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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids 5 Vitamin C SUMMARY Vitamin C functions physiologically as a water-soluble antioxidant by virtue of its high reducing power. It is a cofactor for enzymes involved in the biosynthesis of collagen, carnitine, and neurotransmitters in vitro, and it can quench a variety of reactive oxygen species and reactive nitrogen species in aqueous environments. Evidence for in vivo antioxidant functions of ascorbate include the scavenging of reactive oxidants in activated leukocytes, lung, and gastric mucosa, and diminished lipid peroxidation as measured by urinary isoprostane excretion. To provide antioxidant protection, a Recommended Dietary Allowance (RDA) of 90 mg/day for adult men and 75 mg/day for adult women is set based on the vitamin C intake to maintain near-maximal neutrophil concentration with minimal urinary excretion of ascorbate. Because smoking increases oxidative stress and metabolic turnover of vitamin C, the requirement for smokers is increased by 35 mg/day. Estimates of median dietary intakes of vitamin C for adults are 102 mg/day and 72 mg/day in the United States and Canada, respectively. The Tolerable Upper Intake Level (UL) for adults is set at 2 g/day; the adverse effects upon which the UL is based are osmotic diarrhea and gastrointestinal disturbances. BACKGROUND INFORMATION Vitamin C is a water-soluble vitamin that is essential for all humans and a few other mammals that lack the ability to biosynthesize the compound from glucose because they lack the enzyme gulono-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids lactone oxidase. The term vitamin C refers to both ascorbic acid and dehydroascorbic acid (DHA), since both exhibit anti-scorbutic activity. Ascorbic acid, the functional and primary in vivo form of the vitamin, is the enolic form of an α-ketolactone (2,3-didehydr L -threo-hexano-1,4-lactone). The two enolic hydrogen atoms give the compound its acidic character and provide electrons for its function as a reductant and antioxidant. Its one-electron oxidation product, the ascorbyl radical, readily dismutates to ascorbate and DHA, the two-electron oxidation products. Both the ascorbyl radical and DHA are readily reduced back to ascorbic acid in vivo. However, DHA can be hydrolyzed irreversibly to 2,3-diketogulonic acid. The molecular structure of ascorbic acid contains an asymmetric carbon atom that allows two enantiomeric forms, of which the L form is naturally occurring (the D -form, isoascorbic or erythorbic acid, provides antioxidant but little or no anti-scorbutic activity), as shown in Figure 5-1. Function The biological functions of ascorbic acid are based on its ability to provide reducing equivalents for a variety of biochemical reactions. Because of its reducing power, the vitamin can reduce most physiologically relevant reactive oxygen species (Buettner, 1993). As such, the vitamin functions primarily as a cofactor for reactions requiring a reduced iron or copper metalloenzyme and as a protective antioxidant that operates in the aqueous phase both intra- and extracellularly (Englard and Seifter, 1986; Halliwell and Whiteman, 1997; Tsao, 1997). Both the one- and the two-electron oxidation products of the vitamin are readily regenerated in vivo—chemically and enzymatically—by glutathione, nicotinamide adenine dinucleotide (NADH), and nicotinamide adenine dinucleotide phosphate (NAD-PH) dependent reductases (May et al., 1998; Park and Levine, 1996). Vitamin C is known to be an electron donor for eight human enzymes. Three participate in collagen hydroxylation; two in carnitine biosynthesis; and three in hormone and amino acid biosynthesis. The three enzymes that participate in hormone and amino acid biosynthesis are dopamine-β-hydroxylase, necessary for the biosynthesis of the catecholamines norepinephrine and epinephrine; peptidyl-glycine monooxygenase, necessary for amidation of peptide hormones; and 4-hydroxyphenylpyruvatedioxygenase, involved in tyrosine metabolism. Ascorbate's action with these enzymes in-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids FIGURE 5-1 Chemical structure of ascorbic acid. volves either monooxygenase or dioxygenase activities (Levine et al., 1996b). As a cofactor for hydroxylase and oxygenase metalloenzymes, ascorbic acid is believed to work by reducing the active metal site, resulting in reactivation of the metal-enzyme complex, or by acting as a co-substrate involved in the reduction of molecular oxygen. The
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids best known of these reactions is the posttranslational hydroxylation of peptide-bound proline and lysine residues during formation of mature collagen. In these reactions, ascorbate is believed to reactivate the enzymes by reducing the metal sites of prolyl (iron) and lysyl (copper) hydroxylases (Englard and Seifter, 1986; Tsao, 1997). Evidence also suggests that ascorbate plays a role in or influences collagen gene expression, cellular procollagen secretion, and the biosynthesis of other connective tissue components besides collagen, including elastin, fibronectin, proteoglycans, bone matrix, and elastin-associated fibrillin (Ronchetti et al., 1996). The primary physical symptoms of ascorbic acid's clinical deficiency disease, scurvy, which involves deterioration of elastic tissue, illustrate the important role of ascorbate in connective tissue synthesis. Ascorbic acid is involved in the synthesis and modulation of some hormonal components of the nervous system. The vitamin is a co-factor for dopamine-β-hydroxylase, which catalyzes hydroxylation of the side chain of dopamine to form norepinephrine, and α-amidating monooxygenase enzymes, involved in the biosynthesis of neuropeptides. Other nervous system components modulated by ascorbate concentrations include neurotransmitter receptors, the function of glutamatergic and dopaminergic neurons, and synthesis of glial cells and myelin (Englard and Seifter, 1986; Katsuki, 1996). Because of its ability to donate electrons, ascorbic acid is an effective antioxidant. The vitamin readily scavenges reactive oxygen species (ROS) and reactive nitrogen species (RNS) (e.g., hydroxyl, peroxyl, superoxide, peroxynitrite, and nitroxide radicals) as well as singlet oxygen and hypochlorite (Frei et al., 1989; Halliwell and Whiteman, 1997; Sies and Stahl, 1995). The one- and two-electron oxidation products of ascorbate are relatively nontoxic and easily regenerated by the ubiquitous reductants glutathione and NADH or NAD-PH. The relatively high tissue levels of ascorbate provide substantial antioxidant protection: in the eye, against photolytically generated free-radical damage; in neutrophils, against ROS produced during phagocytosis; and in semen, against oxidative damage to sperm deoxyribonucleic acid (DNA) (Delamere, 1996; Fraga et al., 1991; Levine et al., 1994). Ascorbic acid protects against plasma and low-density lipoprotein (LDL) oxidation by scavenging ROS in the aqueous phase before they initiate lipid peroxidation (Frei et al., 1988; Jialal et al., 1990) and possibly by sparing or regenerating vitamin E (Halpner et al., 1998). Evidence suggests that ascorbate
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids also provides antioxidant protection indirectly by regenerating other biological antioxidants such as glutathione and α-tocopherol back to their active state (Jacob, 1995). Ascorbic acid functions as a reducing agent for mixed-function oxidases in the microsomal drug-metabolizing system that inactivates a wide variety of substrates, such as endogenous hormones or xenobiotics (i.e., other chemical compounds such as drugs, pesticides, or carcinogens that are foreign to humans) (Tsao, 1997). The activity of both microsomal drug-metabolizing enzymes and cytochrome P-450 electron transport is lowered by ascorbate deficiency. The vitamin is involved in the biosynthesis of corticosteroids and aldosterone and in the microsomal hydroxylation of cholesterol in the conversion of cholesterol to bile acids. In reactions similar to the hydroxylation of proline for collagen synthesis, ascorbate is required along with iron at two steps in the pathway of carnitine biosynthesis. Ascorbic acid modulates iron absorption, transport, and storage (Gosiewska et al., 1996). Limited data suggest that ascorbate modulates prostaglandin synthesis and thus exerts bronchodilatory and vasodilatory as well as anticlotting effects (Horrobin, 1996). Physiology of Absorption, Metabolism, and Excretion Absorption and Transport Intestinal absorption of ascorbic acid occurs through a sodium-dependent active transport process that is saturable and dose dependent (Rumsey and Levine, 1998; Tsao, 1997). At low gastrointestinal ascorbate concentrations, active transport predominates, while simple diffusion occurs at high concentrations. Some 70 to 90 percent of usual dietary intakes of ascorbic acid (30 to 180 mg/day) are absorbed; however, absorption falls to about 50 percent or less with increasing doses above 1 g/day (Kallner et al., 1979). The bioavailabilities of the vitamin from foods and supplements are not significantly different (Johnston and Luo, 1994; Mangels et al., 1993). Cellular transport of ascorbic acid and DHA is mediated by transporters that vary by cell type (Jacob, 1999; Tsao, 1997). DHA is the form of the vitamin that primarily crosses the membranes of blood and intestinal cells, after which it is reduced intracellularly to ascorbic acid. Accumulation of ascorbate into neutrophils and lympho-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids cytes is mediated by both high- and low-affinity transporters, and the vitamin is localized mostly in the cytosol. Intracellularly and in plasma, vitamin C exists predominately in the free reduced form as ascorbate monoanion, as shown in Figure 5-1 (Levine et al., 1994). Metabolism and Excretion Since the immediate oxidized forms of vitamin C are readily reduced back to ascorbic acid, relatively small amounts of the vitamin are lost through catabolism. The primary products of oxidation beyond DHA include oxalic and threonic acids, L -xylose, and ascorbate 2-sulfate (Jacob, 1999). With large intakes of the vitamin, unabsorbed ascorbate is degraded in the intestine, a process that may account for the diarrhea and intestinal discomfort sometimes reported by persons ingesting large doses (see section on “Adverse Effects”). Besides dose-dependent absorption, a second primary mechanism for regulation of body ascorbate content is renal action to conserve or excrete unmetabolized ascorbate. Recent studies have shown that little unmetabolized ascorbate is excreted with dietary intakes up to about 80 mg/day and that renal excretion of ascorbate increases proportionately with higher intakes (Blanchard et al., 1997; Melethil et al., 1986). Body Stores Dose-dependent absorption and renal regulation of ascorbate allow conservation of the vitamin by the body during low intakes and limitation of plasma levels at high intakes. Tissue-specific cellular transport systems allow for wide variation of tissue ascorbate concentrations. High levels are maintained in the pituitary and adrenal glands, leukocytes, eye tissues and humors, and the brain, while low levels are found in plasma and saliva (Hornig, 1975). Due to homeostatic regulation, the biological half-life of ascorbate varies widely from 8 to 40 days and is inversely related to the ascorbate body pool (Kallner et al., 1979). Similarly, catabolic turnover varies widely, about 10 to 45 mg/day, over a wide range of dietary intakes due to body pool size. A total body pool of less than 300 mg is associated with scurvy symptoms (Baker et al., 1971), while maximum body pools are limited to about 2 g (Kallner et al., 1979). At very low ascorbate intakes, essentially no ascorbate is excreted unchanged and a minimal loss occurs.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Clinical Effects of Inadequate Intake Scurvy, the classic disease of severe vitamin C deficiency, is characterized by symptoms related to connective tissue defects. Scurvy usually occurs at a plasma concentration of less than 11 µmol/L (0.2 mg/dL). Clinical features of scurvy include follicular hyperkeratosis, petechiae, ecchymoses, coiled hairs, inflamed and bleeding gums, perifollicular hemorrhages, joint effusions, arthralgia, and impaired wound healing (Baker et al., 1971; Chazan and Mistilis, 1963; Levine et al., 1996b). Other symptoms include dyspnea, edema, Sjögren's syndrome (dry eyes and mouth), weakness, fatigue, and depression. In experimental subjects made vitamin C deficient but not frankly scorbutic, gingival inflammation (Leggott et al., 1986) and fatigue (Levine et al., 1996a) were among the most sensitive markers of deficiency. Vitamin C deficiency in infants may result in bone abnormalities such as impaired bone growth and disturbed ossification, hemorrhagic symptoms, and resultant anemia (Jacob, 1999). Lack of ascorbate-related hydroxyproline and hydroxylysine formation needed for collagen cross-linking may explain many of the connective tissue and hemorrhagic manifestations of scurvy, however, the specific histologic defects have not been identified. Oxidative degradation of some blood coagulation factors due to low plasma ascorbate concentrations may contribute to hemorrhagic symptoms (Parkkinen et al., 1996). Scurvy is rare in developed countries but is occasionally seen in individuals who consume few fruits and vegetables, peculiar or restricted diets, or in those who abuse alcohol or drugs. In the United States, low blood ascorbate concentrations are more prevalent in men, especially elderly men, than in women and are more prevalent in populations of lower socioeconomic status (LSRO/FASEB, 1989). Infantile scurvy is rarely seen, because human milk provides an adequate supply of vitamin C and infant formulas are fortified with the vitamin. SELECTION OF INDICATORS FOR ESTIMATING THE REQUIREMENT FOR VITAMIN C Antioxidant Functions There is much support for the role of increased oxidative stress in the pathogenesis of cardiovascular disease (Jialal and Devaraj, 1996; Witztum and Steinberg, 1991). The most plausible and biologically
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids relevant hypothesis is that the oxidative modification of low-density lipoprotein (LDL) and other lipoproteins promote atherogenesis (Berliner and Heinecke, 1996; Devaraj and Jialal, 1996; Witztum and Steinberg, 1991). Several lines of evidence suggest that oxidized LDL (oxLDL) is pro-atherogenic. Furthermore, data support the in vivo existence of oxLDL (Berliner and Heinecke, 1996; Witztum and Steinberg, 1991). In vitro studies have clearly shown that vitamin C at concentrations greater than 40 µmol/L (0.8 mg/dL) inhibits the oxidation of isolated LDL induced by transition metals, free-radical initiators, and activated human neutrophils and macrophages (Jialal and Grundy, 1991; Jialal et al., 1990; Scaccini and Jialal, 1994). This is because vitamin C effectively scavenges aqueous reactive oxygen species (ROS) and reactive nitrogen species (RNS), which prevents them from attacking LDL. Thus, in vitro vitamin C clearly functions as an antioxidant. Studies shown in Table 5-1 examined the effect of vitamin C supplementation alone on biomarkers of lipid peroxidation. Of the 13 studies, 7 showed that vitamin C supplementation resulted in a significant decrease in lipid oxidation products in plasma, LDL, or urine. The vitamin C supplements that resulted in positive effects ranged from 500 to 2,000 mg/day. The most convincing evidence that vitamin C functions as an antioxidant in vivo is the study by Reilly et al. (1996) showing that supplementation of smokers with 2.0 g vitamin C for 5 days was associated with a significant reduction in urinary isoprostanes, an indicator of oxidative stress. In the remaining six studies in which vitamin C was supplemented in amounts ranging from 500 to 6,000 mg/day, there was no significant effect of vitamin C supplementation on lipid oxidation products in plasma, urine, or plasma LDL. Carr and Frei (1999) examined the effect on LDL oxidation of supplementation with vitamin C in combination with vitamin E and β-carotene. Although these investigators have clearly shown that the supplements decrease LDL oxidation, it is difficult to assess the contribution of vitamin C alone. Vitamin C supplementation (2,000 mg/day for 4 to 12 months) in 41 patients with non-atrophic gastritis decreased gastric mucosal nitrotyrosine, a measure of RNS activity (Table 5-2) (Mannick et al., 1996). Thus, from this study and the study by Reilly et al. (1996), it can be concluded that supplementation with vitamin C results in an antioxidant effect in vivo because it significantly reduces nitrotyrosine and urinary isoprostanes. However, with respect to the effect of vitamin C on LDL oxidation, the data are inconclusive. This could be explained by the fact
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids that, because vitamin C is water soluble, it does not partition into the LDL particle. Also, it must be pointed out that in one of the 13 studies summarized in Table 5-1, there was an increase in plasma thiobarbituric acid reactive substances (TBARS), an indicator of oxidative stress, with a 500-mg dose of ascorbic acid (Nyyssonen et al., 1997b). Adhesion of mononuclear cells to endothelium is an early event in atherogenesis and may be triggered by oxidative stress. Smokers have low levels of vitamin C and increased oxidative stress. A recent study showed that monocytes of smokers display greater adhesion to endothelial cells than those of nonsmokers (Weber et al., 1996). When supplemented with 2,000 mg/day of vitamin C, the plasma ascorbate level of smokers increased, and adhesion of their monocytes to endothelium decreased to that seen in nonsmokers. Impaired vascular function is crucial to the clinical manifestation of atherosclerosis. As depicted in Table 5-3, numerous investigators have reported a beneficial effect of high dose vitamin C administration, either orally or intraarterially, on vasodilation. This beneficial effect of vitamin C is most likely related to its antioxidant effect. Endothelium-derived relaxing factor, nitric oxide (NO), promotes vasodilation but is rapidly inactivated by superoxide. Vitamin C improves endothelial function and vasodilation, possibly by scavenging superoxide radicals, conserving intracellular glutathione, or potentiating intracellular NO synthesis. In human endothelial cells in culture, extracellular vitamin C at physiological concentrations increased cellular NO synthesis up to threefold, and the increase in NO synthesis followed a time course similar to ascorbate uptake into the cells (Heller et al., 1999). Antioxidant Functions in Leukocytes The content of vitamin C in leukocytes is especially important because the ROS generated during phagocytosis and neutrophil activation are associated with infectious and inflammatory stresses (Jariwalla and Harakeh, 1996; Levine et al., 1994). Along with pituitary and adrenal glands and eye lens, leukocytes contain the highest vitamin C concentrations of all body tissues (Moser, 1987). Studies with guinea pigs and monkeys show that the concentration of ascorbate in the leukocytes more accurately reflects liver and body pool ascorbate than does the concentration in plasma or erythrocytes (Omaye et al., 1987). The vitamin is transported into leukocytes by an energy-dependent transport system that concentrates the vitamin some twenty-five-, forty-, and eightyfold over plasma levels in neutr-
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids TABLE 5-1 Effect of Vitamin C Supplementation on Biomarkers of Lipid Oxidation in Humans Reference Subjects Vitamin C Dosea (mg/d) Harats et al., 1990 17 smokers 1,000 1,500 Belcher et al., 1993 5 healthy men 1,000 Rifici and Khachadurian, 1993 4 healthy men and women 1,000 Cadenas et al., 1996 21 healthy men 1,000 Fuller et al., 1996 19 smokers (9 placebo) 1,000 Mulholland et al., 1996 16 female smokers (8 placebo) 1,000 Reilly et al., 1996 5 heavy smokers 2,000 Anderson et al., 1997 48 nonsmokers (24 females) 60 6,000 Nyyssonen et al., 1997b 59 male smokers (19 placebo) 500 (Pj) 500 (SRk) Samman et al., 1997 8 male smokers (40) 1,000 Wen et al., 1997 20 nonsmokers (9 placebo) 1,000 Harats et al., 1998 36 healthy men (50) 500 (citrus fruit supplement) Naidoo and Lux, 1998 9 healthy men, 6 healthy women 250, 500, 750 and 1,000 a Amount given in excess of variable amount consumed daily as part of the diet. b LDL = low-density lipoprotein. c TBARS = thiobarbituric acid reactive substances. d LDL oxidizability is measured by the lag time and propagation rate of in vitro lipid peroxidation. e VLDL = very low-density lipoprotein. f CD = conjugated dienes.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Duration Plasma Change Findings 2 wk 2.0-fold ↓ Plasma and LDLb TBARSc 4 wk 2.3-fold ↓ Plasma and LDL TBARS 14 d Not reported LDL oxidationd, no change 10 d Not reported ↓ VLDLe and LDL oxidation (4 hour TBARS) 30 d Not reported Urine TBARS, no change 4 wk 3.9-fold ↓ LDL Oxidizabilityd (TBARS, CDf) 14 d 3.0-fold Serum TBARS, no change 5 d Not reported 18 Urine 8-epi-PGF2a 14 d 1.2-fold Plasma MDAg /HNEh, no change ↑ TACi 14 d 1.8-fold Plasma MDA/HNE, no change ↑ TAC 2 mo 1.3-fold LDL oxidizability, no change 2 mo 1.5-fold Plasma ↑ TBARS with P Vit C No ↑ with SR Vit C (2 wk) (baseline) LDL oxidizability (CD): no change 2 wk 2.0-fold 4 wk 2.2-fold ↓ Plasma MDA (↑ erythrocyte Vit E and GSHl); no change LDL Vit E; no change in LDL oxidizability (TBARS and CD) (1 mo) (baseline) ↓ LDL oxidizability (CD) 2 mo 3.8-fold 2 wk 1.5-fold (250) 2.0-fold (500) 2.0-fold (750 and 1,000) ↓ Plasma MDA and allantoin with 500, 750 and 1,000 mg/d g MDA = malondialdehyde. h HNE = hydroxynonenal. i TAC = Total Antioxidant Capacity. j P = plain. k SR = slow release. l GSH = reduced gluthione.
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DRI DIETARY REFERENCE INTAKES FOR Vitamin C, Vitamin E, Selenium, and Carotenoids Hughes C, Dutton S, Truswell AS. 1981. High intakes of ascorbic acid and urinary oxalate. J Hum Nutr 35:274–280. Hunt JR, Gallagher SK, Johnson LK. 1994. Effect of ascorbic acid on apparent iron absorption by women with low iron stores. Am J Clin Nutr 59:1381–1385. Hunter DJ, Manson JE, Colditz GA, Stampfer MJ, Rosner B, Hennekens CH, Speizer FE, Willett WC. 1993. A prospective study of the intake of vitamins C, E, and A and the risk of breast cancer. N Engl J Med 329:234–240. IOM (Institute of Medicine). 1991. Nutrition During Lactation. Washington, DC: National Academy Press. P. 179. Itoh R, Yamada K, Oka J, Echizen H, Murakami K. 1989. Sex as a factor in levels of serum ascorbic acid in a healthy elderly population. Int J Vitam Nutr Res 59:365–372. Jacob RA. 1995. The integrated antioxidant system. Nutr Res 15:755–766. Jacob RA. 1999. Vitamin C. In: Shils ME, Olson JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease, 9th edition. Baltimore, MD: Williams & Wilkins. Pp. 467–483. Jacob RA, Pianalto FS. 1997. Urinary carnitine excretion increases during experimental vitamin C depletion of healthy men. J Nutr Biochem 8:265–269. Jacob RA, Skala JH, Omaye ST. 1987a. Biochemical indices of human vitamin C status. Am J Clin Nutr 46:818–826. Jacob RA, Skala JH, Omaye ST, Turnlund JR. 1987b. Effect of varying ascorbic acid intakes on copper absorption and ceruloplasmin levels of young men. J Nutr 117:2109–2115. Jacob RA, Otradovec CL, Russell RM, Munro HN, Hartz SC, McGandy RB, Morrow FD, Sadowski JA. 1988. Vitamin C status and nutrient interactions in a healthy elderly population . Am J Clin Nutr 48:1436–1442. Jacob RA, Kelley DS, Pianalto FS, Swendseid ME, Henning SM, Zhang Jz, Ames BN, Fraga CG, Peters JH. 1991. Immunocompetence and oxidant defense during ascorbate depletion of healthy men. Am J Clin Nutr 54:1302S–1309S. Jacob RA, Pianalto FS, Agee RE. 1992. Cellular ascorbate depletion in healthy men. J Nutr 122:1111–1118. Jacob RA, Kutnink MA, Csallany AS, Daroszewska M, Burton GW. 1996. Vitamin C nutriture has little short-term effect on vitamin E concentrations in healthy women. J Nutr 126:2268–2277. Jacques PF, Chylack LT Jr. 1991. Epidemiologic evidence of a role for the antioxidant vitamins and carotenoids in cataract prevention. Am J Clin Nutr 53:352S–355S. Jacques PF, Taylor A, Hankinson SE, Willett WC, Mahnken B, Lee Y, Vaid K, Lahav M. 1997. Long-term vitamin C supplement use and prevalence of early age related lens opacities. Am J Clin Nutr 66:911–916. Jaffe RM, Kasten B, Young DS, MacLowry JD. 1975. False-negative stool occult blood tests caused by ingestion of ascorbic acid (vitamin C). Ann Intern Med 83:824–826. Jama JW, Launer LJ, Witteman JC, den Breeijen JH, Breteler MM, Grobbee DE, Hofman A. 1996. Dietary antioxidants and cognitive function in a population based sample of older persons. The Rotterdam Study. Am J Epidemiol 144:275–280. Jariwalla RJ, Harakeh S. 1996. Antiviral and immunomodulatory activities of asco bic acid. Subcell Biochem 25:213–231. Jarvinen R, Knekt P, Seppanen R, Teppo L. 1997. Diet and breast cancer risk in a cohort of Finnish women. Cancer Lett 114:251–253.
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