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Competing Interests: Declaration of interests We declare no competing interests.

Background: College students may have a risk of fat-soluble vitamin deficiencies due to unhealthy dietary habits, especially for vitamin A and E. They are important members of the human antioxidant network; deficiencies of these vitamins may increase the risk of many critical diseases., Objective: The current study was undertaken to determine the status of vitamin A and E in college students., Methods: Healthy college students were recruited, and fasting blood samples of them were collected and used for determining serum levels of retinol and α-tocopherol by the HPLC method., Results: We found that there was no vitamin A deficiency in college students. However, vitamin E deficiency existed in 34.5% of college students, especially in males. All the students had no vitamin E adequacy. In addition, our findings showed that BMI was inversely associated with serum α-- tocopherol, but not serum retinol., Conclusion: These results suggest that vitamin E deficiency in college students should be given more attention, and it is necessary to consider using vitamin E supplements., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Vitamin E is important because of its antioxidant activity in situations of oxidative stress, especially postnatally. Hence, the objective was to verify whether maternal alpha-tocopherol level is associated with the alpha-tocopherol levels of the newborn and colostrum. This is a cross-sectional study of 58 women and their term newborns from a public hospital. Blood and colostrum were collected to measure alpha-tocopherol levels by high-performance liquid chromatography. Mothers with serum alpha-tocopherol levels <16.2 mmol L(-1) and newborns <11.6 mmol L(-1) were indicative of deficiency or low levels. Mothers were divided into two groups: <16.2 mmol L(-1) and those with levels ≥16.2 mmol L(-1) . The mean (95% confidence interval) serum alpha-tocopherol levels of mothers, umbilical cords and colostrum were 28 (24-32), 6 (5-8) and 39 mmol L(-1) (32-45), respectively (P < 0.001); 19% of the women and 90% of the newborns had low alpha-tocopherol levels. Maternal alpha-tocopherol level was associated with that of the umbilical cord. Newborns from mothers at risk of deficiency had low alpha-tocopherol levels (P < 0.001). Colostrum levels of vitamin E were not influenced by maternal serum. Maternal deficiency influenced the vitamin E level of the umbilical cord but does not in the colostrum, evidencing distinct transfer mechanisms via the mammary gland., (© 2016 John Wiley & Sons Ltd.)

Background: The purpose of this study was to identify the frequency of fat-soluble vitamin deficiencies in children with celiac disease (CD) and to determine the value of routine testing for these deficiencies., Methods: We conducted a retrospective medical record review of patients with a confirmed diagnosis of CD and fat-soluble vitamin levels measured at diagnosis between 1995 and 2012 at Mayo Clinic. Patients' demographics, fat-soluble vitamin levels, and pertinent clinical factors at the time of diagnosis were collected., Results: Eighty-three patients were included in the final analysis: 51 girls and 32 boys, with an average age at diagnosis of 12.8 years in girls and 13.0 years in boys. The most commonly reported symptoms were abdominal pain in 49 patients and diarrhea in 30 patients. Family history of CD was reported in 32 patients. Average vitamin levels for vitamin E, 25-hydroxyvitamin D (25 (OH) D), and vitamin A were 7.5 mg/L, 32.8 ng/mL, and 334.5 μg/dL, respectively. No patients had vitamin A deficiency, 2 patients had vitamin E deficiency, and 9 patients had mild-to-moderate vitamin D deficiency (none had severe deficiency). Both patients with vitamin E deficiency were symptomatic and had complete villous atrophy. Thirty-one patients had insufficiency of 25 (OH) D, which was less than the reported frequency of vitamin D insufficiency in the general pediatric population in the United States in 2004. None of the patients were receiving vitamin supplements at the time of diagnosis., Conclusions: Fat-soluble vitamin deficiencies are uncommon in children with new diagnosis of CD. Routine measuring of fat-soluble vitamins levels may not be necessary.

Background: Nitrogen-bisphosphonates (N-BPs) are the most widely used drugs for bone fragility disorders. Long-term or high-dose N-BP use is associated with unusual serious side effects such as osteonecrosis of the jaw, musculoskeletal pain, and atypical fractures of long bones. It has escaped notice that the pathway N-BPs block is central for the endogenous synthesis of coenzyme Q10, an integral enzyme of the mitochondrial respiratory chain and an important lipid-soluble antioxidant. Our objective was to assess the coenzyme Q10 and antioxidant status in relation to N-BP exposure in women with postmenopausal osteoporosis., Methods: Seventy-one postmenopausal women (age, 73.5 ± 5.5 y) with osteoporosis and no other malignancy were included in this cross-sectional study. Seventeen were treatment naive, 27 were on oral N-BP, and 27 were on i.v. N-BP., Results: Vitamin E γ-tocopherol levels (μmol/mL) were significantly reduced in N-BP users [oral, H(2) = 18.5, P = .02; i.v., H(2) = 25.2, P < .001; mean rank comparisons after Kruskal-Wallis test). Length of time (days) of N-BP exposure, but not age, was inversely associated with the coenzyme Q10/cholesterol ratio (μmol/mol) (β = -0.27; P = .025), which was particularly low for those on i.v. N-BP (mean difference = -35.0 ± 16.9; 95% confidence interval, -65.2 to -4.9; P = .02)., Conclusion: The degree of N-BP exposure appears related to compromised coenzyme Q10 status and vitamin E γ-tocopherol levels in postmenopausal women with osteoporosis. This phenomenon may link to certain adverse N-BP-associated effects. Confirmation of this would suggest that therapeutic supplementation could prevent or reverse certain complications of long-term N-BP therapy for at-risk individuals.

Objective: To describe epidemiological, clinical, and pathological features of neuroaxonal dystrophy in Quarter Horses (QHs) on a single farm., Design: Prospective case series. Animals-148 horses., Procedures: Neurologic, pathological, and toxicological evaluations were completed in selected neurologically affected horses over a 2-year period. Descriptive statistical analysis was performed., Results: 87 QHs and 1 QH-crossbred horse were affected. Most (50/88 [56.8%]) affected horses were 1 to 2 years old (median age, 2 years [range, 2 months to 34 years]). Neurologic deficits included obtundation (53/88 [60%] horses), decreased to absent menace response (33/88 [37.5%]), proprioceptive positioning deficits, wide-based stance, ataxia, and dysmetria (88/88 [100%]). Most (78/88 [88.6%]) horses had mild ataxia, but some (10/88 [11.4%]) had moderate to severe ataxia. Low serum concentrations of vitamin E (≤ 2 mg/L) were detected in 3 index case horses and 16 of 17 randomly selected horses (13/14 affected and 3/3 unaffected) during study year 1. Dietary vitamin E supplementation did not improve neurologic deficits in affected horses; vitamin E administration in pregnant mares appeared to decrease but not prevent disease development among offspring born the following year. Lesions detected at necropsy included bilaterally symmetric neuroaxonal degeneration with axonal spheroids in the nucleus gracilis, nucleus cuneatus medialis, nucleus cuneatus lateralis, and nucleus thoracicus (5/5 horses)., Conclusions and Clinical Relevance: Neuroaxonal dystrophy should be considered in evaluation of young horses with ataxia and proprioceptive positioning deficits. Vitamin E deficiency may contribute to disease severity.

Objective: To determine vitamin A and vitamin E status in very low birth weight (VLBW) infants at the time of birth (TB), at the time of full feeding (TFF) and at term postmenstrual age (TT)., Study Design: An observational study was conducted in VLBW infants. Plasma retinol and α-tocopherol levels were measured at TB, TFF and TT. Multivitamin supplementation was given to all infants to meet the daily requirement., Result: A total of 35 infants were enrolled. The median (interquartile range) of gestational age and birth weight was 30 (28 to 32) weeks and 1157 g (982 to 1406 g). The median of vitamin A and vitamin E intakes from TFF to TT was 832 and 5.5 IU kg(-1) day(-1), respectively. Vitamin A deficiency occurred in 67.7% at birth, 51.6% at TFF and 82.1% at TT. Vitamin E deficiency occurred in 77.4% at birth, 16.1% at TFF and 35.7% at TT. Small-for-gestational age was the only risk factor for vitamin A deficiency. Lower amount of breast milk consumption was associated with higher incidence of vitamin E deficiency. No differences in vitamin A- or vitamin E-related morbidities between infants with and without vitamin deficiencies were found., Conclusion: High prevalence of vitamin A and vitamin E deficiency was found in VLBW infants starting from birth to term postmenstrual age. Therefore, a higher dose of vitamin supplementation is required.

This study was designed to determine the status of selenium, dl-alpha-tocopherol, and all-trans-retinol in adults living in Al-Kharj district using serum and toenail samples, and to look for possible association between these parameters and the etiology of endemic diseases in the same area. For this purpose, we examined a cross section of samples of 743 healthy Saudi adults on routine visits to the Primary Health Care Unites (PHCUs) for different common health problems. The arithmetic mean for selenium, dl-alpha-tocopherol, and all-trans-retinol in serum and toenail selenium levels were 107.045 +/- 23.045 microg/l (n = 743, range 52.600-210.120 microg/l), 1.053 +/- 0.324 mg/dl (n = 737, range 0.29-3.42 mg/dl), 52.561 +/- 25.671 microg/dl (n = 743, range 11.20-400.85 microg/dl), and 0.634 +/- 0.221 microg/g (n = 691, range < DL - 1.797 microg/g), respectively. The average serum selenium concentration seems to be satisfactory and compares favourably with high selenium intake countries. Although none of our participants exhibited serum selenium deficiency (< 45 microg/l), 41% of our participants had toenail selenium < 0.56 microg/g reported low levels in the previous study. The mean serum dl-alpha-tocopherol concentrations fall within the upper limit of the normal range of > 0.698-1.981 mg/dl for alpha-tocopherol as found in previous studies. On the other hand, the mean serum all-trans-retinol is higher than the normal range (20-30 microg/dl). None had exhausted retinol stores trans-retinol and MDA levels in the serum was found as a sign of peroxidative lipid damage, confirming the role of vitamin A in reducing oxidative stress. Our data also revealed a link between the status of selenium, dl-alpha-tocopherol and all-trans-retinol and a number of health problems. However, these observations need larger epidemiological studies for further confirmation.

Alpha-, beta-, gamma- and delta-tocopherol are present in many foods and are, in the absence of fat malabsorption, well absorbed from the gut. Their anti-oxidant property is well known and protects arteries and capillaries as well as blood lipids and nervous tissue against oxidative stress. In contrast to beta-, gamma- and delta-tocopherol, alpha-tocopherol is preferentially conserved by the discriminating action of the liver alpha-tocopherol transfer protein, which also maintains plasma alpha-tocopherol concentration within a range of 20 to 40 microM. In the circulation, alpha-tocopherol, in association with the transfer-protein, is assembled into the very low-density lipoprotein and low-density lipoprotein particles and released for use by the peripheral tissues. Recent data suggest that alpha-tocopherol is not only an anti-oxidant but also a regulator of gene expression through its binding to nuclear receptors. The precise mechanism of regulating gene expression, however, is still unknown. The four tocopherols are ultimately degraded by omega-oxidation and subsequent beta-oxidations followed by the elimination of the metabolites in the bile and in the urine. Patients with a defect of the alpha-tocopherol transfer protein are unable to maintain their alpha-tocopherol reserves and progressively lose tendon reflexes and have signs and symptoms of spinocerebellar ataxia while plasma vitamin E level drops below 2 microg/ml.

Objective: This study sought to determine and evaluate the intakes and plasma concentrations of vitamin E (alpha-tocopherol), gamma-tocopherol, vitamin C, selenium, and carotenoids (alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein/zeaxanthin, and lycopene) of nonsupplemented boys and girls, 4 to 8 years old, of Latino immigrants living in rural Nebraska., Design: Dietary intakes of the Latino children were estimated. Their plasma samples (fasting) were analyzed for vitamin E, vitamin C, selenium, and carotenoid concentrations. Data were evaluated by sex., Subjects: The subjects were a convenience sample of 4- to 8-year-old (n=29), apparently healthy, nonsupplemented children of Latino immigrants living in rural Nebraska., Statistical Analysis: Sex differences in parameter values were determined using general linear models; Pearson r was used for determining correlations., Results: No significant differences in parameter values were observed by sex, with the exception of plasma lutein/zeaxanthin concentration. The majority (69%) had plasma vitamin E (alpha-tocopherol) concentrations<0.516 mg/dL (12 micromol/L), which is indicative of vitamin E inadequacy, and over half (59%) reported consuming less than the Estimated Average Requirement for vitamin E. All subjects had plasma vitamin C and selenium concentrations indicative of adequacy (>0.41 mg/dL or >23 micromol/L, and >6.32 microg/dL or >0.8 micromol/L, respectively), and consumed at least the Recommended Dietary Allowances for these nutrients. The plasma carotenoid concentrations of the children may be useful as norms., Conclusions: These children of Latino immigrants who did not take supplements had low plasma vitamin E (alpha-tocopherol) concentrations but normal plasma vitamin C and selenium concentrations., Implications: Dietetics professionals and others involved in health care need to work with Latino immigrant parents so that their children consume adequate amounts of vitamin E.

In that data were not available on the vitamin E status of young children, the aim of the study was to evaluate the vitamin E status of preschool children by three commonly used criteria: vitamin E intakes, plasma alpha-tocopherol concentrations and plasma alpha-tocopherol/total lipid ratios. Twenty-two ethnically diverse preschool children (13 males and 9 females), aged 2 to 5 years, living in Lincoln, NE, served as subjects. The subjects were in two groups: 2-3 and 4-5 years old. Energy, fat, and alpha- and gamma-tocopherol intakes of the subjects were estimated utilizing two 24-h food recalls. Plasma alpha- and gamma-tocopherol and total lipid concentrations were ascertained. No significant differences by age grouping or gender were observed for vitamin E intakes, plasma alpha-tocopherol concentrations, plasma gamma-tocopherol concentrations and plasma alpha-tocopherol/total lipid ratios of subjects. Plasma alpha-tocopherol concentrations indicative of less than adequate status (<12 micromol/L) were observed in 91% of the children, and values <7 micromol/L (proposed cutoff for pediatric populations) in 68%. Sixty-eight percent of the subjects had plasma alpha-tocopherol/total lipid values <0.8 mg/g. The majority of the 2- to 5-year-old children included in the study had less than adequate vitamin E status.

Chronic gastrointestinal disease can result in nutritional deficiencies that can have a direct effect on the neurologic system. Although acute abnormalities can be corrected, symptoms are rarely reversible. Recognizing the appropriate abnormality is a crucial part of long-term treatment strategies in this population. Because motor and cerebellar symptoms can contribute to poor feeding, aggressive supplementation should begin as soon as symptoms are recognized. We present a patient with delayed onset and progressive hypovitaminosis E and briefly review diagnostic and therapeutic options.

A sheep flock experienced losses in weaned lambs from myopathy and hepatic lipidosis. Investigation revealed painful ambulation, illthrift, and unexpected death in lambs with normal selenium levels, deficient vitamin E levels, and elevated muscle and liver enzyme levels. Vitamin E deficiency should be considered when investigating myopathy and illthrift in lambs.

In order to investigate the pathogenic mechanism responsible for liver injury associated with chronic alcoholism, we studied the effects of different dietary vitamin E levels in chronically ethanol (EtOH)-fed rats on the activity and mRNA regulation of the manganese superoxide dismutase (MnSOD) enzyme. Evidence is accumulating that intermediates of oxygen reduction may in fact be associated with the development of alcoholic liver disease. Since low vitamin E liver content seems to potentiate EtOH-linked oxidative stress, we studied the effect of EtOH treatment in livers from rats fed a diet deficient or supplemented with vitamin E. Chronic EtOH feeding enhanced hepatic consumption of vitamin E in both groups of EtOH-treated animals, irrespectively of the vitamin E level of the basal diet and the effect was observed in both the microsomal and mitochondrial fractions. Both EtOH-fed groups exhibited increased MnSOD gene expression, while the enzyme activity was enhanced only in the vitamin E-deprived group of EtOH-treated animals. The significant increase in manganese liver content found only in this last group could explain the rise of enzyme activity. In fact, in the absence of a parallel increase of the prosthetic ion manganese, MnSOD mRNA induction was not accompanied by a higher enzymatic activity. These findings support the role of oxidative alteration in the EtOH-induced chronic hepatotoxicity in which MnSOD response might represent a primary defence mechanism against the damaging effect of oxygen radical species.

Preterm infants may be susceptible to chronic lung disease and retinopathy of prematurity because of deficient antioxidant mechanisms including deficiency of vitamin E. The aim of this study was to evaluate the status of the antioxidant vitamin E among preterm and term livebirths. Umbilical cord blood samples collected from 40 preterm and 180 term babies were analyzed for vitamin E levels using high performance liquid chromatography. Linear regression analysis was used to examine the relationship of vitamin E with gestational age, birth weight and appropriateness of weight for gestational age. The median vitamin E level of preterm babies (2.61 mg/L) was not significantly different from that of term babies (2.77 mg/L), p = 0.2. Linear regression analysis demonstrated a weak but statistically significant correlation between cord blood vitamin E levels and gestational age (r = 0.14, p = 0.046). Vitamin E levels did not correlate with birth weight or weight for gestational age. Preterm babies had a higher incidence of vitamin E deficiency compared to term babies (38% v 19%, p = 0.02). Our findings lead us to conclude that vitamin E accumulates in the fetus throughout the third trimester so that preterm infants are likely to have vitamin E deficiency.

The investigation dealt with testing vitamins A,E,B1 and B2 levels in the blood of children residing in different regions of Ukraine. The existence of polyhypovitaminosis, especially in children suffering from gastrointestinal tract disease was displayed. 28% of the children may be attributed to a risk group. Some measures directed to polyhypovitaminosis elimination in children, residing in Ukraine, are proposed.

Objective: To determine the oral supplement doses of dl-alpha-tocopheryl-acetate to maintain normal serum alpha-tocopherol concentrations in children with chronic cholestasis and vitamin-E deficient., Background: Malabsorption and deficiency of vitamin E in children with chronic cholestasis causes a progressive, neuromuscular degeneration at approximately 18-24 months of life, if left untreated. Using prompt treatment, it can be completely prevented and reversed to normal., Method: Longitudinal, prospective and comparative study was performed on consecutive sixty vitamin E deficient children with chronic cholestasis divided in three groups. After initial evaluation, therapy was started for 15 days in each group with 100 IU, 200 IU and 400 IU/day of oral dl-alpha-tocopheryl-acetate, respectively; alpha-tocopherol-status, neurological function and biochemical parameters were monitored during therapy., Results: Any oral supplement does administrated for 15 days of dl-alpha-tocopheryl-acetate were enough to maintain the normalization of alpha-tocopherol status (p > 0.06). Neurological function, which had not deteriorated before entry in the trial, stabilized in all after 15 days of therapy. No adverse effects were observed., Conclusions: Oral supplement of dl-alpha-tocopheryl-acetate for 15 days with 100 IU, 200 IU, and 400 IU, in spite of safety, weren't enough to maintain the alpha-tocopherol serum concentration in children with chronic cholestasis and vitamin-E deficient.

Plasma alpha-tocopherol (alpha-T) concentrations, erythrocyte osmotic fragility and detergent sensitivity were measured at 8 week intervals in two 1-year-old male beagle dogs fed a vitamin E-deficient diet (< 0.08 mg per kg alpha-T) and in two control beagles fed the same diet supplemented with vitamin E (> 90 mg per kg alpha-T). Beginning at 24 weeks, dialuric acid haemolysis and spontaneous haemolysis were evaluated also. In the vitamin E-deficient dogs, plasma alpha-T concentrations declined progressively from baseline values of 20.5 and 31.3 micrograms per ml to 0.11 and 0.07 micrograms per ml, respectively, by 90 weeks. The supplemented dogs maintained alpha-T concentrations between 18.3 and 38.4 micrograms per ml. Both dialuric acid haemolysis (R = -0.89) and spontaneous haemolysis (R = -0.91) increased with declining plasma alpha-T concentration. In the dialuric acid haemolysis assay, 50 per cent haemolysis occurred when plasma alpha-T declined to 1.7 micrograms per ml, compared with spontaneous haemolysis in which 50 per cent haemolysis occurred when plasma alpha-T declined to 0.5 micrograms per ml. Osmotic fragility and detergent sensitivity remained unchanged in the vitamin E-deficient dogs throughout the study. Of the four tests, dialuric acid haemolysis was the most sensitive in-vitro assay for vitamin E deficiency in adult dogs.

Thirty elderly long-stay patients were randomly allocated to receive either placebo or dietary supplementation with vitamins A, C and E for 28 days. Nutritional status and cell-mediated immune function were assessed before and after the period of supplementation. Following vitamin supplementation, cell-mediated immune function improved as indicated by a significant increase in the absolute number of T cells (p less than 0.05), T4 subsets (p less than 0.05), T4 to T8 ratio (p less than 0.01) and the proliferation of lymphocytes in response to phytohaemagglutinin (p less than 0.01). In contrast, no significant changes were noted in the immune function of the placebo group. We conclude that supplementation with the dietary antioxidants vitamins A, C and E can improve aspects of cell-mediated immune function in elderly long-stay patients.

Prematurely born, low birth weight infants are abnormal by their very existence ex utero. Thus, the well-documented finding in such infants of low plasma vitamin E concentrations when compared to the adult poses philosophical and pragmatic difficulties as to whether or not a true deficiency state exists: do these low levels represent age-adjusted reference values or do they in fact represent a deficiency state, warranting treatment? We examined multiple measures of vitamin E status in 62 prematurely born, low birth weight infants in order to address this issue. Mathematical and statistical modeling of these measures during the first 21 days of life lead us to conclude that the ex utero antioxidant protective role of vitamin E is best achieved at plasma concentrations of tocopherol very close to those observed in the adult; specifically, when total tocopherol is greater than 0.64 mg/dl and alpha-tocopherol is greater than 0.50 mg/dl. Thus, at birth, a true deficiency in vitamin E exists for most preterm, low birth weight infants and early treatment is warranted.

Pentane, which evolves from the reaction involving omega-6 fatty acids, is a good index of lipid peroxidation. We describe a method for measuring breath pentane excretion in adult humans. After a 4-minute washout period, expired air was analyzed by gas chromatography. Breath was passed through a cooled loop of alumina to adsorb, concentrate, and release, on heating, pentane. Pentane was analyzed by a Porasil-D column with a derived calibration curve. The mean excretion of pentane in 10 normal adults was 6.34 +/- 0.96 pmol X kg-1 X min-1 (mean +/- SEM) and was significantly higher in five patients with plasma vitamin E deficiency (15.39 +/- 1.84 pmol X kg-1 X min-1). There was a significant negative correlation between pentane output and plasma vitamin E levels (r = -0.66, p less than 0.01). Moreover, breath pentane excretion was significantly decreased after a 10-d supplementation with vitamin E in five normal subjects. We conclude that breath pentane output is a sensitive, noninvasive, functional test for assessing vitamin E status.

Experiments with pigs, lambs, sheep, and birds, carried out under various conditions of feeding (with or without supplement or treatment with vitamin E) revealed that the study of the peroxide resistance of erythrocyte lipids could render useful information on the supply of animals with vitamin E. The study of peroxide resistance was shown to be much more accessible than the available chemical methods, and had better reproducibility. This new approach took good consideration of the biologic activity of vitamin E, and was fairly suitable to be employed as a screening diagnostic method. The interpretation of results should take into account the occasional peroxidizing effect produced by heavy metals. With sheep the normal values of erythrocyte lipid peroxidation were 40.3 +/- 1.86; with cattle they were 60.0 +/- 3.2; with pigs--63.7 +/- 3.56; with young birds--64.6 +/- 2.35; and with hen layers--72.8 +/- 4.39.

Vitamin E sufficiency was assessed in 19 children with chronic cholestasis by determining both erythrocyte peroxide hemolysis (EPH) and serum alpha-tocopherol (alpha-T) levels. Eight had normal alpha-T (1.19 +/- 0.67 mg/dl; normal greater than 0.5). The mean EPH in this group was 13.1 +/- 14.3% (normal less than 20%). The remaining 11 patients had low alpha-T levels (0.25 +/- 0.15 mg/dl) and elevated EPH (83.9 +/- 17.1%). Children found to be vitamin E deficient received either oral alpha-T (50-100 IU/kg per day) or parenteral alpha-tocopherol acetate in sesame oil every 2-4 wk (200-300 mg). This permitted serial monitoring of EPH and alpha-T. We found that normalization of the EPH was uniformly accompanied by normalization of the alpha-T level. However, normal alpha-T levels occurred with elevated EPH (between 20% and 80%) on 11 occasions. EPH greater than 80% correctly identified vitamin E deficiency in all cases. Hence, EPH is a satisfactory screening test of vitamin E sufficiently. When the EPH is less than 20%, the patient is vitamin E sufficient. Conversely, when the EPH is greater than 80%, the patient is vitamin E deficient. Serum alpha-T measurements are needed to determine vitamin E sufficiency when the EPH is greater than 20% and less than 80%.

A critical review of the literature on the effects of vitamin E and selenium deficiences on unsaturated fatty acid metabolism reveals that some of these effects are inconsistent with the antioxidant hypothesis of these nutrients as their only biological function. On the basis of these data it is proposed that vitamin E and selenium play a role in the desaturation of n-3 and n-6 polyunsaturated fatty acids by participating in the microsomal electron transport chain and in a proposed peroxidase moiety of the desaturase complex, respectively. A re-interpretation of the experimental literature in terms of the proposed hypothesis is provided, with some suggestions to test its main tenets.

We studied serum vitamin E levels and the ratio of serum vitamin E to serum lipid levels in 11 children with chronic cholestasis complicated by vitamin E deficiency, as defined by characteristic neurologic signs or sural-nerve histopathology in addition to impaired intestinal absorption of vitamin E. Eight of the children had low levels of serum vitamin E, as well as low ratios of serum vitamin E to total lipids and to cholesterol. However, three patients had normal serum vitamin E levels but low ratios of serum vitamin E to total lipids (two of the three had normal ratios of vitamin E to cholesterol). In four patients who were not vitamin E-deficient, all three values were normal. We conclude that vitamin E deficiency may exist in a child with a normal serum vitamin E concentration and that the ratio of serum vitamin E to total serum lipids is the most reliable biochemical index of vitamin E status during chronic childhood cholestasis.

The use of tocopherol levels of either platelets or red blood cells was tested as an index of tissue vitamin E status. Male Wistar rats were fed 0, 5, 10, 20, or 50 ppm of vitamin E (d-alpha-tocopheryl acetate) ad libitum for 10 wk. Over the dosage range from 0 to 20 ppm, response in tocopherol content of most tissues including platelets and red blood cells were linear. Over the whole range from 0 to 50 ppm, responses were curvilinear both directly and logarithmically for all tissues. In a comparison of reproducibility of responses of platelets, plasma and red blood cells, the variation of alpha-tocopherol content within groups fed the same diet was consistently lowest for platelets. Sensitivity (linear slope/SD) for reflecting vitamin E intake was higher for platelets than for either red blood cells or plasma. In vitro spontaneous hemolysis of red blood cells was less than 10% with 10 ppm of vitamin E, greater than 85% with 0 ppm, and was variable (2 to 78%) with 5 ppm. Lipid levels in plasma increased significantly as vitamin E was increased from 5 to 50 ppm of the diets. Over this range, levels of cholesterol and phospholipid increased 20% and levels of triglyceride increased almost 200%.

A rapid and convenient automated procedure for the determination of alpha-tocopherol is described. As little as 0.3 ml of serum or plasma can be used at a sample rate of 20 per hour and carry-over is negligible. Within-batch precision was 4.71% at 5.0 mg alpha-tocopherol per 1, and 3.68% at 20 mg/l, compared with a between-batch precision of 6.98% at 10 mg/l. Using this procedure alpha-tocopherol has been found to be distributed in a log-normal manner and on that basis the range of values for 80 haematologically normal subjects was calculated to be 4.0 to 16.0 mg/l. In pregnancy the alpha-tocopherol was elevated, ranging from 6.7 to 24.0 mg/l. During the first year of life normal infants ranged from 2.0 to 16.0 mg/l which was higher than a small group with various disorders whose values ranged from 1.2 to 8.3 mg/l. The cord blood level was approximately one-fifth of the maternal level.

Serum vitamin E concentrations were determined in 60 term and 26 premature infants during the first 2 months of life. All infants received commercial milk formula containing vitamin E. In addition, premature infants older than 10 days were given vitamin E orally as a multivitamin preparation. Thus, daily intake of vitamin E was nearly 1.2 mg/kg body weight in term infants and 2--3 mg/kg body weight in premature infants. In term infants serum levels of vitamin E rose from 2.6 mg/l (cord blood) to 7.0 mg/l (3rd--13th day) and 9.1 mg/l (16th--25th day) and remained at 10 mg/l (in the second month of life). Hemoglobin concentration and red cell number decreased continuously due to physiological anemia of infancy. In premature infants mean values of vitamin E were the same as in term infants. Vitamin E deficiency with hemolytic anemia could be demonstrated in a 2 months old infant suffering from cystic fibrosis.