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Our objective in this study was to determine whether a mitochondda-targeted vitamin E derivative (MitoVit E) would decrease oxidative stress and associated obesity by preventing a previously proposed aconitase inhibition cascade. Sixty-four mice were fed a high-fat (HF) diet for 5 wk. They were then switched to either a low-fat (LF) or a medium-fat (MF) diet and gavaged with MitoVit E (40 mg MitoVit E kg body [weight.sup.-1]) or drug vehicle (10% ethanol in 0.9% NaCl solution) every other day for 5 wk. Epididymal fat weight, as well as liver lipid and remaining carcass lipid, were significantly lower in the MF group receiving MitoVit E (MF-E) than in the MF group receiving vehicle only (MF-C). Liver mitochondrial [H.sub.2][O.sub.2] production and the protein carbonyl level were also significantly lower in MF-E than in MF-C mice. In contrast, none of the biochemical variables (aconitase activity, ATP and [H.sub.2][O.sub.2] production, and protein carbonyl level) in the muscle mitochondria were modified by MitoVit E in either MF or LF groups. Expression of acetyl-CoA carboxylase and fatty acid synthase in both liver and adipose tissue of MF groups was not affected by MitoVit E. However, expression of carnitine palmitoyltransferase 1 a in the liver and uncoupling protein 2 in adipose tissue were significantly enhanced by MitoVit E in both LF and MF groups. In conclusion, MitoVit E attenuates hepatic oxidative stress and inhibits fat deposition in mice but not through alleviation of the aconitase inhibition cascade. doi: 10.3945/jn.110.121715.

The aim of this experiment was to clarify the contribution of the [alpha]-tocopherol transfer activity of lipoprotein lipase (LPL) to vitamin E transport to tissues in vivo. We studied the effect of Triton WR1339, which prevents the catabolism of triacylglycerol-rich lipoproteins by LPL on vitamin E distribution in rats. Vitamin E-deficient rats fed a vitamin E-free diet for 4 wk were injected with Triton WR1339 and administered by oral gavage an emulsion containing 10 mg of [alpha]-tocopherol, 10 mg of [gamma]-tocopherol, or 29.5 mg of a tocotrienol mixture with 200 mg of sodium taurocholate, 200 mg of triolein, and 50 mg of albumin, [alpha]-Tocopherol was detected in the serum and other tissues of the vitamin E-deficient rats, but [gamma]-tocopherol, [alpha]- and [gamma]-tocotrienol were not detected. Triton WR1339 injection elevated (P < 0.05) the serum [alpha]-tocopherol concentration and inhibited (P < 0.05) the elevation of [alpha]-tocopherol concentration in the liver, adrenal gland, and spleen due to the oral administration of [alpha]-tocopherol. Neither [alpha]-tocopherol administration nor Triton WR1339 injection affected (P [greater than or equal to] 0.05) the [alpha]-tocopherol concentration in the perirenal adipose tissue, epididymal fat, and soleus muscle despite a high expression of LPL in the adipose tissue and muscle. These data show that [alpha]-tocopherol transfer activity of LPL in adipose tissue and muscle is not important for [alpha]-tocopherol transport to the tissue after [alpha]-tocopherol intake or that the amount transferred is small relative to the tissue concentration. Furthermore, Triton WR1339 injection tended to elevate the serum [gamma]-tocopherol (P= 0.071) and [alpha]-tocotrienol (P = 0.053) concentrations and lowered them (P < 0.05) in the liver and adrenal gland of rats administered [gamma]-tocopherol or [alpha]-tocotrienol. These data suggest that lipolysis of triacylglycerol-rich chylomicron by LPL is necessary for postprandial vitamin E transport to the liver and subsequent transport to the other tissues.

Previous studies comparing the biokinetics of deuterated natural (RRR) and synthetic (all-rac) [alpha]-tocopherol (vitamin E) used a simultaneous ingestion or competitive uptake approach and reported relative bioavailability ratios close to 2:1, higher than the accepted biopotency ratio of 1.36:1. The aim of the current study was to compare the biokinetics of deuterated natural and synthetic vitamin E using a noncompetitive uptake model both before and after vitamin E supplementation in a distinct population. Healthy men (n = 10) carrying the apolipoprotein (apo)E4 genotype completed a randomized crossover study, comprised of two 4-wk treatments with 400 mg/d (RRR-[alpha]-tocopheryl and all-rac-[alpha]-tocopheryl acetate) with a 12-wk washout period between treatments. Before and after each treatment period, the subjects consumed a capsule containing 150 mg deuterated [alpha]-tocopheryl acetate in either the RRR or all-rac form depending on their treatment regimen. Blood was obtained up to 48 h after ingestion, and tocopherols analyzed by LC/MS. After deuterated all-rac administration, plasma deuterated tocopherol maximum concentrations and area under the concentration vs. time curves (AUC) were lower than those following RRR administration. The RRR:all-rac ratios determined from the deuterated biokinetic profiles (maximum concentration; [C.sub.max]) and AUCs were 1.35:1 [+ or -] 0.17 and 1.33:1 [+ or -] 0.18, respectively. The 4-wk supplementation with either RRR or all-rac significantly increased plasma [alpha]-tocopherol concentrations (P < 0.001), but decreased the plasma response to newly absorbed deuterated RRR or all-rac [alpha]-tocopherol. Using a noncompetitive uptake approach, the relative bioavailability of natural to synthetic vitamin E in apoE4 males was close to the currently accepted biopotency ratio of 1.36:1. KEY WORDS: * tocopherol * natural * synthetic * biokinetics * bioavailability * apoE4

Previous studies have shown that deficiencies in selenium (Se) and/or vitamin E (VE) can exacerbate the infectivity and pathogenesis of coxsackievirus B3 and influenza. Both Se and VE play a role in immune function and antioxidant defense. To determine whether these deficiencies would affect the normal course of infection with a metazoan parasite, mice were made deficient in Se and/or VE and inoculated with the gastrointestinal nematode parasite Heligmosomoides polygyrus. Both primary and secondary infections were assessed. Although the course of a primary infection with H. polygyrus was unaffected by diet, diets deficient in Se, VE, and both Se and VE (Se/VE double-deficiency) all caused delayed adult worm expulsion and increased fecundity during a secondary infection; suggesting an impaired intestinal response. H. polygyrus-induced IL-4 levels were diet-independent; but Se/VE double-deficiency blocked the H. polygyrus-induced IL-4 receptor-associated decrease in sodium-dependent glucose absorption in the jejunum that contributes to worm expulsion. In contrast, Se/VE double-deficiency had no effect on the infection-induced, IL-4R-associated increase in epithelial cell permeability that accompanies the infection. These results suggest that both Se and VE are required for specific IL-4-related changes in intestinal physiology that promote host protection against H. polygyrus. KEY WORDS: * selenium * vitamin E * parasite * immunity * gastrointestinal

Vitamin E is a lipophilic chain-breaking antioxidant that prevents lipid peroxidation. Although cigarette smoke is a potent source of oxidative stress that depletes vitamin E in vitro, it is unclear whether it has a similar effect in vivo, particularly in humans. Therefore, this review will discuss the role of cigarette smoke on [gamma]-tocopherol ([gamma]-T) nitration, its effect on [alpha]-tocopherol ([alpha]-T) biokinetics in smokers, and the changes in the synthesis, plasma concentrations, and urinary excretion of the vitamin E metabolite (CEHC; carboxy-ethyl-hydroxy-chroman). Last, the possibility of CEHC as a biomarker of vitamin E status will be assessed as will the question whether smokers have increased dietary requirements of vitamin E.

In this study, the effect of dietary vitamin E on the hepatic tumor-promoting activity of PCB-77 and PCB-153 in female Sprague-Dawley rats (175-200 g) was investigated. One week after diethylnitrosamine injection, rats were fed purified diets containing 10, 50, or 250 mg/kg vitamin E in the form of [alpha]-tocopheryl acetate. Starting 1 wk later, we injected rats i.p. with vehicle (corn oil) or PCB-77 or PCB-153 (300 [micro]mol/kg) every 14 d for 4 injections. All rats were killed 10 d after the last PCB injection. The number and volume of placental glutathione S-transferase (PGST)-positive foci were increased by PCB-77 but not by PCB-153. Vitamin E did not affect the induction of PGST-positive foci. PCB-77, but not PCB-153, increased hepatic NF-[kappa]B activity. In conclusion, dietary vitamin E supplementation does not protect against the induction of altered hepatic focal lesions by PCBs. KEY WORDS: * polychlorinated biphenyls * vitamin E * altered hepatic foci * NF-[kappa]B

During a study of the effect of vitamin E in activated mouse macrophages, we observed a reduction in the viability of cells treated with various forms of vitamin E. We show this report that some tocopherols (both [gamma]- and [delta]-tocopherol) are cytotoxic to some but not all cell types. Mouse macrophages were especially sensitive (40 [micro]mol/L), whereas human hepatocytes and bovine endothelial cells were almost completely refractory (90 [micro]mol/L). The fully methylated tocopherol, [alpha]-tocopherol ([alpha]-Toc), was not cytotoxic in any cell type tested. The cytotoxicity observed with [delta]-tocopherol ([delta]-Toc) was associated with 2 markers of apoptosis. Vitamer-specific cytotoxicity was not due to differences in cellular uptake/accumulation because both [alpha]-Toc and [delta]-Toc accumulated equally in any cell type tested. In contrast, the cell-specific cytotoxicity was related in part to uptake/accumulation of the tocopherols. Macrophages accumulated nearly 5 times more tocopherol compared with hepatocytes cultured under similar conditions. To address the hypothesis that uptake accounted for the cell-specific sensitivity, we developed a macrophage 'subtype' that was markedly resistant (>150 [micro]mol/L) to [delta]-Toc. Under many different cell culture conditions (including human serum) uptake/accumulation of tocopherols was reduced in this subtype by ~50%. Further selection and evaluation of this phenotype, however, demonstrated no cytotoxicity even when cellular levels were elevated. Our results show that undermethylated tocopherols are cytotoxic to macrophages and that there are independent and selectable processes that determine cellular tocopherol uptake/accumulation and [delta]-Toc cytotoxicity. KEY WORDS: * tocopherol * macrophage * cellular accumulation * vitamin E * toxicity

Epidemiological studies suggest that consumption of vegetables rich in the xanthophylls lutein (LUT) and zeaxanthin (ZEA) reduces the risk for developing age-related cataract, a leading cause of vision loss. Although LUT and ZEA are the only dietary carotenoids present in the lens, direct evidence for their photoprotective effect in this organ is not available. The present study examined the effects of xanthophylls and [alpha]-tocopherol ([alpha]-TC) on lipid peroxidation and the mitogen-activated stress signaling pathways in human lens epithelial (HLE) cells following ultraviolet B light (UVB) irradiation. When presented with LUT, ZEA, astaxanthin (AST), and [alpha]-TC as methyl-[beta]-cyclodextrin complexes, HLE cells accumulated the lipophiles in a concentration- and time-dependent manner with uptake of LUT exceeding that of ZEA and AST. Pretreatment of cultures with either 2 [micro]mol/L xanthophyll of 10 [micro]mol/L [alpha]-TC for 4 h before exposure to 300 J/[m.sup.2] UVB radiation decreased lipid peroxidation by 47-57% compared with UVB-treated control HLE cells. Pretreatment with the xanthophylls and [alpha]-TC also inhibited UVB-induced activation of c-JUN N[H.sub.2]-terminal kinase (JNK) and p38 by 50-60 and 25-32%, respectively. There was substantial inhibition of UVB-induced JNK and p38 activation for cells containing 2.3 nmol [alpha]-TC/mg protein was required to significantly decrease UVB-induced stress signaling. These data suggest that xanthophylls are more potent than [alpha]-TC for protecting human lens epithelial cells against UVB insult. KEY WORDS: * lutein * zeaxanthin * MAPK stress signaling * lipid peroxidation * human lens epithelial cells

Oxidized fats affect animal metabolism in several ways. To gain a comprehensive understanding of the molecular mechanisms underlying the effects of dietary oxidized rats in rats at varying dietary vitamin E concentrations, the gene expression profile of the liver was monitored with an array containing 1176 binding sites for cDNAs. Rats were fed diets with a fresh fat and vitamin E concentrations of 25 or 250 mg [alpha]-tocopherol/kg (FF25, FF250 rats) or a fat heated at 50[degrees]C for 38 d, with vitamin E concentrations of 25 or 250 mg [alpha]-tocopherol/kg (OF25, OF250 rats) for 63 d. Differences in gene expression were considered to be significant at a ratio of at least 1.4. In the OF25 rats, the expression of 47 genes was altered; in the OF250 rats, the expression of 37 genes was altered, and in the FF250 rats, the expression of 21 genes was altered compared with FF25 rats. In both OF25 and OF250 rats, a series of target genes of the peroxisome proliferator-activated receptor [alpha] (PPAR[alpha]) was upregulated. Determination of gene expression of acyl CoA oxidase and activity of catalase confirmed that oxidized fats caused peroxisome proliferation in the liver. In OF25 and OF250 rats, there was also upregulation of 12 and 5 genes involved in xenobiotic metabolism and stress response, of 7 and 7 genes involved in protein metabolism, of 5 and 2 genes encoding intracellular effectors or modulators and of 5 and 6 genes, respectively, encoding activators or repressors of transcription or translation. In conclusion, this study provides indirect evidence that dietary oxidized fats cause an activation of the PPAR[alpha], irrespective of the dietary vitamin E concentration. Identification of several other differentially regulated genes may be helpful to understand the effects of oxidized rats on animal metabolism. KEY WORDS: * rats * oxidized rats * vitamin E * cDNA array * gene expression

We showed previously that dietary antioxidant depletion enhances tumor reactive oxygen species (ROS) and apoptosis, resulting in a reduction in brain tumor size in the [TgT.sub.121] transgenic mouse model, a nonmetastatic tumor model. Here, in a transgenic mouse model of mammary tumorigenesis with defined rates of tumor growth and lung-targeted metastasis, we determined the ability of dietary antioxidant depletion to inhibit tumor growth and metastasis. Compared with control mice fed a standard diet, antioxidant-depleted mice exhibited tumor-targeted generation of ROS manifested by increased levels of oxidatively modified DNA/RNA (8-hydroxy-2'-deoxyguanine, 8-hydroxyguanine) and lipid peroxidation (4-hydroxy-2-nonenal) in primary and metastatic tumor foci. In addition to increased tumor-targeted ROS, the number of apoptotic cells was increased approximately 500% (P < 0.01) and terminal dUTP nucleotide DNA end-labeling-positive cells 200% (P < 0.01) in mice fed the antioxidant-depleted diet, whereas the percentage of tumor cells undergoing mitosis was >50% lower than in controls (P < 0.01). The proportional distribution of small ( KEY WORDS: * antioxidant * apoptosis * mammary neoplasm * metastasis * reactive oxygen species

The effects of oral doses of canthaxanthin on tissue distribution of [Alpha]- and [Gamma],-tocopherols were investigated in three experiments in male and female Balb/c mice. Mice were assigned to receive canthaxanthin [7 or 14 [[micro]gram]/(g body weight * d)] or placebo (olive oil) by gavage for different periods of time (0, 1, 2, 4 and 6 wk). A 2 wk-treatment with canthaxanthin resulted in incorporation of the carotenoid in all tissues analyzed, including liver, spleen, kidney, lung and heart. In liver, the maximum accumulation of the carotenoid was reached after 2 wk of dosing in female mice and after 6 wk in male mice. Canthaxanthin incorporation was accompanied by changes in [Alpha]- and -[Gamma]-tocopherol concentrations in plasma and tissues. These included the following: 1) a significant increase (P < 0.001) in [Alpha]-tocopherol concentration in spleen (21 and 27% in male and female mice, respectively) after 2 wk and in liver ([approximately]50% in both male and female mice) after 6 wk; 2) a significant decrease in [Gamma]-tocopherol concentration in plasma (P < 0.05) and tissues (P < 0.001) after 2 wk of treatment. In female mice, this decrease was 55% in plasma, 45% in liver, 44% in kidney, 71% in lung and 70% in heart. In male mice, the decrease was observed only in plasma (30%), kidney (54%) and heart (46%). In liver, the decrease in [Gamma]-tocopherol concentration was both dose- and time-dependent and significantly (P < 0.001) greater in female than in male mice. We conclude that dietary administration of canthaxanthin modifies tocopherol status in murine tissues. KEY WORDS: * canthaxanthin * [Alpha]-tocopherol * [Gamma]-tocopherol * mice * tissue distribution

The effect of a short-term, high-dose intramuscular injection of d-[Alpha]-tocopherol was studied in pigs given a challenge dose of lipopolysaccharide (LPS). Twenty-four pigs surgically fitted with jugular catheters were used in a 2 x 2 factorial design. Pigs received either 0 or 600 mg d-[Alpha]-tocopherol by intramuscular injection for 3 d before receiving an intraperitoneal injection of saline containing either 0 or 5 [[micro]gram]/kg body weight Escherichia coil LPS. Blood was collected from indwelling jugular catheters at 0, 1, 2, 4, 6, 8, 12 and 24 h after injection of LPS. Plasma [Alpha]-tocopherol levels were 13-fold greater (P < 0.01) at time 0 in pigs pretreated with 600 mg d-[Alpha]-tocopherol (9.9 [+ or -] 1.3 mg/L) than in those not treated with d-[Alpha]-tocopherol (0.74 [+ or -] 0.09 mg/L). Injection of LPS increased (P < 0.05) plasma levels of interleukin-6 (IL-6) and cortisol at 2-h postinjection, regardless of vitamin E treatment. However, pigs that received [Alpha]-tocopherol before the LPS challenge had substantially lower (P < 0.05) peak levels of IL-6 and cortisol than pigs not receiving [Alpha]-tocopherol. These results suggest that supplementation with a surfeit level of vitamin E reduces the response of pigs to endotoxin. KEY WORDS: * vitamin E * lipopolysaccharide * interleukin-6 * cortisol * pigs

The reaction of superoxide (a reactive oxygen species) and nitric oxide (one of the nitrogen oxides with numerous biological functions) results in the production of peroxynitrite. The characteristics of oxidation of [Alpha]-tocopherol (vitamin E) in synaptosomes (nerve ending particles) and mitochondria by peroxynitrite were studied. The subcellular fractions were isolated from brain hemispheres of 4-month-old male Fischer 344 rats by standard centrifugation procedures involving Ficoll gradients. Peroxynitrite treatment oxidized [Alpha]-tocopherol in KEY WORDS: rats brain vitamin E tocopherol oxidation peroxynitrite

Dietary intakes of retinol equivalents, [Alpha]-tocopherol equivalents, vitamin D and phylloquinone were estimated from three sets of 4-d weighed diet records and compared to three corresponding fasting plasma concentrations of retinol, 25-hydroxyvitamin D, [Alpha]-tocopherol, and phylloquinone measured in 34 healthy adults over 20 wk. The magnitude of the correlation between dietary vitamin intake and its corresponding biochemical measure is in part determined by the reproducibility of each of the measures, so within-to-between subject variance ratios were calculated for both dietary intakes and plasma concentrations. Phylloquinone was the only fat-soluble vitamin with a significant correlation between dietary intake and fasting plasma concentration (r = 0.51, P = 0.004). This correlation improved with an increase in both the number of independent diet records and independent plasma measures. Of the dietary intake measures, all the fat-soluble vitamins had greater within than between subject variance, with the highest measured for phylloquinone (6.86:1). Of the plasma measures, only phylloquinone had a within-to-between subject variance ratio greater than one (5.36:1). Comparisons across age and sex for dietary intake and plasma concentrations differed in pattern among the fat-soluble vitamins. KEY WORDS: * vitamin A * vitamin D * vitamin E * vitamin K * humans

The antioxidant effect of dietary [Beta]-carotene supplementation on the peroxidation potential of plasma was investigated in a randomized double-blind, placebo-controlled study. Twelve healthy women (62-80 y) supplemented their usual daily diet with 90 mg of [Beta]-carotene (n = 6) or placebo (n = 6) capsules for 3 wk. Plasma concentrations of [Beta]-carotene, [Alpha]- and [Gamma]-tocopherol, ascorbate, urate, bilirubin and in vitro production of phosphatidylcholine hydroperoxides (PC-OOH) and utilization of plasma antioxidants in the presence of 50 mmol/L 2,2[prime]-azobis (2-aminopropane) hydrochloride (AAPH), a free radical generator, at 37 [degrees] C were measured before and after dietary treatment. Plasma [Beta]-carotene increased from 0.76 [+ or -] 0.16 to 6.45 [+ or -] 1.16 [[micro]mol]/L (P < 0.05) in supplemented but not placebo-treated subjects. The plasma concentrations of other antioxidants did not change significantly in either group. [Beta]-Carotene supplementation did not affect basal levels of plasma PC-OOH as measured by HPLC post-column chemiluminescence but did affect AAPH-induced production of PC-OOH. Before supplementation, the induction period of plasma PC-OOH production was 2.4 [+ or -] 0.4 h, with levels reaching 5.39 [+ or -] 1.50 [[micro]mol]/L after 6 h of incubation. After supplementation, the induction period increased significantly to 4.2 [+ or -] 0.4 h (P < 0.01), with a lower PC-OOH production of 2.16 [+ or -] 0.90 [[micro]mol]/L after 6 h (P < 0.05). In this system, plasma ascorbate concentrations were depleted first, followed by loss of bilirubin and [Alpha]-tocopherol and then by the sequential loss of [Gamma]-tocopherol, urate and [Beta]-carotene. These results indicate that [Beta]-carotene supplementation increases the plasma antioxidant capacity of older women. INDEXING KEY WORDS: * tocopherol * humans * age * [Beta]-carotene * lipid peroxidation

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS, which is functionally similar to human AIDS. Vitamin E effects on immune functions, cytokine production and nutritional concentrations in retrovirus-infected mice were determined. Retrovirus infection inhibited release of inter-leukin-2 (IL) and interferon-[Gamma](IFN) and some immune functions, whereas it stimulated secretion of IL-4, IL-5, IL-6 and tumor necrosis factor-[Alpha] (TNF) and immunoglobulin (Ig) production. Furthermore, retrovirus infection induced some nutritional deficiencies in the tissues. A 15-fold increase in dietary vitamin E largely restored concentrations of some micronutrients (vitamins A and E, zinc and copper) in the liver, intestine, serum and thymus. It also partially restored production of IL-2 and IFN-[Gamma] by splenocytes. Retrovirus-induced elevated production of IL-4, IL-5 and IL-6 by splenocytes in vitro was normalized by vitamin E. Elevated release of IL-6, TNF-[Alpha], IgA and IgG produced by splenocytes in vitro during murine AIDS were also completely or partially normalized by vitamin E. Vitamin E also prevented retrovirus-induced suppression of splenocyte proliferation and natural killer cell activity. These data indicate that vitamin E supplementation during routine AIDS can help to ameliorate the disorders during routine AIDS, suggesting vitamin E usefulness in treatment of AIDS in humans. INDEXING KEY WORDS: vitamin E; cytokine; mice; murine AIDS; immune response

Vitamin E activity of sesame seed, which contains only gamma-tocopherol, a compound that has vitamin E activity equal to only 6-16% that of alpha-tocopherol, was examined in two experiments. In the first experiment, groups of rats were fed four diets: vitamin E-free control diet, alpha-tocopherol- containing diet, gamma-tocopherol-containing diet and sesame seed-containing diet. Changes in red blood cell hemolysis, plasma pyruvate kinase activity, and peroxides in plasma and liver, as indices of vitamin E activity, were examined. The sesame seed diet has high vitamin E activity, whereas this activity was low in the gamma-tocopherol diet. In plasma and liver, alpha-tocopherol was found in high concentration only in the alpha-tocopherol-fed group, and gamma-tocopherol was found in high concentration only in the sesame seed-fed group, with negligible amounts of gamma-tocopherol in liver of the gamma-tocopherol-fed group. In the second experiment, two diets containing sesame lignan (sesaminol or sesamin) and gamma-tocopherol were tested. Results in both of the sesame lignan-fed groups were comparable to those observed in the sesame seed-fed group in Experiment 1. These experiments indicate that gamma-tocopherol in sesame seed exerts vitamin E activity equal to that of alpha-tocopherol through a synergistic interaction with sesame seed lignans. J. Nutr. 122: 2440-2446, 1992.

This study was conducted to compare the effects of enterally infused phosphatidylcholine (PC) and lysophosphatidylcholine (lysoPC) on the lymphatic absorption of [Alpha]-tocopherol ([Alpha]TP) in male rats. In expt. 1, bile-diverted rats with mesenteric lymph cannulas were infused at 3.0 mL/h for 8 h with a lipid emulsion containing 5.0/[micro]mol [Alpha]TP, 565/[micro]mol [sup.14]C-triolein ([sup.14]C-OA) and 396/[micro]mol [Na.sup.+]-taurocholate with 80/[micro]mol 1,2-dipalmitoyl PC (DPPC) or 1,2-dilinoleoyl PC (DLPC) or without PC (NoPC) in 24 mL phosphate-buffered saline (pH 6.6). In expt. 2, the effects of 1,2-dioleoyl PC (DOPC) and 1-oleoyl-2-hydroxy-PC (lysoPC) on [Alpha]TP and [sup.14]C-cholesterol absorption were compared in rats with lymph cannulas. When DPPC or DLPC was infused, the lymphatic absorption of [Alpha]TP was lowered drastically. The cumulative absorptions of [Alpha]TP in rats infused with DPPC and DLPC were 45 and 52%, respectively, of the control values (NoPC). No significant difference was noted between the PC groups. In contrast, the absorption of [sup.14]C-OA was increased by 42 to 43% in rats infused with DPPC or DLPC compared with that in NoPC rats. Phospholipid outputs also were significantly higher in DPPC (34.0 [+ or -] 5.5/[micro]mol/8 h) and DLPC (32.4 [+ or -] 2.4/[micro]mol/8 h) rats than in NoPC rats (21.2 [+ or -] 4.2/[micro]mol/8 h). When lysoPC was infused, the absorptions of [Alpha]TP and [sup.14]C-cholesterol were increased markedly compared with those for DOPC, with no significant difference in PL output between groups infused with DOPC and lysoPC. These observations provide clear evidence that PC present in a lipid emulsion inhibits [Alpha]TP absorption, whereas it enhances the absorption of fat. The data also demonstrate that lysoPC simultaneously increases the absorption of [Alpha]TP and cholesterol. The findings indicate that luminal PC inhibits the absorption of [Alpha]TP and that hydrolysis of PC is critical to improving the intestinal absorption of the vitamin. J. Nutr. 131: 717-722, 2001. KEY WORDS: * absorption * [Alpha]-tocopherol * cholesterol * lysophosphatidylcholine * phosphatidylcholine * rats

Tocopherols act as second-line defenses against increased stress of (n-3) fatty acids and should be considered in the study of protective enzymes responsible for the generation of reactive oxygen species. Furthermore, the higher urinary and thiobarbituric acid-reactive substances observed in female rats compared to male rats was explained on the basis of the difference among sexes in the pattern of fatty acid incorporation in tissues.