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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood in neonates shows several peculiar properties which affect its rheological properties. 1. The haematocrit in neonates may be as high as 0.65 l/l without any clinical signs. 2. Both plasma viscosity and red cell aggregation are markedly lower in neonates than in adults because of low protein levels in neonates. This results in decreased blood viscosity at given haematocrit, particularly at low shear forces. 3. Deformability of neonatal red cells is similar to that of adult cells when studied under controlled conditions (e.g. rheoscope, ektacytometer). However, neonatal red cells are less filterable and require higher pressures for entering narrow micropipettes than adult red cells due to the larger size of neonatal red cells. 4. Neonatal leukocytes require higher pressure for the passage of 5 microns filter pores or 5 microns micropipettes than adult cells. The following haemorheological disorders have been observed in neonates: 1. Polycythaemia in infants with late cord-clamping, severe asphyxia, growth retardation and diabetic mothers. 2. Markedly decreased red cell deformability in septicaemia, necrotizing enterocolitis and in vitamin E deficiency (after exposure to oxidizing agents). 3. Moderately decreased red cell deformability in infants with diabetic mothers, growth retardation and severe acidosis. 4. Increased red cell aggregation in septicaemia. 5. Lack of red cell aggregation in immature neonates. 6. Decreased ability of leukocytes from septic neonates to pass filter pores and micropipettes. Treatment may be either haemodilution (in polycythaemia) or exchange transfusion (in septicaemia and necrotizing enterocolitis). Haemorheological drugs have not been used in neonates.
Baillieres Clin Haematol 1987 Sep
PMID:Blood rheology in the newborn infant. 332 66

We measured serum levels of vitamins A, E, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D, as well as levels of abnormal (des-gamma-carboxy) prothrombin, in 52 patients with primary biliary cirrhosis. Decreased serum levels of retinol (vitamin A) and 25-hydroxyvitamin D and elevated levels of abnormal prothrombin were common in these patients and correlated with the histologic stage of the disease and with the clinical severity of disease as judged by elevated serum bilirubin levels and decreased serum albumin levels. The increased levels of abnormal prothrombin were due primarily to vitamin K deficiency but also, in part, to the severity of the liver disease itself. Vitamin E deficiency was rare. Only 1 patient had clinical manifestations of fat-soluble vitamin deficiency, night blindness, and gastrointestinal bleeding related to a marked prolongation of the prothrombin time. Deficiencies of fat-soluble vitamins are most likely to be present in jaundiced patients with long-standing, severe cholestasis. We suggest that fat-soluble vitamin status be determined in all patients with primary biliary cirrhosis by appropriate blood tests and that vitamin supplements be given only to those patients who require them.
Gastroenterology 1988 Sep
PMID:Fat-soluble vitamin nutriture in primary biliary cirrhosis. 339 23

The efficiency of alpha-tocopherol as a 7-etoxycumarine deethylase protector in rat liver microsomes damaged by phospholipase A2 at various levels of vitamin E was studied. No selective damage of cytochrome P-450 isoforms possessing a catalytic activity towards 7-etoxycumarine under vitamin E deficiency was observed. Phospholipase A2 decreased the deethylase activity of cytochrome P-450, the efficiency of the damaging action being dependent on vitamin E content in the liver. Exogenous alpha-tocopherol exerts an antiphospholipase effect and protects 7-etoxycumarine deethylase; the protective action is inversely proportional to vitamin E level in the liver. Under normal conditions the damaging effect of phospholipase A2 on cytochrome P-450 is mainly provided for by lysophospholipids, while under vitamin E deficiency both lysophospholipids and free fatty acids exert a damaging action. A possible mechanism of the stabilizing effect of alpha-tocopherol may consist in the interaction of the chromanol nucleus in the vitamin E molecyule both with lysophospholipids and with free fatty acids.
Biokhimiia 1986 Sep
PMID:[Non-antioxidative mechanism of cytochrome P-450 stabilization by alpha-tocopherol: the effectiveness in avitaminosis E]. 349 Feb 81

It has been established in the experiments on rats resistant to encephalomyelitis that vitamin E deficiency promoted and thymaline administration prevented the onset of the disease. The experiments on guinea-pigs sensitive to encephalomyelitis have shown that the combined administration of alpha-tocopherol and thymaline prevented the development of the disease. The results obtained make it possible to suggest that the resistance to encephalomyelitis depends on the level of membrane antioxidant defense and the condition of T-cell immunity.
Biull Eksp Biol Med 1987 Sep
PMID:[Effect of vitamin E and thymalin on the development of experimental allergic encephalomyelitis]. 366 10

1. Studies were made on the vitamin E status of the newborn as judged by cord serum vitamin E and erythrocyte haemolysis in vitro in relation to gestational age, birth weight and maternal vitamin E status in subjects belonging to low (LIG)- and high (HIG)-income groups in urban Baroda. 2. In the case of full-term infants, the mean values for maternal serum vitamin E (mg/l) for LIG (n 73) and HIG (n 43) were 9.9 (SE 0.4) and 11.6 (SE 0.5). The corresponding values for cord serum vitamin E were 3.6 (SE 0.2) and 4.6 (SE 0.2) mg/l. 3. Serum vitamin E levels (mg/l) were lower in premature infants (2.3 (SE 0.2); n 20) and low-birth-weight full-term infants (2.9 (SE 0.2); n 25) than in full-term normal infants (4.2 (SE 0.1); n 91). This was associated with differences in maternal serum vitamin E levels (7.4 (SE 0.5), 8.2 (SE 0.5) and 11.1 (SE 0.3) respectively). The differences were more marked for LIG. 4. A negative correlation was found between serum vitamin E and erythrocyte haemolysis in vitro in the case of maternal blood but not in cord blood. 5. These results suggest that maternal vitamin E deficiency is one of the features associated with prematurity and intra-uterine growth retardation.
Br J Nutr 1987 Sep
PMID:Vitamin E status of the newborn in relation to gestational age, birth weight and maternal vitamin E status. 367 41

Cystic fibrosis patients with pancreatic insufficiency are at risk for the development of vitamin E deficiency. We report here the outcome of screening 13 cystic fibrosis patients with conventional descriptive measures of vitamin E status and a new functional test. The results were compared with those from age appropriate controls. Nine patients were found to be vitamin E sufficient based upon normal plasma vitamin E levels, the ratio of plasma vitamin E to total plasma lipids, and normal levels of in vitro erythrocyte malondialdehyde formation, the new functional measure of vitamin E status. Four patients considered vitamin E deficient, based upon low plasma vitamin E levels and plasma vitamin E to total plasma lipid ratios, demonstrated increased erythrocyte malondialdehyde formation in vitro when compared to age-matched controls. Since limited reference data in children are available to define normal plasma vitamin E levels and plasma vitamin E to total plasma lipid ratios, we suggest that for cystic fibrosis patients the functional in vitro malondialdehyde formation test may be a better measure of vitamin E status than static plasma levels.
Eur J Pediatr 1987 Sep
PMID:Application of a new test for vitamin E deficiency to cystic fibrosis. 367 78

To test whether vitamin E deficiency might influence the course of essential fatty acid (EFA) deficiency, Long Evans rats were fed diets containing a marginal amount (1.5% of calories) of 18:2 omega 6 or 18:3 omega 3 fatty acid with complete absence of the other and with or without vitamin E. Vitamin E contents decreased continuously in serum and liver in all rats fed the E-free diets but in the brains of only the rats fed the marginal 18:3 omega 3, E-free diet. It is considered that the vitamin E is cooxidized in the liver with 22:6 omega 3, since this fatty acid is very low in livers of the rats fed the marginal 18:2 omega 6 diet but much higher in livers of the rats fed the marginal 18:3 omega 3 diet. Brain 22:6 omega 3 values are comparable for both groups. The source of 22:6 omega 3 is evidently in the mother's milk, since following weaning there is a precipitous drop in 22:6 omega 3 in serum, liver and carcass of rats on the 18:2 omega 6--containing diet. No significant signs of EFA deficiency were seen in the E-deficient rats.
Lipids 1986 Sep
PMID:A relationship between essential fatty acid and vitamin E deficiency. 376 33

Plasma tocopherol was measured in 85 alcoholic patients and 40 control subjects from a local factory. Cholesterol, triglycerides and phospholipids were measured individually and summed to give an estimate of total serum lipids. Plasma tocopherol concentrations of the alcoholics were significantly lower than those of the controls and showed wide variation from marked deficiency to the upper limit of the normal range. Using regression analysis, 1.11 mumol tocopherol/mmol total lipids were calculated as the threshold of deficiency equivalent to 0.8 mg tocopherol/g total lipid established by Horwitt et al. The sensitivity and specificity of other tocopherol:lipid ratios for identifying vitamin E deficiency was compared with the tocopherol:total lipid ratio. Thresholds of deficiency for the different tocopherol:lipid ratios were calculated. The tocopherol:cholesterol+triglyceride ratio was found to be almost as powerful in identifying vitamin E deficiency as the tocopherol:total lipid ratio (sensitivity 95%, specificity 99%). Of the tocopherol:individual lipid ratios, the tocopherol:cholesterol ratio gave the best results (sensitivity 86%, specificity 94%).
Ann Clin Biochem 1986 Sep
PMID:The use of different lipids to express serum tocopherol: lipid ratios for the measurement of vitamin E status. 376 86

As determined by in vivo studies using [1-14C] L-leucine and [1-14C] glycine, vitamin E deficiency in young rabbits caused a higher turnover rate of liver proteins and of plasma albumin and globulin fractions. This effect was most clearly and consistently observed in animals fed a diet containing 10 mg of the non-absorbable polymeric antioxidant Anoxomer per g of fat in the diet.
Z Ernahrungswiss 1986 Sep
PMID:Vitamin E deficiency in rabbits receiving a high PUFA diet with and without a non-absorbable antioxidant. II. Incorporation of 14C-labelled glycine and L-leucine into liver and plasma proteins. 377 42

Selenium deficiency and vitamin E deficiency both affect xenobiotic metabolism and toxicity. In addition, selenium deficiency causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione metabolism in isolated hepatocytes from selenium-deficient, vitamin E-deficient, and control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during the 5-h incubation. Freshly isolated hepatocytes had the same glutathione concentration regardless of diet group. During the incubation, however, the glutathione concentration in selenium-deficient hepatocytes rose to 1.4 times that in control hepatocytes. The selenium-deficient cells also released twice as much glutathione into the incubation medium as did the control cells. Total glutathione (intracellular plus extracellular) in the incubation flask increased from 47.7 +/- 8.9 to 152 +/- 16.5 nmol/10(6) selenium-deficient cells over 5 h compared with an increase from 46.7 +/- 7.1 to 92.0 +/- 17.4 nmol/10(6) control cells and from 47.7 +/- 11.7 to 79.5 +/- 24.9 nmol/10(6) vitamin E-deficient cells. This overall increase in glutathione concentration suggested that glutathione synthesis was accelerated by selenium deficiency. The activity of gamma-glutamylcysteine synthetase was twice as great in selenium-deficient liver supernatant (105,000 X g) as in vitamin E-deficient or control liver supernatant (105,000 X g). Hemoglobin-free perfused livers were used to determine the form of glutathione released and its route. Selenium-deficient livers released 4 times as much GSH into the caval perfusate as did control livers. Plasma glutathione concentration in selenium-deficient rats was found to be 2-fold that in control rats, suggesting that increased GSH synthesis and release is an in vivo phenomenon associated with selenium deficiency.
J Biol Chem 1982 Sep 25
PMID:Effect of selenium deficiency and vitamin E deficiency on glutathione metabolism in isolated rat hepatocytes. 612 15


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