Cerebrospinal fluid levels of alpha-tocopherol (vitamin E) in Parkinson's disease

We compared CSF and serum levels, and the CSF/serum ratio of alpha-tocopherol (vitamin E), measured by HPLC, in 34 patients with Parkinson's disease (PD) and 47 controls. CSF and serum vitamin E levels were correlate. The mean CSF and serum vitamin E levels, and the CSF/serum ratio of PD patients did not differ significantly between the groups. There was no influence of antiparkinsonian therapy on CSF vitamin E levels. CSF vitamin E levels did not correlate with age, age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale of the Hoehn and Yahr staging in the PD group. These results suggest that CSF vitamin E concentrations are unrelated with the risk for PD.     

Alpha tocopherol in CSF of subjects taking high-dose vitamin E in the DATATOP study. Parkinson Study Group

Alpha-Tocopherol concentrations were determined in the CSF of patients with early untreated Parkinson's disease receiving 2,000 IU vitamin E orally per day. After treatment the concentrations increased significantly (p < 0.001) by 76+/-10 (SE)%. The net increases in CSF alpha-tocopherol concentrations after treatment showed a significant positive correlation with the number of days of vitamin E ingestion (p < 0.001). Thus, high-dose vitamin E treatment results in elevating CSF vitamin E levels and possibly brain vitamin E levels.     

The effect of excessive dietary vitamin A on performance and vitamin E status in swine fed diets varying in dietary vitamin E

A study was conducted to evaluate the effects of high dietary vitamin A on vitamin E status and performance of growing-finishing pigs fed diets supplemented with varying levels of vitamin E. Treatments consisted of corn-soybean meal-based diets supplemented with retinyl acetate to provide 2,000 or 20,000 IU of vitamin A/kg of diet and with DL-alpha-tocopheryl acetate to provide 0, 15, or 150 IU of added vitamin E/kg in a 2 x 3 factorial arrangement. The trial involved 84 crossbred pigs (26 kg initial BW) allotted to pens of two pigs each (one gilt, one barrow). Serum was obtained from all pigs on d 0, 3, 7, 21, 35, 63, and 77 of the 83- or 90-d feeding period. Tissue samples (liver, leg, and neck muscle, backfat, and leaf fat) were collected from one pig (barrow) in each pen at the end of the feeding period. Average daily gain and gain:feed were .93 kg and .30, respectively, without treatment differences (P > .10). Serum alpha-tocopherol increased linearly (P < .01) by d 3 with increasing level of dietary vitamin E supplementation. High dietary vitamin A resulted in a small decrease (P < .01) in serum alpha-tocopherol on d 3, but serum alpha-tocopherol concentration was not affected (P > .10) on other days. Tissue alpha-tocopherol increased linearly (P < .001) as dietary vitamin E increased in all tissues examined. No consistent evidence was found to indicate that a high level of dietary vitamin A interfered with performance or with blood serum or tissue alpha-tocopherol concentrations in growing-finishing swine.     

Effect of alpha-tocopherol on the respiratory burst of neutrophils, blast transformation of lymphocytes, and activity of human natural killer cells in blood

The effect of vitamin E on immunological reactions of blood cells was studied. The addition of vitamin E in concentration of 100 microM to neutrophils caused the increase of superoxide production. But this index was decreased when incubation of these cells with A23187 or FMLP was accompanied by alpha-tocopherol in concentration of 100 microM followed by the removal of free ligand or alpha-tocopherol in concentration of 0.5 microM. In the presence of PMA the inhibiting action of alpha-tocopherol was not found (under the 0.5 microM of alpha-tocopherol) or was small (under the concentration of it 100 microM of alpha-tocopherol). The addition of alpha-tocopherol in concentration of 0.5 microM and 50 microM caused the inhibition of blasttransformation of lymphocytes and activity of natural killer cells. This effect was expressed more under the low contents of this vitamin in the incubation medium. The level of blasstransformation of blood in vitamin E-deficient rats was by 20% less than in normal. The exogenous addition of alpha-tocopherol in concentration of 0.5 microM did not affect this value. It was suggested that vitamin E can affect the respiration burst of neutrophils, blasttransformation of lymphocytes and activity of natural killer cells and these actions depend on its concentrations.     

Fine-needle aspiration biopsy findings in a case of follicular dendritic cell tumor

OBJECTIVES: To measure blood selenium concentration and glutathione peroxidase (GSH-Px) activity and serum concentrations of vitamin A and alpha-tocopherol, and to determine the correlation between blood selenium concentration and GSH-Px activity of llamas fed alfalfa hay. DESIGN: Mean (+/- SD) serum vitamin A and alpha-tocopherol concentrations, blood selenium concentrations, and GSH-Px activity were calculated from 9 sequential blood samples collected from llamas fed a diet of alfalfa hay. ANIMALS: 15 clinically normal llamas (8 males, 7 females) between 10 and 14 months of age. PROCEDURE: Llamas were fed alfalfa hay for 40 days prior to sample collection and then for the duration of the trial. Vitamin E, selenium, and concentrations of vitamin A precursors were measured in the hay. Blood samples were collected on days 0, 6, 7, 9, 13, 20, 42, 64, and 98. Blood selenium concentrations were measured, using an inductively coupled spectrometric method. Blood GSH-Px activity was measured with a spectrophotometer, using a modification of a previously described assay. Isocratic high-performance liquid chromatography with florescent detection was used to determine serum alpha-tocopherol and vitamin A concentrations. RESULTS: The alfalfa hay contained 0.2 mg/kg of selenium, 5 mg/kg of vitamin E, and 0.9 mg/kg of vitamin A precursors. The mean (+/- SD) blood selenium concentration and GSH-Px activity were 0.179 +/- 0.032 micrograms/ml and 25.76 +/- 6.53 mU NADPH oxidized/min/mg of Hb, respectively, with a correlation coefficient of 0.97. The mean (+/- SD) concentrations for serum alpha-tocopherol and vitamin A were 128.1 +/- 41.7 and 74.8 +/- 5.5 micrograms/dl, respectively. CONCLUSIONS: Blood selenium concentrations in llamas are highly correlated to GSH-Px activity. Blood selenium concentrations in llamas appear to be similar to other domestic ruminants and diets containing 0.2 mg/kg of selenium appear to provide an adequate dietary source. The concentrations of vitamin A precursors and vitamin E in the hay were below currently recommended dietary levels for llamas, and alfalfa hay appears to provide an unreliable source of vitamins A and E in this species. Further studies are required to determine optimal dietary concentrations and to substantiate a reference range for these vitamins in llamas.     

Cerebrospinal fluid selenium and chromium levels in patients with Parkinson's disease

We compared CSF and serum levels of selenium and chromium, measured by atomic absorption spectrophotometry, in 28 patients with Parkinson's disease (PD) and 43 matched controls. The CSF and serum levels of these trace metals did not differ significantly between PD patients and controls. CSF selenium and chromium levels were not correlated with age, age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale of the Hoehn and Yahr staging in the PD group. Although antiparkinsonian therapy did not influence significantly the CSF levels of selenium, PD patients not treated with levodopa had significantly higher CSF selenium levels than controls (p < 0.01). It is possible that increased CSF selenium levels could indicate an attempt of protection against oxidative stress. The normality of CSF and serum chromium levels suggest that these values are not related with the risk for PD.     

Effect of insecticides on vital activity, hepatic enzymes and red blood cell acetyl cholinesterase activity of rabbits in Makkah

Vitamin E is important in maintaining normal neurological structure and function. In this study, 100 children with protein-energy malnutrition (PEM) were studied and compared to a suitably age-matched control group. Posterior column deficits, cerebellar deficits, and problems with fine motor coordination were present to a significant degree in the PEM subjects. The presence of neurological signs was correlated with various parameters of vitamin E deficiency, including low serum alpha-tocopherol levels and a low tocopherol/total lipid ratio which was present in 92 per cent of subjects. There was good concordance between vitamin E levels and vitamin E to serum lipid ratio in assessing vitamin E deficiency. We conclude that vitamin E deficiency is prevalent, to a hitherto unsuspected degree, in children with PEM and that these malnourished children have significant neurological deficits attributable to low vitamin E levels. This observation is of clinical significance as the neurological deficits are potentially reversible with vitamin E supplementation.     

Cerebrospinal fluid levels of transition metals in patients with Parkinson's disease

We compared CSF and serum levels of iron, copper, manganese, and zinc, measured by atomic absorption spectrophotometry, in 37 patients with Parkinson's disease (PD) and 37 matched controls. The CSF levels of zinc were significantly decreased in PD patients as compared with controls (p < 0.05). The serum levels of zinc, and the CSF and serum levels of iron, copper, and manganese, did not differ significantly between PD-patient and control groups. There was no influence of antiparkinsonian therapy on CSF levels of none of these transition metals. These values were not correlated with age, age at onset, duration of the disease, scores of the Unified Parkinson Disease Rating Scale of the Hoehn and Yahr staging in the PD group, with the exception of CSF copper levels with the duration of the disease (r = 0.38, p < 0.05). These results suggest that low CSF zinc concentrations might be related with the risk for PD, although they could be related with oxidative stress processes.     

The effect of alpha-tocopherol and beta-carotene supplementation on COPD symptoms

The effects of alpha-tocopherol (50 mg/d) and beta-carotene (20 mg/d) supplementation on symptoms of chronic obstructive pulmonary disease were studied among the 29,133 participants of the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study undertaken to investigate the effects of these two substances in the prevention of lung and other cancers. During the follow-up the supplementations did not affect the recurrence or incidence of chronic cough, phlegm, or dyspnea. The prevalence of chronic bronchitis and dyspnea at baseline was lower among those with high dietary intake of beta-carotene (OR = 0.78 and 0.67, respectively) or vitamin E (OR = 0.87 and 0.77) and high serum beta-carotene (OR = 0.59 and 0.62) and alpha-tocopherol (OR = 0.76 and 0.82). High intake and serum levels of retinol were associated with low prevalence of dyspnea (OR = 0.84 and 0.80, respectively) but not with chronic bronchitis. The results indicate no benefit from supplementation with alpha-tocopherol or beta-carotene on the symptoms of chronic obstructive pulmonary disorders but support the beneficial effect of dietary intake of fruits and vegetables rich in these compounds.     

Fish oils lower rat plasma and hepatic, but not immune cell alpha-tocopherol concentration

These studies were designed to measure the impact of different fish oil sources of dietary (n-3) polyunsaturated fatty acid on the alpha-tocopherol content of rat immune cells. In the first experiment, rats were fed diets containing either lard, corn oil, menhaden fish oil or cod liver oil. In the second study, sardine fish oil replaced corn oil. Dietary fat source did not significantly influence body weights or the yield of immune cells in either study. In both studies, plasma and liver alpha-tocopherol concentrations were significantly lower in (n-3) polyunsaturated fatty acid-fed rats than in rats fed lard. In the first study, immune cell alpha-tocopherol concentrations followed those observed in the plasma and liver. These concentrations closely paralleled the amount of RRR-alpha-tocopheryl acetate added to diets and not the total vitamin E present, which was the same for all treatment groups. However, in the second study, alpha-tocopherol concentration of immune cells was not significantly different among rats fed lard, menhaden fish oil, and sardine fish oil. In that study both the amount and form of vitamin E were carefully balanced across dietary treatment groups. In conclusion, despite having similar amounts of (n-3) polyunsaturated fatty acids, two out of three fish oils tested did not lower immune cell alpha-tocopherol concentration even in the face of significantly reduced plasma and liver alpha-tocopherol concentrations.     

Liver alpha-tocopherol transfer protein and its mRNA are differentially altered by dietary vitamin E deficiency and protein insufficiency in rats

To study how the expression of alpha-tocopherol transfer protein (alpha-TTP) and its mRNA are affected by protein and vitamin E status, Long-Evans male weanling rats were fed a vitamin E-deficient (DE), high vitamin E (HE, 5 g/kg diet of all-rac-alpha-tocopheryl acetate) or control (C) diet for 12 wk in Experiment 1; and fed a low-protein (LP) or control (C) diet for 6 wk in Experiment 2. The high and deficient vitamin E status of HE and DE groups in Experiment 1 were confirmed by changes in plasma pyruvate kinase activity as well as the concentrations of alpha-tocopherol in plasma and liver. As shown by the Northern and Western Blot Analysis, the expression of alpha-TTP in the liver of the DE group was significantly lower than, while that of the HE group was not different from, that of the controls. In contrast, the alpha-TTP mRNA levels did not differ among the C, DE and HE groups. alpha-Tocopherol in most peripheral tissues of rats fed the LP diet in Experiment 2 was significantly lower than that of the C. Both the alpha-TTP and its mRNA were significantly lower in the LP group than in the C. The results suggested that dietary vitamin E does not affect alpha-TTP gene expression except that the protein levels in the liver were lowered by vitamin E deficiency. On the other hand, protein inadequacy appeared to down-regulate the expression of the alpha-TTP gene.     

Methods for determination of vitamins A and E our simple HPLC assay

Biological effects of reactive oxygen species and other radicals which are controlled by antioxidant mechanism are exerted on the basis of enzymes and substrates. Antioxidant substrates are divided into lipophilic and hydrophilic groups. Main representants of lipophilic antioxidants are retinol and tocopherol which are closely related to ascorbate in the hydrophilic compartment. Described methods for detection of retinol and alpha-tocopherol are simple, sensitive, specific and precise. They are reliable, economic and fast. Only small amounts of serum are used for one analysis which is convenient for patients, too. Our methods can be recommended for routine use in laboratories of clinical biochemistry. Haemodialyzed patients, retinol serum level was higher than that in blood donors while alpha-tocopherol serum level did not differ. Both vitamin A and E serum levels were similar in alcoholics compared to controls.     

Serum beta-carotene and antioxidant micronutrients in children with cancer. The 'Cancer in Children and Antioxidant Micronutrients' French Study Group

Serum antioxidant vitamins A (retinol) and E (alpha-tocopherol), beta-carotene, zinc and selenium for 418 children with newly diagnosed malignancy were compared with those of 632 cancer-free controls. Incident cancer cases and controls were 1-16 years old and recruited in 1986-1989. Age- and sex-adjusted serum concentrations of retinol, beta-carotene and alpha-tocopherol were significantly inversely associated with cancer. In similar models, the odds ratio (OR) comparing the highest with the lowest quintile was 2.06 (95% confidence interval [CI] 1.40-3.02) for retinol, 3.87 (95% CI: 2.54-5.90) for beta-carotene, 2.15 (95% CI: 1.48-3.10) for alpha-tocopherol, 1.29 (95% CI: 0.75-2.23) for selenium, and 1.94 (95% CI: 1.17-2.23) for zinc. The cancer sites that were associated with serum beta-carotene were, in general, leukaemia, lymphoma, central nervous system, bone and renal tumours. Moreover, leukaemia was associated with low mean serum levels of retinol, selenium and zinc. Subjects with lymphoma, bone and renal tumours also had lower mean retinol and alpha-tocopherol levels than controls. Brain tumour patients had low vitamin E levels. Low serum values of antioxidant vitamins were associated with childhood neoplasm occurrence. Some site-specific effect was reported. Low peripheral nutrient levels are not considered as cancer promoters but rather as an impairment of the body's defence mechanism occurring during the cancer-related metabolic and nutritional disturbances and inflammation processes.     

Pretreatment of young pigs with vitamin E attenuates the elevation in plasma interleukin-6 and cortisol caused by a challenge dose of lipopolysaccharide

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

Factors affecting the ultrasonic properties of equine digital flexor tendons

Dietary treatment with three diets differing in vitamin E, Low E (15 mg of vitamin E/kg diet), Medium E (150 mg/kg), or High E (1,500 mg/kg), resulted in guinea pigs with low (but nondeficient), intermediate, or high heart alpha-tocopherol concentration. Neither the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and reductase, nor the nonenzymatic antioxidants, GSH, ascorbate, and uric acid were homeostatically depressed by increases in heart alpha-tocopherol. Protection from both enzymatic (NADPH dependent) and nonenzymatic (ascorbate-Fe2+) lipid peroxidation was strongly increased by vitamin E supplementation from Low to Medium E whereas no additional gain was obtained from the Medium E to the High E group. The GSH/GSSG and GSH/total glutathione ratios increased as a function of the vitamin E dietary concentration closely resembling the shape of the dependence of heart alpha-tocopherol on dietary vitamin E. The results show the capacity of dietary vitamin E to increase the global antioxidant capacity of the heart and to improve the heart redox status in both the lipid and water-soluble compartments. This capacity occurred at levels six times higher than the minimum daily requirement of vitamin E, even in the presence of optimum dietary vitamin C concentrations and basal unstressed conditions. The need for vitamin E dietary supplementation seems specially important in this tissue due to the low constitutive levels of endogenous enzymatic and nonenzymatic antioxidants present of the mammalian heart in comparison with those of other internal organs.     

Atherosclerosis, with special reference to vitamin E

The relationship between atherosclerosis and fat soluble vitamin, especially vitamin E is reviewed on the basis of oxidised modification of low density lipoprotein (LDL). Data now support the notion that the oxidised LDL is present in the blood and arterial wall and antioxidant drugs such as probucol and vitamin E, beta-carotene, may prevent the progression of atherosclerosis. LDL alpha-tocopherol levels are generally correlated to the plasma concentrations and supplementation with alpha-tocopherol increases its content in LDL. There is a significant correlation between the LDL alpha-tocopherol level and the resistance to oxidative modification. Epidemiological data also shows the relation between low levels of plasma vitamin E and the increased incidence of coronary heart disease. Clinical application of vitamin E should be clarified in detail to inhibit the progression of atherosclerosis.     

Cerebral metabolic monitoring experience in critical neurological patients

The effects of vitamin E on lipid peroxidation, intracellular free Ca2+ concentration ([Ca2+]i), and cell death were investigated in the postischemic immature cerebellum. Deprivation of oxygen and glucose for 10-min in a suspension of freshly dissociated granule cells from the cerebellum of 9-day-old male rat pups resulted in a recovery-induced consumption of cell nonenzymatic antioxidants (ascorbic acid, glutathione, and alpha-tocopherol) and development of membrane lipid peroxidation as measured by the thiobarbituric acid method. The rate of lipid peroxidation of the postischemic cells was stimulated, not reduced, by treatment of the cells with vitamin E (5-30 microM alpha-tocopherol phosphate). In flow-cytometric studies a 10-min period of ischemia resulted in a small increase in intracellular calcium concentration, lipid peroxidation products and cell death, but in the presence of alpha-tocopherol the same treatment caused a dramatic increase in cell death, accompanied by a large increase in [Ca2+]i and lipid peroxidation products. Pretreatment of the cells with a mixture of three antioxidants (vitamin C/rutin/ubiquinol-10, 10/5/1) or nickel (Ni2+) reduced the alpha-tocopherol-induced increases in [Ca2+]i, and cell death. Hydrogen peroxide (1 mM) and the water-soluble analogue of vitamin E, trolox (50 microM), mimicked the effect of vitamin E on lipid peroxidation in the postischemic cells. Pretreatment of the cells with the intracellular Ca2+ chelator BAPTA-AM, reduced both the alpha-tocopherol-induced increase in [Ca2+]i and cell death. The effect of vitamin E on [Ca2+]i was age dependent and decreased abruptly during maturation of the cerebellum between the first and second weeks of life. Results of in vitro treatment of the immature cerebellar cells with the water-soluble form of vitamin E (alpha-tocopherol phosphate) suggest that, after consumption of cellular co-antioxidants, vitamin E may be converted to an alpha-tocopheroxyl radical, which act as a toxic prooxidant as cellular bioenergetics deteriorate.     

Effect of alpha-tocopherol succinate on free radical and lipid peroxidation levels in BL6 melanoma cells

Numerous studies have proposed a radical or oxidant involvement in a number of degenerative diseases such as cancer. This has led to suggestions that the supplementation of antioxidants such as alpha-tocopherol (vitamin E) may function to reduce the growth of cancer. In this study, a nonmalignant Monkey kidney (LLCMK) and a malignant Murine melanoma (BL6-F10) cell line were supplemented with varying levels of alpha-Tocopherol acid succinate (vitamin E succinate) ranging from 1 to 10 microg/ml. BL6-F10 cells supplemented with 5, 7, and 10 microg/ml vitamin E succinate, showed significant decreases in cell proliferation, and this decrease was accompanied by a concomitant increase rather than a decrease in the levels of free radicals and lipid peroxidation. LLCMK cells supplemented with 1-10 microg/ml vitamin E succinate showed no significant increase or decrease in growth, while the levels of lipid peroxidation were shown to be insignificantly elevated at 5, 7, and 10 microg/ml vitamin E succinate. Free radical levels in LLCMK cells were significantly decreased at 1 microg/ml vitamin E succinate, while at 3, 5, 7, and 10 microg/ml supplementary vitamin E succinate, free radical levels increased compared to the 1 microg/ml group, but not compared to control cultures. These results suggest that the inhibitory effects of vitamin E succinate on BL6-F10 cell growth in vitro is not a consequence of its antioxidant properties, but may, in fact, be due to one or more of its other potential roles within the cells, such as the regulation of cellular enzyme activities involved in growth.     

Surgical treatment of chronic pulmonary thromboembolism

It has become increasingly obvious that free radicals and lipid peroxidation contribute to brain damage from trauma by mediating edema formation and ischemia. It should, therefore, be expected that the actual level of endogenous antioxidants, as for example, vitamin C and E in plasma, has an influence on the extent of free radical-induced injury. In this communication we investigate the effect of dietary changes in the free radical scavenger alpha-tocopherol on posttraumatic cerebral swelling in Sprague-Dawley rats. Low, normal, and high plasma levels of alpha-tocopherol were established by respective diets supplied over 2 weeks. Animals of all groups received the same food without alpha-tocopherol. One group was fed a vitamin E-free diet. The pellet-food for the other animals was supplemented either with 5-mg alpha-tocopherol/100 g or 250-mg alpha-tocopherol/100 g dry mass, respectively. The vitamin E-free diet lowered the alpha-tocopherol level in plasma to 30% of control, whereas supplementation with 250 mg/100 g led to a plasma concentration of 200% of control. The animals were then subjected to a focal cold injury of the left cerebral hemisphere. Twenty-four hours after trauma the brain was removed and the water content of each hemisphere was determined by the wet-dry weight method. Swelling of the traumatized hemisphere was calculated as the difference in weight between the traumatized and contralateral control hemisphere. The 2-week alpha-tocopherol supplementation or -deletion diet, respectively, did not either afford significant reduction or lead to an enhancement of traumatic brain swelling. Likewise, the increase in brain water content of the traumatized hemisphere was not affected. It is concluded that supplementation or depletion of alpha-tocopherol for 2 weeks, resulting in a marked increase or decrease of the vitamin E plasma level, does not influence formation of posttraumatic vasogenic brain edema.     

Vitamin E inhibits retinal pigment epithelium cell proliferation in vitro

Retinal pigment epithelium (RPE) cells migrating through the damaged retina play an important role in the pathogenesis of proliferative vitreoretinopathy (PVR). We found that alpha-tocopherol (vitamin E) inhibits proliferation of human RPE in culture without exerting cytotoxic effects. Maximal inhibition was achieved with 100 microM alpha-tocopherol. Our result could explain the observation that vitamin E supplements have an adverse effect on light-damaged retina and on the course of retinitis pigmentosa. Since it has been shown that supplemental oral administrations of vitamin E can raise the RPE concentration of alpha-tocopherol well above 100 microM and supplementation is not associated with any clinical relevant adverse effect, we believe that vitamin E could be beneficial in the treatment of PVR.