (5). AR are also found in high levels in other types of Triticum and in triticale (Triticosecale X) and in low amounts in barley (Hordeum vulgare) (5). Cereal AR are present as odd-numbered alkyl-chain length homologues between 15:0 and 25:0 (5). AR analogs with an unsaturated and/or oxygenated alkyl chain are also present in high amounts in rye (~15–20% of total AR) (5–7).

Interest in the nutritional properties of AR was first sparked by the work of Wieringa (8), who suggested that AR were responsible for the decreased growth of animals fed rye. Another study in rats showed decreased growth of rats fed diets high in semipure synthetic AR (9). Later studies found that the decreased growth was due mainly to the soluble fiber fraction of rye, and not to AR (10,11).

In vitro, AR have been reported to have anticancer, enzyme-inhibiting, and DNA-cleaving properties (12). Although AR are reported to be antioxidants (13), the hydroxyl substituents are in the meta position on the phenolic ring; thus they are weak antioxidants in vitro compared with {alpha}-tocopherol (11,14). Because AR are amphiphilic, they can form monolayers and insert into phospholipid membranes (12). This property may enable them to interfere with lipid absorption in the gastrointestinal tract. AR were also reported to interfere with enzymes that synthesize triacylglycerols in vitro (15,16) and inhibit the accumulation of triacylglycerols in cultured adipocytes (17). AR are also of interest as biomarkers of whole-grain wheat and rye intake in humans (11).

AR are absorbed by rats (18), pigs (18), and humans (19), at levels varying from 33 to 79%, suggesting that they may be absorbed in sufficient quantities to be biologically active. AR concentrations in the plasma of humans consuming high amounts of whole-grain rye were ~300 nmol/L (20). After rats consumed a single dose of radiolabeled AR, almost all (>99.9%) radioactivity was excreted after 6 d (18), although because AR are strongly lipophilic, they may accumulate in fatty tissues if they are consumed regularly.

Because AR are amphiphilic phenolic lipids with some structural similarities to tocopherols and tocotrienols, we hypothesized that they might interfere with their absorption and/or metabolism. In this study, the effect of three levels of AR on plasma and tissue total lipid, tocopherol, and cholesterol levels was tested in rats. The inhibition of tocopherol-{omega}-hydroxylase by AR in vitro as a possible mechanism of the effects of AR on tocopherols in vivo was also investigated.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 LITERATURE CITED
 
    Isolation of alkylresorcinols. AR were isolated from rye bran as described by Kozubek (21). The purity and homologue composition of the AR extract were determined by NMR and GC (22).

    Experimental animals, diets, and study design. Male, 21- to 23-d-old Sprague-Dawley rats (n = 32; B&K Universal AB) with a mean body weight of 52 g on d 0 were used for the study. The conditions for housing the rats were reported previously (23). The experiment was carried out in accordance with the guidelines of and approved by the Ethical Committee for Animal Experiments in the Uppsala region.

The composition of the semisynthetic basal diet was reported elsewhere (23). AR were added to the basal diet at concentrations of 1, 2, and 4 g/kg. The 32 rats were weighed and assigned to 4 groups of 8, with similar mean body weights. Rats were fed diets containing 0, 1, 2, and 4 g AR/kg feed for 4 wk and body weights were measured twice each week. The amount of feed given each day was adjusted for mean body weight so that the rats would consume all their feed. At the end of the experiment, the rats were deprived of feed for 12 h before i.p. injection of an overdose of sodium pentobarbital and killed by exsanguination. Blood samples were withdrawn from the vena cava, collected in EDTA tubes, and centrifuged (1000 x g, 10 min); blood plasma was transferred to test tubes with screw caps and stored at -20°C until analysis. Liver, lungs, and perirenal adipose tissue were excised, weighed, transferred to vials filled with 2-propanol, and stored at -80°C.

    Analysis of rat tissue samples. Plasma, lung, and liver lipids were extracted and analyzed for tocopherols, cholesterol, and fatty acids as described previously (24). In the plasma samples, lipoprotein fractions were separated and the tocopherol and cholesterol levels, and fatty acid distribution were determined (24). AR in perirenal adipose tissue samples were extracted by refluxing with chloroform for 2 h, followed by purification using solid phase extraction. After purification, AR were analyzed by TLC and staining with Fast Blue B (7) and GC (22). Blood cells (the pellet remaining after centrifugation of blood to separate plasma) were broken up by dilution with distilled water, followed by sonication in an ultra-sonic bath. AR from the blood cells were then extracted 3 times with 3 times volume ethyl acetate, with resonication in between each extraction. AR were then purified using solid phase extraction, and analyzed with TLC and GC as for the adipose tissue samples.

    Tocopherol-{omega}-hydroxylase activity. The effect of AR on tocopherol-{omega}-hydroxylase activity was evaluated in a hepatocyte cell culture assay. HepG2 cells (subclone C3A; American Type Culture Collection) were grown in DMEM containing 10% fetal bovine serum (FBS) under conditions recommended by the supplier and used 3–5 d postconfluence. Ethanolic stock solutions of purified synthetic 15:0 AR (14) and purified rye bran AR described earlier were first added drop-wise to FBS, which was then diluted 10-fold with DMEM for a final concentration of either 5 or 20 µmol/L. Sesamin (2 µmol/L; Cayman Chemicals) was used as a positive control. Cells were preincubated with a medium containing the AR for 4 h, after which the medium was changed to one containing 25 µmol/L {gamma}-tocopherol and either 5 or 20 µmol/L of either 15:0 or purified rye bran AR. After 48 h of incubation, the concentrations of {gamma}-tocopherol metabolites, 3'- and 5'-{gamma}-carboxychromanol, in the medium were determined by GC-MS of their trimethylsilyl ethers, using d9-{alpha}-3'-carboxychromanol as an internal standard, as previously described (25). Total cell protein was determined by dye binding (Bio-Rad Protein Assay; Bio-Rad Laboratories). Experiments were carried out in triplicate.

    Statistical analyses. Statistical analysis was performed using one-way ANOVA with Tukey’s pairwise comparisons (Minitab version 11). Differences were considered significant at P < 0.05.


   RESULTS AND DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
LITERATURE CITED
 
The purified rye AR fed to the rats were estimated to be >99% AR or AR analogs, of which ~20% were present as unsaturated or other derivatives of AR. The homologue composition of the purified AR (15:0, 1.5%; 17:0, 25.7%; 19:0, 34.4%; 21:0, 22.7%; 23:0, 9.0%; 25:0, 6.7%) differed slightly from rye AR in whole kernels (22) with a slightly higher proportion of shorter-chain AR homologues (15:0 and 17:0). The levels of AR fed to rats in this study were selected to be similar to those in whole-grain rye (1 g/kg) and rye bran (4 g/kg). Food products made from the whole grain or the bran of wheat and rye contain 0.2–1.8 g AR/kg (5). The total intake for a person consuming a diet high in whole-grain wheat has been estimated to be 200 mg AR/d (18), or ~3 mg AR/(kg body weight · d). In this study, the rats were fed between 100 and 410 mg AR/(kg body weight · d), a higher dose than what is possible in a normal human diet, but perhaps possible for animals fed high amounts of whole-grain wheat or rye, or wheat or rye bran.

Rats fed 1 and 2 g AR/kg diet did not differ in weight from the control rats throughout the study, whereas rats fed 4 g AR/kg diet weighed slightly, but significantly less during the first 9 d (P < 0.01); however, they did not differ from the rats fed the other diets during the last 2 wk of the study (Table 1). Liver, lung, and perirenal adipose tissue weights did not differ among rats when they were killed (data not shown). Studies on the effect of AR on rats have focused on their effect as appetite- and growth-depressing substances in rye, as proposed by Wieringa (8) and Sedlet et al. (9). The rats in this study always ate all their feed, with no apparent appetite-suppressing effect of AR as previously suggested (9). Other studies in rats showed that AR have no effect on growth (26) or performance (27). Rakowska et al. (28) found that 1 g AR/kg diet had no effect on growth, but 2 g AR/kg diet did, suggesting that AR may be growth inhibiting at high doses. The idea that AR have an antinutritional effect cannot be ruled out by this study because we did not directly test this. However, the results suggest that a diet extremely high in AR may have a small, short-term effect on the growth of young rats, but otherwise does not negatively affect their performance.


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  		TABLE 1 Weekly live body weights of rats fed 0, 1, 2, or 4 g alkylresorcinols/kg diet1

 
Compared with controls, rats fed AR had elevated {gamma}-tocopherol ({gamma}-T) concentrations in the liver and lungs (P < 0.01), whereas the effects on plasma {alpha}-T were minor (Table 2). AR did not affect plasma cholesterol concentrations or fatty acid composition (results not shown). The 4 g AR/kg diet caused a 47% decrease in liver cholesterol (P < 0.001) and a 35% decrease in the percentage of cholesterol in liver lipids compared with the control diet (P < 0.05) (Table 3).


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  		TABLE 2 Plasma and tissue tocopherol concentrations of rats fed 0, 1, 2, or 4 g alkylresorcinols/kg diet for 4 wk1

 

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  		TABLE 3 Liver lipid and cholesterol concentrations of rats fed 0, 1, 2, or 4 g alkylresorcinols/kg diet for 4 wk1

 
We hypothesized that the observed increase in liver and lung {gamma}-T in rats fed AR was via inhibition of elimination of {gamma}-T by the tocopherol-{omega}-hydroxylase pathway recently described (29). This was investigated by testing the effect of AR on the metabolism of {gamma}-T to its water-soluble hydroxychroman metabolites in Hep G2 cell cultures previously shown to express this activity (30). Both synthetic AR (15:0) and purified rye AR inhibited the synthesis of {gamma}-T metabolites in a dose-dependent manner (Fig. 1). The alkyl chain of AR may undergo metabolism by {omega}-oxidation (31) in a manner analogous to that of tocopherols. Sesamin is a lignan that strongly inhibits tocopherol-{omega}-hydroxylase activity in hepatocytes (24) by blocking cytochrome P450-dependent {omega}-hydroxylation of tocopherols (29). Sesamin had a more pronounced effect on {gamma}-T levels in rats (32,33) than the AR in this study, and inhibited tocopherol metabolism in Hep G2 cells by 95% at a concentration of 2 µmol/L (Fig. 1). The moderate increase in {gamma}-T levels in rats fed AR and the weaker effects on tocopherol metabolite formation in vitro compared with sesamin suggest that AR may competitively inhibit tocopherol metabolism. This was supported by the dose-dependent increase in {gamma}-T concentrations in the liver of rats with increasing doses of AR (Table 2) and by the finding of AR metabolites in human urine, apparently resulting from ß-oxidation of the alkyl chain (11,31). Synthetic AR (15:0) had a greater inhibitory effect on tocopherol metabolism than similar concentrations of purified rye AR (84 and 47% inhibition at 20 µmol/L, respectively). This difference may be due to the difference in overall lipophilicity of 15:0 compared with the mixed rye AR (15:0–25:0). In vitro and in vivo, the less methylated tocopherols ({gamma}-T and {delta}-T) are more extensively metabolized via the tocopherol-{omega}-hydroxylase pathway than the more lipophilic {alpha}-T (29). Alternatively, AR with alkyl chains longer than 15 carbons (close to that of tocopherols) may be poorer substrates for {omega}-oxidation, at least by the enzyme responsible for {omega}-hydroxylation of tocopherols, and therefore less able to compete for enzyme binding.



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  		FIGURE 1 Inhibition of {gamma}-tocopherol metabolism by alkylresorcinols in HepG2 cells in vitro. Rye alkylresorcinols = purified (99%) rye AR (15:0–25:0); 15:0 = synthetic pentadecylresorcinol. Sesamin is a positive control. {gamma}-Tocopherol metabolites measured were 3'- and 5'-{gamma}-carboxychromanol. Values are means ± SEM, n = 3. Bars not sharing a letter differ, P < 0.05.

 
There is no ready explanation for why 4 g/kg AR dramatically decreased liver cholesterol when similar effects did not occur in plasma or in the other groups fed AR. Because AR are amphiphilic and can disrupt and form membranes that can incorporate other lipid components (34), they may interfere with the absorption of lipids, or compete for lipid transport, as observed for phytosterols (35); if this was the case, a difference in plasma cholesterol should have also been observed. It is also possible that AR inhibit some of the enzymes involved in cholesterol synthesis. Sesamin, which increases {gamma}-T levels in rats (32,33), also lowers cholesterol levels in rats, by inhibiting both its absorption and synthesis (36).

Perirenal adipose tissue samples from rats consuming AR diets contained unchanged AR that could be detected by both TLC and GC. The amount recovered was ~2–4 µg AR/g fresh adipose tissue, although the efficiency of the recovery of AR was not determined. Because AR are highly lipophilic [octanol/water coefficient (log P) of rye AR ranges from 8.5 to 13.4 (11)], they would probably partition into fatty tissues, as appeared to be the case in this study. Low amounts of unchanged AR were also detected in the blood cells (blood minus the plasma) of the rats fed AR. Previous studies showed that AR from rye can insert into and alter the structure of erythrocyte membranes (37,38). Further studies are required to determine whether AR can be detected in other tissues and whether they affect the tissues in which they are present.

Consumption of a diet rich in whole-grain cereals was demonstrated to decrease the risk of coronary heart disease (8) by a mechanism that has not been fully explained, but has been suggested to involve dietary fiber, minerals, vitamins, and other beneficial phytochemicals (4). A low concentration of {gamma}-T has been associated with an increased risk of coronary heart disease (39), suggesting that compounds that can increase levels of this form of vitamin E in the body may contribute to the prevention of heart disease. AR may be one of many compounds present in whole-grain wheat and rye that could play a role in the health benefits arising from regular consumption of these cereals.


   ACKNOWLEDGMENTS
 
The authors thank Siv Tengblad and Barbro Simu (Department of Public Health and Caring Sciences/Geriatrics, Uppsala University) for their skilled technical assistance.


   FOOTNOTES
 
2 Y.C. was funded by the LiFT (Future Technologies for Food Production) programme. Back

3 Abbreviations used: AR, alkylresorcinol(s); FBS, fetal bovine serum; T, tocopherol. Back

Manuscript received 29 October 2003. Initial review completed 1 December 2003. Revision accepted 10 December 2003.


   LITERATURE CITED
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 LITERATURE CITED
 

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R. Landberg, A.-M. Linko, A. Kamal-Eldin, B. Vessby, H. Adlercreutz, and P. Aman
Human Plasma Kinetics and Relative Bioavailability of Alkylresorcinols after Intake of Rye Bran
J. Nutr., November 1, 2006; 136(11): 2760 - 2765.
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W.-H. Wu, Y.-P. Kang, N.-H. Wang, H.-J. Jou, and T.-A. Wang
Sesame Ingestion Affects Sex Hormones, Antioxidant Status, and Blood Lipids in Postmenopausal Women
J. Nutr., May 1, 2006; 136(5): 1270 - 1275.
[Abstract] [Full Text] [PDF]

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