Serum Α-tocopherol Levels Research Articles

Thiobarbituric acid reactive substances and vitamin E in serum and cerebrospinal fluid from patients with cerebral apoplexy

Thiobarbituric acid (TBA) reactive substances in serum and cerebrospinal fluid from patients with cerebral apoplexy were determined and their relationship to this disease was studied. TBA reactants in serum were elevated in patients with cerebral apoplexy, but there was no difference between patients with brain tumor or other neurological disease and healthy persons. TBA reactants in cerebrospinal fluid in patients with cerebral aneurysm, cerebral arterial and venous anomalies or intracerebral hematoma, and its levels in patients with cerebral infarction or brain tumor were also higher than in healthy persons. Serum α-tocopherol levels were elevated in patients with cerebral infarction, but were relatively low in patients with cerebral aneurysm, cerebral arterial and venous anomalies or intracerebral hematoma. The reverse was the case with cerebrospinal fluid levels of α-tocopherol. That is, the sequence of decreasing level of α-tocopherol in cerebrospinal fluid was intracerebral hematoma, cerebral aneurysm, cerebral arterial and venous anomalies, and cerebral infarction. The levels of TBA reactive substances in patients with cerebral apoplexy showed a positive correlation between serum and cerebrospinal fluid, and the levels of α-tocopherol showed a similar correlation.

Serum α-tocopherol, lipids, potassium, and creatine phosphokinase in normal and malabsorption patients

Serum α-tocopherol, lipids, potassium, and creatine phosphokinase levels were measured in 20 adult male control patients and eight malabsorption patients. The malabsorption group had significantly lower serum α-tocopherol levels than the control group. This change was independent of serum total lipid levels that were not significantly different among the two groups. Serum potassium and creatine phosphokinase levels that are normally used to assess muscle pathology in man did not correlate with serum α-tocopherol levels in either the control or the malabsorption groups. Body mass indices that are directly related to adiposity of the individuals were calculated. Among the control patients, there was a significant increase in serum α-tocopherol and serum total lipids with increase in body mass index. Similar correlations did not exist in the malabsorption group. In the latter group serum α-tocopherol levels may have reached low enough levels to be independent of factors such as adiposity and serum total lipids.

Vitamin E deficiency in β-thalassemia major: changes in hematological and biochemical parameters after a therapeutic trial with α-tocopherol

Serum α-tocopherol (vitamin E) levels less than 0.5 mg/100 ml were found in β-thalassemia major and intermedia. Vitamin E deficiency in thalassemia is not associated with malabsorption, but could be due to its consumption while neuthlizing oxidative damage in red blood cell (RBC) membrane and other tissues. A therapeutic trial with vitamin E was carried out in eight patients with β-thalassemia major with 750 to 1000 IU/day for an average period of 16 months. Serum vitamin E levels were determined consecutively in these patients and in seven untreated patients throughout that period. The treated patients showed: 1) A 4-fold increase in both serum and RBC vitamin E levels; 2) serum vitamin E dropped to the low pretreatment values after discontinuation of the therapeutic trial; 3) decrease in abnormally high malonyldialdehyde levels, which were generated after oxidant stress and indicate peroxidative damage to the lipid portion of the RBC membrane; 4) no changes in the low titratable sulfhydryl groups calculated per RBC membrane protein; 5) in three of seven patients prolonged RBC survival was found after administration of vitamin E for 12 months; 6) no significant changes were found in transfusion requirements between the treated and untreated groups followed for a period of 16 and 18 months, respectively. While there seem to be practical and theoretical indications to treat thalassemic patients with vitamin E, this by itself is incapable of correcting the variety of changes in RBC membrane components.

脳卒中発作後の血清ビタミンE, 過酸化脂質, 総コレステロール, 遊離脂肪酸に対するビタミンE投与の影響

Serum levels of α-tocopherol, lipoperoxide (TBARS), total cholesterol (TC) and free fatty acid (FFA) were studied before and after the administration of vitamin E (dl-α-tocopheryl acetate) for 4 weeks (400mg/d im for the first week, thereafter 600mg/d po) in the acute stage of cerebrovascular accident (stroke).Serum α-tocopherol was significantly lower, but TBARS was higher than that of the control on the first day of outbreak. Then, vitamin E administration elevated serum α-tocopherol level in a few days, but did not affect on TC level. On the other hand, serum TBARS level did not arise and was in plateau during 4 weeks. These result led us to have a conclusion that administrated vitamin E must inhibit the elevation of TBARS, which otherwise, was observed in most cases in the first week. Lastly, there were three stroke patients whose serum α-tocopherol had been happenly measured 2 or 4 months prior to attack, and two of them had revealed low level of α-tocopherol (less than 0.5mg/dl) at that time. Soon after stroke developing, seum α-tocopherol was commonly proven to be lower, as others, in three patients.These findings might roughly suggest that low level of serum α-tocopherol could be one of risk factors of cerebrovascular accident.

Lipid peroxidation in the hemolytic uremic syndrome

Based on recent evidence of a genetic influence on prognosis (1) and the existence of red cell membrane phospholipid depletion with low or absent serum α-tocopherol (2) levels in three children with the Hemolytic Uremic Syndrome (H.U.S.), we wish to suggest the existence of an inborn error of antioxident capacity as the basic pathogenetic mechanism in the development of the hemolytic uremic syndrome (H.U.S.).