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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids 6 Vitamin E SUMMARY Vitamin E is thought to function primarily as a chain-breaking antioxidant that prevents the propagation of lipid peroxidation. Overt deficiency is very rare, seen only in individuals unable to absorb the vitamin or with inherited abnormalities that prevent the maintenance of normal blood concentrations. Thus, current dietary patterns appear to provide sufficient vitamin E to prevent deficiency symptoms such as peripheral neuropathy. Estimates of vitamin E intake are underreported, due in part to underreporting of amounts of dietary fat consumed and lack of specificity of sources in the diet. Data on human experimental vitamin E deficiency are very limited but provide some guidance as to the appropriate Recommended Dietary Allowance (RDA). The values recommended here are based largely on induced vitamin E deficiency in humans and the correlation between hydrogen peroxide-induced erythrocyte lysis and plasma α-tocopherol concentrations. The RDA for both men and women is 15 mg (35 µmol)/day of α-tocopherol. Vitamin E activity of α-tocopherol as defined in this report is limited to that available from the naturally occuring form (RRR-) and the other three synthetic 2R-stereoisomer forms (RSR-, RRS-, and RSS-) of α-tocopherol for purposes of establishing the human requirement for vitamin E. Other naturally occurring forms of vitamin E (β-, γ-, and δ-tocopherols and the tocotrienols) do not contribute toward meeting the vitamin E requirement because (although absorbed) they are not converted to α-tocopherol by humans and are recognized poorly by the α-tocopherol transfer protein (α-TTP) in the liver. Therefore, the RDA is based only on the α-tocopherol form of vitamin E which represents a change
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids from most recent recommendations. A large and growing body of experimental evidence suggests that high intakes of vitamin E may lower the risk of some chronic diseases, especially heart disease. However, the limited and discordant clinical trial evidence available precludes recommendations at this time of higher vitamin E intakes to reduce chronic disease risk. The Tolerable Upper Intake Level (UL) for adults is set at 1,000 mg (2,325 µmol)/day of any form of supplemental α-tocopherol based on the adverse effect of increased tendency to hemorrhage. BACKGROUND INFORMATION Definition of Vitamin E Of the eight naturally occurring forms of vitamin E (see section on “Naturally Occurring Forms” and Figure 6-1) only the α-tocopherol form of the vitamin is maintained in human plasma (Traber, 1999). Furthermore, the only forms of α-tocopherol that are maintained in plasma are RRR-α-tocopherol [2,5,7,8-tetramethyl-2R-(4′R, 8′R, 12′ trimethyltridecyl)-6-chromanol], the form of α-tocopherol that occurs naturally in foods, and the 2R-stereoisomeric forms of α-tocopherol (RRR-, RSR-, RRS-, and RSS-α-tocopherol) present in synthetic all racemic- (all rac-) α-tocopherol [2,5,7,8-tetramethyl-2RS-(4′RS, 8′RS, 12′ trimethyltridecyl)-6-chromanol (Traber, 1999) (Figure 6-2). Since the 2S-stereoisomers of α-tocopherol (SRR-, SSR-, SRS-, and SSS-α-tocopherol), part of the synthetic all rac-α-tocopherol, are not maintained in human plasma (Acuff et al., 1994; Kiyose et al., 1997; Traber, 1999) or tissues (Burton et al., 1998), they are not included in the definition of active components of vitamin E for humans. Therefore, vitamin E is defined in this report as limited to the 2R-stereoisomeric forms of α-tocopherol to establish recommended intakes. All forms of supplemental α-tocopherol are used as the basis of establishing the Tolerable Upper Intake Level (UL) for vitamin E. These recommended intakes and ULs are at variance with past definitions and recommendations for vitamin E (NRC, 1989). Structure Naturally Occurring Forms Naturally occurring structures (Figure 6-1) classified in the past as having vitamin E antioxidant activity include 4 tocopherols (α-tocopherol, trimethyl [3 methyl groups on the chromanol ring]; β-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids FIGURE 6-1 Structures of tocopherols and tocotrienols. The four tocopherols are shown in A and the four tocotrienols in B. All tocopherols are in the RRR-form. SOURCE: Adapted from Traber (1999).
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids FIGURE 6-2 all rac-α-Tocopherol structures. Shown are the eight different stereoisomers in synthetic vitamin E (all rac-α-tocopherol): RRR-, RSR-, RRS-, RSS-, SRR-, SSR-, SRS-, and SSS-. All eight stereoisomers are formed in equal amounts. One stereoisomer, RRR-α-tocopherol, is also naturally present in food. The structure differences occur in the side chain and most importantly at the ring/tail junction. or γ-tocopherols, dimethyl [2 methyl groups on the chromanol ring at different positions]; and δ-tocopherol, monomethyl [1 methyl group on the chromanol ring]) and 4 tocotrienols (α-tocotrienol, trimethyl; β- or γ-tocotrienols, dimethyl; and δ-tocotrienol, monomethyl) (IUPAC-IUB Joint Commission on Biochemical Nomenclature, 1974). The tocopherols are characterized by a substituted, hydroxylated ring system (chromanol ring) with a long, saturated (phytyl) side chain (Figure 6-1). Tocotrienols differ from tocopherols only in that they have an unsaturated side chain. All tocopherols that occur naturally in foods have the RRR stereochemistry in the side chain. However, the various forms of vitamin E are not inter-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids convertible in the human and thus do not behave the same metabolically. Synthetic Vitamin E Synthetic forms of α-tocopherol are present in fortified foods and in vitamin supplements. Vitamin E supplements are sold as esters of either the natural RRR- or the synthetic mixture (all rac-) forms of α-tocopherol. Because α-tocopherol has three asymmetric carbon atoms, it has eight possible stereoisomers, seven of which are only found in synthetic preparations. Synthetic vitamin E, all rac-α-tocopherol (historically and incorrectly labeled dl-α-tocopherol) (Horwitt, 1976),1 is produced by coupling trimethylhydroquinone with isophytol; it contains all eight stereoisomers in equal amounts (Figure 6-2). Four of the stereoisomers are in the 2R-stereoisomeric form (RRR-, RSR-, RRS-, and RSS-α-tocopherol) and four are in the 2S-stereoisomeric form (SRR- SSR-, SRS-, and SSS-α-tocopherol). Although RRR-α-tocopherol is the most biologically active of the eight stereoisomers in rats, the other 2R-stereoisomers generally have a higher activity than the 2S stereoisomers (Weiser and Vecchi, 1982; Weiser et al., 1986). The naturally occurring stereoisomer is RRR-α-tocopherol (historically and incorrectly labeled d-α-tocopherol) (Horwitt, 1976). RRR-α-Tocopherol can be derived by methylating γ-tocopherol isolated from vegetable oil. This is labeled “natural source” vitamin E when marketed. Esterification of the labile hydroxyl (OH) group on the chromanol ring of vitamin E prevents its oxidation and extends its shelf life. This is why esters of α-tocopherol are often used in vitamin E supplements and in fortified foods. In apparently healthy humans, 1 The original international standard for vitamin E, dl-α-tocopheryl acetate (one asymmetric carbon atom in the 2 position on the chromal ring, ambo-α-tocopheryl acetate) is no longer commercially available. It was synthesized from natural phytol and was a mixture of two stereoisomers of α-tocopherols, RRR-α-tocopheryl acetate and SRR-α-tocopheryl acetate (Horwitt, 1976). For practical purposes at the time, the activity of 1 mg of dl-α-tocopheryl acetate was defined as equivalent to one IU of vitamin E. The dl-α-tocopheryl acetate of commerce currently available is synthesized from synthetic isophytol, has eight stereoisomers, and is labeled as dl-α-tocopheryl acetate. However, it is more accurately called all rac-α-tocopheryl acetate (AIN, 1990; IUPAC, 1974) because it contains three asymmetric carbon atoms in the 2, 4', and 8' positions (2RS, 4'RS, 8'RS-α-tocopherol). The all rac and ambo-α-tocopheryl acetates were shown to have the same biological activity in rats (Weiser et al., 1986).
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids the esters (e.g., α-tocopheryl acetate or α-tocopheryl succinate) are hydrolyzed and absorbed as efficiently as α-tocopherol (Cheeseman et al., 1995). Interconversion of Vitamin E Units Before 1980, for pharmacological uses, one international unit (IU) of vitamin E activity was defined as 1 mg of all rac-α-tocopheryl acetate by the United States Pharmacopeia (USP) (USP, 1979). Using the rat fetal resorption assay, 1 mg of RRR-α-tocopherol was calculated to be equivalent to 1.49 IU of vitamin E (Weiser and Vecchi, 1981). After 1980, the IU was changed to the USP unit where one USP unit of vitamin E was still defined as having the activity of 1 mg of all rac-α-tocopheryl acetate, 0.67 mg RRR-α-tocopherol, or 0.74 mg RRR-α-tocopheryl acetate (USP, 1980). Although IUs are no longer recognized, many fortified foods and supplements still retain this terminology while USP units are now generally used by the pharmaceutical industry in labeling vitamin E supplements. Both systems are based on the same equivalency. Since the USP unit was defined before studies were published indicating that the 2S-stereoisomers of all rac-α-tocopherol were not maintained in human plasma (Acuff et al., 1994; Kiyose et al., 1997: Traber, 1999) or in tissues (Burton et al., 1998), it is recommended that the present equivalency used in the USP system be redefined based on the definition presented in this report of what contributes to the active form of vitamin E in humans. Vitamin E is defined here as limited to the 2R-stereoisomeric forms of α-tocopherol (RRR-, RSR-, RRS-, and RSS-α-tocopherol) to establish recommended intakes. Based on this definition, all rac-α-tocopherol has one-half the activity of RRR-α-tocopherol found in foods or present with the other 2R stereoisomeric forms (RSR-, RRS- and RSS-) of α-tocopherol in fortified foods and supplements. Thus to achieve the RDA recommended in this report of 15 mg/day of α-tocopherol, a person can consume 15 mg/day of RRR-α-tocopherol or 15 mg/day of the 2R-stereoisomeric forms of α-tocopherol (e.g., 30 mg/day of all rac-α-tocopherol) or a combination of the two. The factors necessary to convert RRR- and all rac-α-tocopherol and their esters based on this new definition of vitamin E to USP units (IUs) are shown in Table 6-1.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids TABLE 6-1 Factors for Converting International Units of Vitamin Ea to α-Tocopherolb (mg) to Meet Recommended Intake USP Conversion Factorsc Molar Conversion Factorsd α-Tocopherol Conversion Factorse IU/mg mg/IU µmol/IU mg/IU Synthetic Vitamin E and Esters dl-α-Tocopheryl acetate 1.00 1.00 2.12 0.45 dl-α- Tocopheryl succinate 0.89 1.12 2.12 0.45 dl-α-Tocopherolf 1.10 0.91 2.12 0.45 Natural Vitamin E and Esters d-α-Tocopheryl acetate 1.36 0.74 1.56 0.67 d-α-Tocopheryl succinate 1.21 0.83 1.56 0.67 d-α-Tocopherolg 1.49 0.67 1.56 0.67 a Vitamin E supplements are historically and incorrectly labeled d- or dl-α-tocopherol. Vitamin E compounds include the all racemic (all rac)-α-tocopherol (dl-α-tocopherol [RRR-, RRS-, RSR-, RSS-, SSS-, SRS-, SSR-, and SRR-] or synthetic) form and its esters and the RRR-α-tocopherol (d-α-tocopherol or natural) form and its esters. All of these compounds of vitamin E may be present in fortified foods and multivitamins. Not all stereoisomers function to meet vitamin E requirements in humans. b α-Tocopherol as defined in this report to meet recommended intakes includes RRR-α-tocopherol (historically and incorrectly labeled d-α-tocopherol) the only form of α-tocopherol that occurs naturally in foods, and the other 2R-stereoisomeric forms of α-tocopherol (RSR-, RRS-, and RSS-α-tocopherol) that are synthesized chemically and thus are found in fortified foods and supplements (Figure 6-2). c Official United States Pharmacopeia (USP) conversions where one IU is defined as 1 mg of all rac-α-tocopheryl acetate (USP, 1979, 1999). All of the conversions are based on rat fetal resorption assays that were conducted in the 1940s. The amounts of the free and succinate forms have been adjusted for their different molecular weights relative to the all rac-α-tocopheryl acetate (incorrectly labeled dl-α-tocopheryl acetate). d To convert mg to µmol divide the mg by the molecular weight of the vitamin E compound (α-tocopheryl acetate = 472; α-tocopheryl succinate = 530; α-tocopherol = 430) and multiply by 1,000. Because the amount of free and succinate compounds are adjusted for their different molecular weights relative to α-tocopheryl acetate, these forms have the same conversion factors as the corresponding tocopherol compounds. e To convert the µmol of the vitamin E compound to mg of α-tocopherol, multiply the µmol by the molecular weight of α-tocopherol (430) and divide by 1,000. The activities of the three synthetic α-tocopherol compounds have been divided by 2 because the 2S-stereoisomers contained in synthetic-α-tocopherol are not maintained in the blood. f dl-α-Tocopherol = all rac-(racemic) α-tocopherol = synthetic vitamin E; all rac-α-tocopherol = RRR-, RRS-, RSR-, RSS-, SSS-, SRS-, SSR-, and SRR-α-tocopherol isomers. g d-α-Tocopherol = RRR-α-tocopherol = natural vitamin E.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Units of Vitamin E Activity It is now known that vitamin E forms are not interconvertible in the human and that their plasma concentrations are dependent on the affinity of hepatic α-tocopherol transfer protein (α-TTP) for them (see section on “Hepatic α-Tocopherol Transfer Protein”). Kinetic studies have shown that while RRR-α-tocopherol concentrations are maintained in human plasma, the same is not true for either synthetic SRR-α-tocopherol or natural γ-tocopherol (Traber et al., 1990a, 1992). These compounds are efficiently absorbed and delivered to the liver in chylomicrons but are packaged poorly into newly secreted lipoproteins for delivery to peripheral tissues (see section on “Preferential Secretion of α-Tocopherol from the Liver”). In light of these new findings in humans, it becomes necessary to reevaluate the relative biological potencies of different forms of vitamin E. Therefore, it is best to measure and report the actual concentrations of each of the various vitamin E forms in food and biological samples. Current information suggests that the number of methyl groups and the stereochemistry of the phytyl tail at the point where it meets the chromanol ring (2 position) determine the affinity of the α-TTP for the vitamin E form and that this protein in turn determines the effective vitamin E biological activity (Hosomi et al., 1997). Since the 2S-stereoisomers (Figure 6-2) are not maintained in human plasma or in tissues, the difference in relative activity of all rac-α-tocopherol compared to RRR-α-tocopherol is 50 percent as demonstrated in Figure 6-3. Vitamin E activity in food is often reported as α-tocopherol equivalents (α-TE) (Bieri and Evarts, 1973, 1974; Eitenmiller and Landen, 1995) as have been dietary recommendations (NRC, 1989). Previously, factors for the conversion of the tocopherols and tocotrienols to α-TE units were based on the biological activity of the various forms as determined using the rat fetal resorption assay (Bieri and McKenna, 1981). α-TEs were defined as α-tocopherol, mg × 1.0; β-tocopherol, mg × 0.5; γ-tocopherol, mg × 0.1; δ-tocopherol, mg × 0.03; α-tocotrienol, mg × 0.3; and β-tocotrienol, mg × 0.05 (NRC, 1989). The biological activities of γ- and δ-tocotrienol were below detection. Based on a review of the data, the 2R-stereoisomeric forms of α-tocopherol (RRR-, RSR-, RRS-, and RSS-α-tocopherol) are now used to estimate the vitamin E requirement. The 2S-stereoisomeric forms of α-tocopherol and the other tocopherols (β-, γ-,and δ-tocopherol) and the tocotrienols are not used to estimate the vitamin E require-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids FIGURE 6-3 Plasma labeled (d3 and d6) α-tocopherols (means ± standard error, n = 6) following administration of a single dose containing 150 mg each d3RRR-α-and d6all rac-α-tocopherol acetates. SOURCE: Adapted from Traber et al. (1998). ment because of their failure to bind with the α-TTP. Thus, the Estimated Average Requirements (EARs), Recommended Dietary Allowances (RDAs), and Adequate Intakes (AIs) that follow apply only to intake of the 2R-stereoisomeric forms of α-tocopherol from food, fortified food, and multivitamins. The ULs apply to any forms of supplemental α-tocopherol. Currently, most nutrient databases, as well as nutrition labels, do not distinguish between the different tocopherols in food. They often present the data as α-tocopherol equivalents and include the contribution of all eight naturally occurring forms of vitamin E (Figure 6-1), after adjustment for bioavailability of the various forms (see above). Because these other forms of vitamin E occur naturally in foods (e.g., γ-tocopherol is present in widely consumed oils such
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids as soybean and corn oils), the intake of α-tocopherol equivalents is greater than the intake of α-tocopherol (2R-stereoisomeric forms) alone (see later section “Intake of Vitamin E” for suggested conversion factor). Function Unlike most nutrients, a specific role for vitamin E in a required metabolic function has not been found. Vitamin E's major function appears to be as a non-specific chain-breaking antioxidant. Antioxidant Activity Vitamin E is a chain-breaking antioxidant that prevents the propagation of free-radical reactions (Burton and Ingold, 1986; Burton et al., 1983; Ingold et al., 1987; Kamal-Eldin and Appelqvist, 1996; Packer, 1994; Tappel, 1962). The vitamin is a peroxyl radical scavenger and especially protects polyunsaturated fatty acids (PUFAs) within membrane phospholipids and in plasma lipoproteins (Burton et al., 1983). Peroxyl radicals (abbreviated ROO•) react with vitamin E (abbreviated Vit E-OH) 1,000 times more rapidly than they do with PUFA (abbreviated RH) (Packer, 1994). The phenolic hydroxyl group of tocopherol reacts with an organic peroxyl radical to form the corresponding organic hydroperoxide and the tocopheroxyl radical (Vit E-O•) (Burton et al., 1985): In the presence of vitamin E: ROO•+Vit E-OH → ROOH + Vit E-O• In the absence of vitamin E: ROO•+RH → ROOH+R•R•+ O2 → ROO• The tocopheroxyl radical can then undergo several possible fates. It can (1) be reduced by other antioxidants to tocopherol (see section on “ Antioxidant Interactions ”), (2) react with another tocopheroxyl radical to form non-reactive products such as tocopherol dimers, (3) undergo further oxidation to tocopheryl quinone (see section on “ Metabolism ”), and (4) act as a prooxidant and oxidize other lipids (see section on “ Antioxidant Interactions ”). Biochemical and Molecular Biologic Activities In addition to its direct antioxidant function, α-tocopherol reportedly has specific molecular functions, α-Tocopherol inhibits
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids protein kinase C activity, which is involved in cell proliferation and differentiation, in smooth muscle cells (Boscoboinik et al., 1991; Chatelain et al., 1993; Clement et al., 1997; Stauble et al., 1994; Tasinato et al., 1995), human platelets (Freedman et al., 1996), and monocytes (Cachia et al., 1998; Devaraj et al., 1996). Protein kinase C inhibition by α-tocopherol is in part attributable to its attenuating effect on the generation of membrane-derived diacylglycerol, a lipid that facilitates protein kinase C translocation, thus increasing its activity (Kunisaki et al., 1994; Tran et al., 1994). Vitamin E enrichment of endothelial cells downregulates the expression of intercellular cell adhesion molecule (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), thereby decreasing the adhesion of blood cell components to the endothelium (Cominacini et al., 1997). Vitamin E also upregulates the expression of cytosolic phospholipase A2 (Chan et al., 1998a; Tran et al., 1996) and cyclooxygenase-1 (Chan et al., 1998b). The enhanced expression of these two rate-limiting enzymes in the arachidonic acid cascade explains the observation that vitamin E, in a dose-dependent fashion, enhanced the release of prostacyclin, a potent vasodilator and inhibitor of platelet aggregation in humans (Szczeklik et al., 1985; Tran and Chan, 1990). Physiology of Absorption, Metabolism, and Excretion Absorption and Transport Intestinal Absorption. While the efficiency of vitamin E absorption is low in humans, the precise rate of absorption is not known with certainty. In the early 1970s, vitamin E absorption was estimated to be 51 to 86 percent, measured as fecal radioactivity following ingestion of α-tocopherol (Kelleher and Losowsky, 1970; MacMahon and Neale, 1970). However, when Blomstrand and Forsgren (1968) measured vitamin E absorption in two individuals with gastric carcinoma and lymphatic leukemia, respectively, they found fractional absorption in the lymphatics to be only 21 and 29 percent of label from meals containing α-tocopherol and α-tocopheryl acetate, respectively. Vitamin E absorption from the intestinal lumen is dependent upon biliary and pancreatic secretions, micelle formation, uptake into enterocytes, and chylomicron secretion. Defects at any step lead to impaired absorption (Gallo-Torres, 1970; Harries and Muller, 1971; Sokol, 1993; Sokol et al., 1983, 1989). Chylomicron
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Kohlschütter A, Hubner C, Jansen W, Lindner SG. 1988. A treatable familial ne romyopathy with vitamin E deficiency, normal absorption, and evidence of increased consumption of vitamin E. J Inher Metab Dis 11:149–152. Kostner GM, Oettl K, Jauhiainen M, Ehnholm C, Esterbauer H, Dieplinger H. 1995. Human plasma phospholipid transfer protein accelerates exchange/transfer of alpha-tocopherol between lipoproteins and cells. Biochem J 305:659–667. Krasavage WJ, Terhaar CJ. 1977. d-alpha-Tocopheryl poly(ethylene glycol) 1000 succinate. Acute toxicity, subchronic feeding, reproduction, and teratologic studies in the rat. J Agric Food Chem 25:273–278. Krendel DA, Gilchrist JM, Johnson AO, Bossen EH. 1987. Isolated deficiency of vitamin E with progressive neurologic deterioration . Neurology 37:538–540. Kuhlenkamp J, Ronk M, Yusin M, Stolz A, Kaplowitz N. 1993. Identification and purification of a human liver cytosolic tocopherol binding protein. Protein Expr Purif 4:382–389. Kunisaki M, Umeda F, Inoguchi T, Watanabe J, Nawata H. 1990. Effects of vitamin E administration on platelet function in diabetes mellitus. Diabetes Res 14:37–42. Kunisaki M, Bursell SE, Umeda F, Nawata H, King GL. 1994. Normalization of diacylglycerol-protein kinase C activation by vitamin E in aorta of diabetic rats and cultured rat smooth muscle cells exposed to elevated glucose levels. Diab tes 43:1372–1377. Kushi LH, Folsom AR, Prineas RJ, Mink PJ, Wu Y, Bostick RM. 1996. Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women. N Engl J Med 334:1156–1162. Laditan AA, Ette SI. 1982. Plasma alpha-tocopherol (vitamin E) levels and tocopherol-lipid ratio among children with protein-energy malnutrition (PEM). Ann Trop Paediatr 2:85–88. Lammi-Keefe CJ, Jensen RG, Clark RM, Ferris AM. 1985. Alpha tocopherol, total lipid and linoleic acid contents of human milk at 2, 6, 12, and 16 weeks. In: Schaub J, ed. Composition and Physiological Properties of Human Milk. New York: Elsevier Science. Pp. 241–245. Lammi-Keefe CJ, Ferris AM, Jensen RG. 1990. Changes in human milk at 0600, 1000, 1400, 1800, and 2200 h. J Pediatr Gastroenterol Nutr 11:83–88. Laplante P, Vanasse M, Michaud J, Geoffroy G, Brochu P. 1984. A progressive neurological syndrome associated with an isolated vitamin E deficiency. Can J Neurol Sci 11:561–564. Lehmann J, Martin HL, Lashley EL, Marshall MW, Judd JT. 1986. Vitamin E in foods from high and low linoleic acid diets. J Am Diet Assoc 86:1208–1216. Leo MA, Ahmed S, Aleynik SI, Siegel JH, Kasmin F, Lieber CS. 1995. Carotenoids and tocopherols in various hepatobiliary conditions. J Hepatol 23:550–556. Leske MC, Chylack LT Jr, Wu SY. 1991. The Lens Opacities Case-Control Study. Risk factors for cataract. Arch Ophthalmol 109:244–251. Lohr JB, Cadet JL, Lohr MA, Jeste DV, Wyatt RJ. 1987. Alpha-tocopherol in tardive dyskinesia. Lancet 1:913–914. Lohr JB, Kuczenski R, Bracha HS, Moir M, Jeste DV. 1990. Increased indices of free radical activity in the cerebrospinal fluid of patients with tardive dyskinesia. Biol Psychiatry 28:535–539. London RS, Sundaram GS, Murphy L, Manimekalai S, Reynolds M, Goldstein PJ. 1985. The effect of vitamin E on mammary dysplasia: A double-blind study . Obstet Gynecol 65:104–106.
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Representative terms from entire chapter: