The aim of this study was to evaluate tissue distribution of vitamin E isoforms such as α- and γ-tocotrienol and γ-tocopherol and interference with their tissue accumulation by α-tocopherol. Rats were fed a diet containing a tocotrienol mixture or γ-tocopherol with or without α-tocopherol, or were administered by gavage an emulsion containing tocotrienol mixture or γ-tocopherol with or without α-tocopherol. There were high levels of α-tocotrienol in the adipose tissue and adrenal gland, γ-tocotrienol in the adipose tissue, and γ-tocopherol in the adrenal gland of rats fed tocotrienol mixture or γ-tocopherol for 7 weeks. Dietary α-tocopherol decreased the α-tocotrienol and γ-tocopherol but not γ-tocotrienol concentrations in tissues. In the oral administration study, both tocopherol and tocotrienol quickly accumulated in the adrenal gland; however, their accumulation in adipose tissue was slow. In contrast to the dietary intake, α-tocopherol, which has the highest affinity for α-tocopherol transfer protein (αTTP), inhibited uptake of γ-tocotrienol to tissues including adipose tissue after oral administration, suggesting that the affinities of tocopherol and tocotrienol for αTTP in the liver were the critical determinants of their uptake to peripheral tissues. Vitamin E deficiency for 4 weeks depleted tocopherol and tocotrienol stores in the liver but not in adipose tissue. These results indicate that dietary vitamin E slowly accumulates in adipose tissue but the levels are kept without degradation. The property of adipose tissue as vitamin E store causes adipose tissue-specific accumulation of dietary tocotrienol.
SummaryWe previously found that 2,7,8-trimethyl-2(2 ′ -carboxyethyl)-6-hydroxychroman ( ␥ CEHC), a metabolite of the vitamin E isoforms ␥ -tocopherol or ␥ -tocotrienol, accumulated in the rat small intestine. The aim of this study was to evaluate tissue distribution of vitamin E metabolites. A single dose of ␣ -tocopherol, ␥ -tocopherol or a tocotrienol mixture containing ␣ -and ␥ -tocotrienol was orally administered to rats. Total amounts of conjugated and unconjugated metabolites in the tissues were measured by HPLC with an electrochemical detector, and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (trolox) was used as an internal standard. Twenty-four hours later, the vitamin E isoforms were detected in most tissues and in the serum. However, 2,5,7,8-tetramethyl-2(2 ′ -carboxyethyl)-6-hydroxychroman ( ␣ CEHC), a metabolite of ␣ -tocopherol or ␣ -tocotrienol, and ␥ CEHC accumulated in the serum and in some tissues including the liver, small intestine and kidney. Administration of ␣ -tocopherol increased the ␥ CEHC concentration in the small intestine, suggesting that ␣ -tocopherol enhances ␥ -tocopherol catabolism. In contrast, ketoconazole, an inhibitor of cytochrome P450 (CYP)-dependent vitamin E catabolism, markedly decreased the ␥ CEHC concentration. These data indicate that vitamin E metabolite accumulates not only in the liver but also in the small intestine and kidney. We conclude that some dietary vitamin E is catabolized to carboxyethyl-hydroxychroman in the small intestine and is secreted into the circulatory system. Key Words carboxyethyl-hydroxychroman, tocopherol, tocotrienol, vitamin E Vitamin E is a fat-soluble antioxidant that inhibits lipid peroxidation in biological membranes. In nature, compounds with vitamin E activity are ␣ -,  -, ␥ -or ␦ -tocopherol and ␣ -,  -, ␥ -or ␦ -tocotrienol. ␣ -and ␥ -tocopherol are abundant in dietary vitamin E while tocotrienol is only present in some plant sources, such as palm oil and rice bran, while daily foods contain low levels of tocotrienol. The dietary vitamin E isoforms are absorbed in the small intestine, secreted with triacylglycerol-rich chylomicrons into the lymph and blood, and then transported to the liver ( 1 , 2 ). The vitamin E isoform ␣ -tocopherol is preferentially incorporated into VLDL and transported to tissues by lipoprotein ( 3 , 4 ) because of its high affinity for ␣ -tocopherol transfer protein ( ␣ TTP) ( 5 ). In contrast, the other vitamin E isoforms, including ␥ -tocopherol and tocotrienol, are catabolized and excreted. Therefore, ␣ -tocopherol has the highest biological activity among vitamin E isoforms.All vitamin E isoforms undergo catabolism to phytyl short-chain carboxyethyl hydroxychromans (CEHC) such as 2,5,7,8-tetramethyl-2(2 ′ -carboxyethyl)-6-hydroxychroman ( ␣ CEHC), a metabolite of ␣ -tocopherol and ␣ -tocotrienol, and 2,7,8-trimethyl-2(2 ′ -carboxyethyl)-6-hydroxychroman ( ␥ CEHC), a metabolite of ␥ -tocopherol and ␥ -tocotrienol ( 6-8 ). The catabolic pathway involves -hydroxylation of the phytyl chain and ...
We have shown that intake of sesame seed and its lignan increases vitamin E concentrations and decreases urinary excretion levels of vitamin E metabolites in male Wistar rats, suggesting inhibition of vitamin E catabolism by sesame lignan. The aim of this study was to examine whether dietary sesame seed also increased vitamin K concentrations, because its metabolic pathway is similar to that of vitamin E. To test the effect of sesame lignan on vitamin K concentrations, male Wistar rats were fed a control diet or a diet with 0.2% sesamin (a sesame lignan) for 7 d in experiment 1. Liver phylloquinone (PK), menaquinone-4 (MK-4), and γ-tocopherol were greater in rats fed sesamin than in control rats. To test the effect of sesame seed on vitamin K concentrations, male Wistar rats were fed a control diet or a diet with 1, 5, or 10% sesame seed for 3 d in experiment 2. Liver and kidney PK and γ-tocopherol but not MK-4 were greater in rats fed sesame seed than in control rats, although differences in dietary amounts of sesame seed did not affect the PK concentrations. For further confirmation of the effect of sesame seed, male Wistar rats were fed a control diet or a diet with 20% sesame seed for 40 d in experiment 3. Kidney, heart, lung, testis, and brain PK and brain MK-4 were greater in rats fed sesame seed than in control rats. The present study revealed for the first time, to our knowledge, that dietary sesame seed and sesame lignan increase not only vitamin E but also vitamin K concentrations in rat tissues.
Excess α-tocopherol decreased extrahepatic PK in rats fed PK but not MK-4 in rats fed MK-4.
From an enzyme kinetic study using rat liver microsomes, α-tocopherol has been suggested to accelerate the other vitamin E catabolism by stimulating vitamin E ω-hydroxylation, the late limiting reaction of the vitamin E catabolic pathway. To test the effect of α-tocopherol on catabolism of the other vitamin E isoforms in vivo, we determined whether α-tocopherol accelerates depletion of γ-tocopherol and tocotrienol and excretion of their metabolites in rats. Male Wistar rats were fed a γ-tocopherol-rich diet for 6 weeks followed by a γ-tocopherol-free diet with or without α-tocopherol for 7 days. Intake of γ-tocopherol-free diets lowered γ-tocopherol concentrations in serum, liver, adrenal gland, small intestine, and heart, but there was no effect of dietary α-tocopherol on γ-tocopherol concentrations. The level of urinary excretion of γ-tocopherol metabolite was not affected by dietary α-tocopherol. Next, the effect of α-tocopherol on tocotrienol depletion was examined using rats fed a tocotrienol-rich diet for 6 weeks. Subsequent intake of a tocotrienol-free diet with or without α-tocopherol for 7 days depleted concentrations of α- and γ-tocotrienol in serum and tissues, which was accompanied by a decrease in the excretion of γ-tocotrienol metabolite. However, neither the tocotrienol concentration nor γ-tocotrienol metabolite excretion was affected by dietary α-tocopherol. These data showed that dietary α-tocopherol did not accelerate the depletion of γ-tocopherol and tocotrienol and their metabolite excretions, suggesting that the positive effect of α-tocopherol on vitamin E ω-hydroxylase is not sufficient to affect the other isoform concentrations in tissues.
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