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• W1975109406 abstract "Patients with parenteral nutrition depend on an adequate supply of micronutrients, in particular, antioxidant vitamins and cofactors such as selenium. In cases of oxidative stress (eg, chronic inflammation, sepsis, lung distress syndrome, and organ failure), there is a higher need for antioxidants. One of the most important antioxidant vitamins is vitamin E. For very low birth weight infants the plasma level is an indicator for adequate supply and for safety. Safe and effective blood levels are between 23 and 46 μmol/L, maintained with a dose of 2.8 IU/kg body weight (1–2 mg/day). For safety reasons a plasma level of 80 μmol/L should not be exceeded. For adults, 10 IU/day (9.1 mg/day) are recommended. Whether this dose is sufficient to ensure body stores and sufficient antioxidant activity is controversial. If parenteral lipid emulsions are supplied there is an additional need for vitamin E to protect the lipids (polyunsaturated fatty acids) from lipid peroxidation and to deliver additional vitamin E. Dietary guidelines for healthy adults recommend an intake of polyunsaturated fatty acids equal to 10% of total energy and an intake of α-tocopherol greater than 0.4 mg/g of polyunsaturated fatty acids. Randomized clinical trials are performed using special formulations of vitamin E solutions because vitamin E is available only in lipid emulsions to protect lipids, but not in an isolated solution for parenteral supply. Patients with parenteral nutrition depend on an adequate supply of micronutrients, in particular, antioxidant vitamins and cofactors such as selenium. In cases of oxidative stress (eg, chronic inflammation, sepsis, lung distress syndrome, and organ failure), there is a higher need for antioxidants. One of the most important antioxidant vitamins is vitamin E. For very low birth weight infants the plasma level is an indicator for adequate supply and for safety. Safe and effective blood levels are between 23 and 46 μmol/L, maintained with a dose of 2.8 IU/kg body weight (1–2 mg/day). For safety reasons a plasma level of 80 μmol/L should not be exceeded. For adults, 10 IU/day (9.1 mg/day) are recommended. Whether this dose is sufficient to ensure body stores and sufficient antioxidant activity is controversial. If parenteral lipid emulsions are supplied there is an additional need for vitamin E to protect the lipids (polyunsaturated fatty acids) from lipid peroxidation and to deliver additional vitamin E. Dietary guidelines for healthy adults recommend an intake of polyunsaturated fatty acids equal to 10% of total energy and an intake of α-tocopherol greater than 0.4 mg/g of polyunsaturated fatty acids. Randomized clinical trials are performed using special formulations of vitamin E solutions because vitamin E is available only in lipid emulsions to protect lipids, but not in an isolated solution for parenteral supply. Oxidative stress is believed to be involved in acute and/or chronic postoperative complications such as lung distress syndrome, inadequate wound healing, sepsis, and multiple organ failure.1Quinlan G.J. Evans T.W. Gutteridge J.M.C. Oxidative damage to plasma proteins in adult respiratory distress syndrome.Free Radic Res. 1994; 20: 289-298Crossref PubMed Scopus (100) Google Scholar, 2Vincent J. Preiser J. Friedman G. et al.Endothelial cell function in the critically ill.in: Reinhart K. Eyrich K. Sprung C. Sepsis, current perspectives in pathophysiology and therapy. Berlin, Springer1994: 174-180Google Scholar Oxidative stress is defined as an imbalance between the extent of reactive oxygen species and a comparable low antioxidative capacity of a biological system.3Sies H. Physiological society symposium: impaired endothelial and smooth muscle cell function in oxidative stress—oxidative stress: oxidants and antioxidants.Exp Physiol. 1997; 82: 291-295PubMed Google Scholar A major component of this antioxidative network is vitamin E, the most important lipid-soluble antioxidant. This vitamin helps to prevent membrane destabilizing lipid peroxidation by breaking lipid radical chain reactions.4DiMascio P. Murphy M.E. Sies H. Antioxidant defense systems: the role of carotenoids, tocopherols, and thiols.Free Radic Biol Med. 1991; 11: 215-232Crossref PubMed Scopus (403) Google Scholar, 5Erin A.N. Spirin M.M. Tabidza L.V. et al.Formulation of α-tocopherol complexes with fatty acids: a hypothetical mechanism of stabilization of biomembranes by vitamin E.Biochim Biophys Acta. 1984; 774: 96-102Crossref PubMed Scopus (132) Google Scholar, 6Niki E. Antioxidants in relation to lipid peroxidation.Chem Phys Lipids. 1987; 44: 227-253Crossref PubMed Scopus (655) Google Scholar Increased lipid peroxidation occurs during ischemia/reperfusion as a result of increased formation of superoxide anion and consecutive production of hydroxyl radicals owing to the iron-catalyzed Fenton reaction. Sources of superoxide anion formation during ischemia/reperfusion are conversion of xanthine dehydrogenase to xanthine oxidase7McCord J.M. Oxygen-derived free radicals in post-ischemic tissue injury.N Engl J Med. 1985; 312: 159-163Crossref PubMed Scopus (4984) Google Scholar and activation of polymorphonuclear cells.8Grinyó J.M. Reperfusion injury.Transplant Proc. 1997; 29: 59-62Abstract Full Text PDF PubMed Scopus (27) Google Scholar Combined oral supplementation with α-tocopherol and ascorbic acid—the water-soluble counterpart of vitamin E—prevents ischemia/reperfusion-induced damage in experimental studies.9Cadenas S. Rojas C. Pérez-Campo R. et al.Vitamin E protects guinea pig liver from lipid peroxidation without depressing levels of antioxidants.Int J Biochem Cell Biol. 1995; 27: 1175-1181Crossref PubMed Scopus (42) Google Scholar, 10Willy C. Thiery J. Menger M. et al.Impact of vitamin E supplement in standard laboratory animal diet on microvascular manifestation of ischemia reperfusion injury.Free Radic Biol Med. 1995; 19: 919-926Crossref PubMed Scopus (32) Google Scholar Indeed, primary prevention during ischemia/reperfusion injury might be achieved by using oral supplementation. Yet, this approach is not practical during acute episodes of oxidative stress. In these situations parenteral vitamin E might seem to be more appropriate management. α-Tocopherol is the naturally occurring compound with the highest vitamin E activity. It has 3 chiral centers (at 2′, 4′, and 8′ in Figure 1) at which the methyl groups are in the R-configuration but can exist as 7 other isomers. According to International Union of Pure and Applied Chemistry (IUPAC), the correct name is therefore 2R, 4R, and 8R-α-tocopherol. It usually is accompanied by small amounts of β-, γ-, and δ-tocopherol, which differ by the number and positions of the methyl groups attached to the ring. In addition, there are naturally occurring tocotrienols with 3 additional double bonds in the phytyl side chain (Figure 2). Finally, various synthetic or half-synthetic α-tocopherols are always mixtures of the various stereoisomers. The most common form of synthetic vitamin E consists of 8 stereoisomers, and has only a 12.5% RRR-α-tocopherol content. The mixture is called all-rac-α-tocopherol. IUPAC recommends the use of the biochemical nomenclature (in analogy to vitamin A): vitamin E comprises all tocopherols and tocotrienols that have the same qualitative biological activity as RRR-α-tocopherol. However, quantitatively, their biological effects vary greatly. All naturally occurring tocopherols/tocotrienols show less than 50% of the activity of RRR-α-tocopherol (=100%). The all-rac-α-tocopherol form shows 74%, and all-rac-α-tocopherol acetate, which frequently is used in medications and esterified for increased stability, shows 67%. To account for these various degrees of vitamin E activity, nutrient tables use the term α-tocopherol equivalents, for purposes of which the effect of RRR-α-tocopherol is equivalent to 100%. Vitamin E in medications and in pure compounds have been described in international units (IU) or USP (United States Pharmacopeia), although milligram (mg) is preferred.Figure 2Structure of the naturally occurring tocotrienols.View Large Image Figure ViewerDownload (PPT) Vitamin E is absorbed in the intestine together with lipids after any tocopheryl esters have been hydrolyzed by lipases or mucosal esterases. The average absorption rate is 30%, with α-tocopherol and its esters being better absorbed than the other forms. The absorbed vitamin E is transported rapidly to the liver; only small amounts are released from the chylomicrons by lipoprotein lipase on the surface of endothelial cells. Vitamin E incorporated in very low density lipoproteins (VLDL) is released back into the bloodstream. There, a dynamic equilibrium exists between all lipoprotein fractions owing to a rapid interchange. Uptake into the target cells occurs either through release by endothelium-based lipoprotein lipase or via receptor-mediated low-density lipoprotein (LDL) endocytosis. Vitamin E is stored in fatty tissue and muscle, preferentially as RRR-α-tocopherol. Recently, an explanation for this was found in a cloned human gene that encodes for a hepatic α-tocopherol transfer protein. It causes RRR-α-tocopherol to be incorporated preferentially into VLDL, whereas other forms of vitamin E are excreted quickly via bile fluid. In animal cells, α-tocopherol is a component of all biological membranes. According to the current state of knowledge, its most important function is to protect membranes from lipid peroxidation. Because of exposure to light, heat, and/or chemicals, as well as through many metabolic processes, free radicals form in the body. If a polyunsaturated fatty acid (PUFA) is attacked by a radical X, 1 of the 2 H atoms is removed from the methylene group between the 2 double bonds, resulting in a highly reactive lipid radical (missing electron). When the latter bonds with O2, a highly reactive lipid peroxide radical is formed. The latter either will react with another fatty acid to form a stable, nonphysiologic, but cytotoxic lipid peroxide or fuse with another peroxide molecule. During the transfer of the H atom, an additional lipid radical is formed, triggering an autocatalytic chain reaction. Uninterrupted, this process quickly can destroy the affected biological membrane's function. Vitamin E has a very strong affinity for lipid peroxide radicals: transfer of an H atom from vitamin E to the lipid peroxide radical results in a stable lipid hydroperoxide and a vitamin E radical. Because the latter is resonance-stabilized and therefore extremely inert, this interrupts the chain reaction. The tocopherol radical, which is anchored in the cell membrane, is reconverted to vitamin E by ascorbic acid (vitamin C) inside the watery cytosol (Figure 3). Plant germs and seeds, as well as their oils, and products derived from them are the best sources of vitamin E. In wheat germ, sunflower seeds, cotton-seed, and olive oil, RRR-α-tocopherol makes up most (50%–100%) of the vitamin E, whereas γ-tocopherol, which has only 10% of the biological activity, dominates in soy and corn oil. Most oils sold as vegetable oil contain various amounts of soy, corn, and cottonseed oils; margarines contain mostly soy, corn, and sunflower oils. Their natural vitamin E activity depends on their sunflower or cottonseed components, otherwise, synthetic vitamin E may be added as a stabilizer. Cold-pressed wheat germ oil has the highest natural vitamin E content. Estimates of adequate vitamin E intakes depend on the intake of PUFAs: 0.5 mg RRR-α-tocopherol should be supplied for every gram of diene fatty acids; even many plant oils do not contain these amounts (eg, soy oil contains approximately 0.3 mg). An intake of 24 mg of diene equivalents (18 g linolenic acid) therefore would mean a calculated requirement of 12 mg of α-tocopherol per day. A severe vitamin E deficiency with typical clinical signs is rare. Ataxia with isolated vitamin E deficiency is a rare autosomal-recessive neurodegenerative disease caused by mutation in the α-tocopherol transfer protein. As a consequence, the transfer of vitamin E into VLDL within the liver is impaired and low plasma levels (<3 mg/dL) of vitamin E are the consequence despite adequate intake. Clinical signs are gait and limb ataxia, dysarthria, lower-limb areflexia, loss of vibration and positional sense, and bilateral extensor planar reflexes. Besides the genetic reason for vitamin E deficiency, low levels of plasma vitamin E are seen in children with chronic fat malabsorption11Muller D.P. Lloyd J.K. Wolff D.H. Vitamin E and neurological function: abetalipoproteinemia and other disorders of fat absorption.CIBA Found Symp. 1983; 101: 106-117PubMed Google Scholar such as biliary tract disease.12Sokol R.J. Heubi J.E. Iannaccone S.T. et al.Vitamin E deficiency with normal serum vitamin E concentrations in children with chronic cholestasis.N Engl J Med. 1984; 310: 1209-1212Crossref PubMed Scopus (166) Google Scholar In preterm infants immature fat absorption and low body stores of vitamin E both contribute to a borderline vitamin E status. Iron supplementation and milk formula with high linoleic acid and PUFA enhance the signs of deficiency,13Ritchie J.H. Fish M.B. McMasters V. et al.Edema and hemolytic anemia in premature infants A vitamin E deficiency syndrome.N Engl J Med. 1968; 279: 1185-1190Crossref PubMed Scopus (100) Google Scholar, 14Williams M.L. Shoot R.J. O'Neal P.L. et al.Role of dietary iron and fat on vitamin E deficiency anemia of infancy.N Engl J Med. 1975; 292: 887-890Crossref PubMed Scopus (101) Google Scholar which are edema formation, thrombocytosis, and hemolytic anemia. The clinical assessment of vitamin E deficiency in preterm infants is difficult because plasma levels do not reflect tissue concentrations.15Greer F.R. Vitamin metabolism and requirements in the micropremie.Clin Perinatol. 2000; 27: 95-118Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar A tocopherol-to-lipid ratio of 0.8 mg/g has been recommended as a sufficient vitamin E status.16Johnson L. Vitamin E nutrition in fetuses and newborn.in: Polin R.A. Fox W.W. Fetal and neonatal physiology. 2nd ed. WB Saunders, Philadelphia1998: 425-442Google Scholar Newborn or premature infants in most instances do not show abnormalities in circulating lipid levels. Furthermore, because of inadequate sample size vitamin E status is expressed primarily as μmol/L in newborns. α-Tocopherol levels less than 10 μmol/L are associated with increased red blood cell peroxide hemolysis, an indicator for vitamin E deficiency. Plasma levels between 12 and 35 μmol/L can be achieved in term infants and in children with a parenteral supply of 7 mg all-rac-α-tocopherol.17Greene H.L. Moore M.E. Phillips B. et al.Evaluation of a pediatric multiple vitamin preparation for total parenteral nutrition II. Blood levels of vitamins A, D, and E.Pediatrics. 1986; 77: 539-547PubMed Google Scholar Deficiency in adults may result from the earlier-mentioned mutation of the gene responsible for formation of the α-tocopherol transfer protein or a β-lipoproteinemia. The cause of the latter is an absence of apoprotein B, which results in a failure to absorb and transport vitamin E. Dietary reasons for vitamin E deficiency are the result of long-lasting fat malabsorption. In adults with fat malabsorption early vitamin E deficiency generally is asymptomatic. Typical neurologic signs such as ataxia, weakness, and visual changes occur with chronic advanced deficiency.18Satya-Murti S. Howard L. Krohel G. et al.The spectrum of neurological disorders from vitamin E-deficiency.Neurology. 1986; 36: 917-921Crossref PubMed Google Scholar Vitamin E supplementation (200 mg/day) improves neurologic symptoms in cases of long-standing fat malabsorption (short-bowel syndrome) a few months after normalization of vitamin E status.19Howard L. Ovesen L. Satya-Murti S. et al.Reversible neurological symptoms caused by vitamin E deficiency in a patient with short bowel syndrome.Am J Clin Nutr. 1982; 36: 1243-1249PubMed Scopus (75) Google Scholar Vitamin E deficiency also may be a problem in patients undergoing long-term parenteral nutrition (PN). However, critical studies evaluating the incidence, consequences, and time course of vitamin E deficiency in these patients still are unavailable. Porter et al20Porter L. Reynolds N. Ellis J.D. Total parenteral nutrition, vitamin E, and reversible macular dysfunction morphologically mimicking age related macular degeneration.Br J Ophthalmol. 2005; 89: 1530-1532Crossref PubMed Scopus (8) Google Scholar described a case of long-term PN with vitamin E deficiency (plasma level, <12 μmol/L; normal range, 14–39 mmol/L) in which the patient developed visual symptoms and signs of macular degeneration. The patient described altered color perception and enlarging central scotomata. Treatment with vitamin supplementation led to complete resolution of symptoms in 3 weeks. What route, dose, and formulation of vitamin E treatment was used to manage the symptomatic deficiency? The original text of the case report does not provide this information. Vitamin E deficiency favors formation of lipofuscin in the retinal pigment epithelium and the deficiency may result in retinal degeneration. Neurologic symptoms caused by vitamin E deficiency, as described earlier, are potentially reversible if vitamin E is supplemented. Consequently, plasma vitamin E levels should be monitored on a regular basis for patients receiving long-term PN. Low levels of vitamin E may exist without detectable clinical signs or symptoms and can present acutely as a result of oxidative stress, as in major trauma or surgery. Plasma levels of vitamin E decrease during surgery and as a consequence of trauma they decrease to very low levels. Frey et al21Frey B. Johnen W. Haupt R. et al.Bioactive oxidized lipids in the plasma of cardiac surgical intensive care patients.Shock. 2002; 18: 14-17Crossref PubMed Scopus (10) Google Scholar showed that in patients who had undergone cardiac surgery and developed postoperative complications, systemic inflammatory response syndrome, or multiorgan failure, the ratio of α-tocoquinone (degradation product of vitamin E) to α-tocopherol in plasma increased significantly compared with a control group without complications. These data suggest that α-tocopherol is degraded in multiorgan failure and systemic inflammatory response syndrome patients owing to increased lipid peroxidation. Plasma α-tocopherol levels may be used to detect deficiency. Levels below 11.6 μmol/L suggest vitamin E deficiency. In fat malabsorption, low plasma lipid levels can affect plasma vitamin E levels, thus a low ratio of plasma α-tocopherol to plasma lipids (<0.8 mg/g total lipid) is the most accurate indicator in adults. Plasma levels greater than 12 μmol/L do not necessarily indicate a sufficient vitamin E supply, especially in patients on home PN (HPN). Patients receiving PN for 69 ± 45 months (mean ± SD) showed normal plasma levels compared with controls, but lower α-tocopherol/cholesterol ratios in adipose tissue. The mean values were not significantly different, although were lower in PN patients (55 ± 36 vs 106 ± 63, respectively; P < .04).22Steephen A.C. Traber M.G. Ito Y. et al.Vitamin E status of patients receiving long-term parenteral nutrition: is vitamin E supplementation adequate?.JPEN J Parenter Enteral Nutr. 1991; 15: 647-652Crossref PubMed Scopus (37) Google Scholar This suggests that current vitamin E supplementation may not be sufficient to ensure adequate tissue stores. The reason for low tissue stores may be a result of an overestimation of the contribution of γ-tocopherol, the major vitamin E compound in soybean oil. Based on kinetic data the γ-tocopherol content of lipid emulsions cannot be used to assess vitamin E status.23Traber M.G. Carpentier Y.A. Kayden H.J. et al.Alterations in plasma alpha- and gamma-tocopherol concentrations in response to intravenous infusion of lipid emulsions in humans.Metabolism. 1993; 42: 701-709Abstract Full Text PDF PubMed Scopus (31) Google Scholar Tissue levels may be determined using the recently described buccal mucosa assay.24Erhardt J.G. Mack H. Sobeck U. et al.Beta-carotene and alpha-tocopherol concentration and antioxidant status in buccal mucosal cells and plasma after oral supplementation.Br J Nutr. 2002; 87: 471-475Crossref PubMed Scopus (39) Google Scholar In smokers the levels of α-tocopherol in buccal mucosa cells are significantly (P = .002) lower (74.9 ng/106 cells) than in nonsmokers (141.1 ng/106 cells) despite nonsignificant differences in α-tocopherol plasma levels (1.48 vs 1.73 μg/dL, respectively).25Gabriel H.E. Liu Z. Crott J.W. et al.A comparison of carotenoids, retinoids, and tocopherols in the serum and buccal mucosa of chronic cigarette smokers versus nonsmokers.Cancer Epidemiol Biomarkers Prev. 2006; 15: 993-999Crossref PubMed Scopus (37) Google Scholar Dietary vitamin E intake of smokers (4 mg/kcal) was lower than that of nonsmokers (9.3 mg/kcal), yet not significantly different. Regarding dietary intake vitamin E is a critical micronutrient. Data from the National Health and Nutrition Examination Survey (NHANES) 2001–2002 survey in US adults showed that only 5% of men and 4% of women met the vitamin E recommended daily requirement (15 mg/day), and only 10%–11% and 7%–8%, respectively, met the Estimated Average Requirements (12 mg/day).26Gao X. Wilde P.E. Lichtenstein A.H. et al.The maximal amount of dietary alpha-tocopherol intake in U.S. adults (NHANES 2001–2002).J Nutr. 2006; 136: 1021-1026PubMed Scopus (64) Google Scholar Based on studies with apples fortified with deuterium-labeled α-tocopheryl acetate the amount of dietary vitamin E needed daily to replace irreversible losses is ≤15 mg/day.27Bruno R.S. Leonard S.W. Park S.I. et al.Human vitamin E requirements assessed with the use of apples fortified with deuterium-labeled alpha-tocopheryl acetate.Am J Clin Nutr. 2006; 83: 299-304PubMed Scopus (75) Google Scholar Because the vitamin E plasma level is regulated via the activity of the tocopherol binding protein, a normal level may exist despite low tissue levels. To define patients at risk for inadequate intake, different risk groups or risk profiles have to be considered. Instructions to reduce fat intake as part of weight management results in a 50% reduction in vitamin E intake.28Mueller-Cunningham W.M. Quintana R. Kasim-Karakas S.E. An ad libitum, very low-fat diet results in weight loss and changes in nutrient intakes in postmenopausal women.J Am Diet Assoc. 2003; 103: 1600-1606Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar, 29Ernst B. Thurnheer M. Schmid S.M. et al.Evidence for the necessity to systematically assess micronutrient status prior to bariatric surgery.Obes Surg. 2009; 19: 66-73Crossref PubMed Scopus (173) Google Scholar, 30Kumar N. Nutritional neuropathies.Neurol Clin. 2007; 25: 209-255Abstract Full Text Full Text PDF PubMed Scopus (84) Google Scholar In cases of bariatric surgery this problem may increase. Patients with fat malabsorption because of either inflammatory bowel diseases or cystic fibrosis are at risk for inadequate supply of fat-soluble micronutrients, in particular vitamin E.31Back E.I. Frindt C. Nohr D. et al.Antioxidant deficiency in cystic fibrosis: when is the right time to take action?.Am J Clin Nutr. 2004; 80: 374-384PubMed Scopus (60) Google Scholar In general, as described earlier, vitamin E intake is rather low, a fact that should be considered in cases of PN. Preterm infants may be more susceptible to liver damage from high intakes of vitamin E. A parenteral supply of 25–100 mg α-tocopherol-acetate (E-ferol Aqueous solution; Carter Glogau Labs, Inc, Glendale, AZ) to very low birthweight infants for as little as 1 week resulted in coagulopathy with liver failure. However, it is not clear whether this truly was caused by the vitamin E32Johnson L. Bowen Jr, F.W. Abbasi S. et al.Relationship of prolonged pharmacologic serum levels of vitamin E to incidence of sepsis and necrotizing enterocolitis in infants with birth weight 1,500 grams or less.Pediatrics. 1985; 75: 619-638PubMed Google Scholar, 33Phelps D.L. Toxicity of pharmacologic parenteral doses of vitamin E in neonatal kitten.Pediatr Res. 1979; 13: 372Google Scholar or by the solubilizer polysorbate. In general, toxic effects from high doses of vitamin E are quite rare even after a high intake for several years.34Bell S.J. Grochoski G.T. How safe is vitamin E supplementation?.Crit Rev Food Sci Nutr. 2008; 48: 760-774Crossref PubMed Scopus (35) Google Scholar Irrespective from the oral dose given, plasma level seldom exceeded 2–3 times that of normal value; plasma saturation often is achieved at 200 mg/day. This is because of the controlled transfer of vitamin E to VLDL and because of an intricate yet undefined mechanism controlling gut absorption.35Traber M.G. Vitamin E regulatory mechanisms.Ann Rev Nutr. 2007; 27: 347-362Crossref PubMed Scopus (303) Google Scholar, 36Lodge J.K. Vitamin E bioavailability in humans.J Plant Physiol. 2008; 32: 201-209Google Scholar From numerous studies on the prophylactic and therapeutic use of vitamin E it has been concluded that vitamin E, even in large supplemental oral doses of up to 3200 IU/day, causes no consistent adverse effects. Data regarding the toxicity of parenteral vitamin E do not exist. Indeed, the risk of an intake below the individual's need seems much more probable than the risk of toxicity. Vitamin E can be degraded by photooxidation in parenteral solutions. The mechanism of degradation involves a photocatalyzed reaction with oxygen. Consequently, factors influencing the availability of oxygen (the filling process or permeation through the bag) will influence the rate and degree of degradation. Because of the lower antioxidant activity of the synthetic vitamin E formulation (all-RAC-α-tocopheryl-acetate) frequently used in parenteral products, natural vitamin E (RRR-α-tocopherol) or the 2-R-isomers are preferred to ensure better stability. In addition, the relative content of the bioactive α-tocopherol to γ-tocopherol (less active) differs within different lipid emulsions. As a consequence, the protective effect in vitro and in vivo might be lower depending on the ratio of the isomers.37Gutcher G.R. Lax A.A. Farrell P.M. Tocopherol isomers in intravenous lipid emulsions and resultant plasma concentrations.JPEN J Parenter Enteral Nutr. 1984; 8: 269-273Crossref PubMed Scopus (34) Google Scholar The photooxidation of vitamin E may be prevented by the presence of ascorbic acid (competition for oxygen) and the type of bag used; multilayered bags substantially reduce oxidation reactions by preventing oxygen permeation from the air into the solution.38Allwood M.C. Martin H.J. The photodegradation of vitamins A and E in parenteral nutrition mixtures during infusion.Clin Nutr. 2000; 19: 339-342Abstract Full Text PDF PubMed Scopus (60) Google Scholar The study of Allwood and Martin38Allwood M.C. Martin H.J. The photodegradation of vitamins A and E in parenteral nutrition mixtures during infusion.Clin Nutr. 2000; 19: 339-342Abstract Full Text PDF PubMed Scopus (60) Google Scholar indicated that vitamin E is relatively stable, even if not light-protected during administration, in multilayered bags. This also has been documented by Haas et al39Haas C. Genzel-Boroviczény O. Koletzko B. Losses of vitamin A and E in parenteral nutrition suitable for premature infants.Eur J Clin Nutr. 2002; 56: 906-912Crossref PubMed Scopus (20) Google Scholar in PN suitable for premature infants. In contrast, there is a substantial loss in 2-in-1 mixtures in ethylene vinyl acetate bags. Fat emulsions provide some, but not sufficient, protection. In 3-in-1 mixtures vitamins will be degraded and lipids may undergo peroxidation owing to light and oxygen exposure. As recently documented, the formulation of the mixture may influence the degradation process.37Gutcher G.R. Lax A.A. Farrell P.M. Tocopherol isomers in intravenous lipid emulsions and resultant plasma concentrations.JPEN J Parenter Enteral Nutr. 1984; 8: 269-273Crossref PubMed Scopus (34) Google Scholar Vitamin E (α- and γ-tocopherol) were more stable in mixtures containing medium chain triglycerides (MCT) than in soy and olive oil, and vitamin E (α-tocopherol) is significantly more stable in lyophilized multivitamin mixtures than in an emulsified form.40Guidetti M. Sforzini A. Bersani G. et al.Vitamin A and vitamin E isoforms stability and peroxidation potential of all-in-one admixtures for parenteral nutrition.Int J Vitam Nutr Res. 2008; 78: 156-166Crossref PubMed Scopus (10) Google Scholar Skouroliakou et al41Skouroliakou M. Matthaiou C. Chiou A. et al.Physicochemical stability of parenteral nutrition supplied as all-in-one for neonates.JPEN J Parenter Enteral Nutr. 2008; 32: 201-209Crossref PubMed Scopus (24) Google Scholar evaluated the stability of vitamin E in all-in-one mixtures for PN of neonates. In these all-in-one mixtures vitamin E (6.4 mg) remained stable (90%) within 24 hours, but started to decrease after 24 hours. However, 24 hours after the preparation of the all-in-one mixture, the peroxide load increased about 8 times and after 7 days it increased 14 times. This increase seems to be related to the α-tocopherol concentration as suggested by the investigators. The data regarding vitamin E and peroxide level strengthen the importance of adequate vitamin E concentration in fat emulsions to protect PUFA and to deliver vitamin E. The approach of Skouroliakou et al,41Skouroliakou M. Matthaiou C. Chiou A. et al.Physicochemical stability of parenteral nutrition supplied as all-in-one for neonates.JPEN J Parenter Enteral Nutr. 2008; 32: 201-209Crossref PubMed" @default.
• W1975109406 created "2016-06-24" @default.
• W1975109406 creator A5025078895 @default.
• W1975109406 date "2009-11-01" @default.
• W1975109406 modified "2023-09-24" @default.
• W1975109406 title "Vitamin E Requirements in Parenteral Nutrition" @default.
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