Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acanthocytic red cells in patients with abetalipoproteinemia are morphologically similar to the red cells in spur cell anemia. Fluidity of membrane lipids is decreased in spur cells due to their excess cholesterol content. Acanthocyte membranes have an increased content of sphingomyelin and a decreased content of lecithin. To assess the effect of this abnormality of acanthocyte membrane lipid composition on membrane fluidity, we studied red cells from five patients with abetalipoproteinemia and four obligate heterozygote family members. Membrane fluidity was measured in terms of microviscosity ( eta) at 37 degrees C, assessed by means of the fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene. It was increased from 3.2+/-0.1 poise in normals to 4.01-4.14 poise in acanthocytes. This was associated with an increase in the sphingomyelin/lecithin ratio from 0.84+/-0.08 in normals in 1.45-1.61 in acanthocytes. The eta of acanthocyte membranes was not influenced by the degree of vitamin E deficiency. Similar changes in eta were observed in liposomes prepared from red cell lipids. Heterozygotes had normal sphingomyelin/lecithin ratios and normal values for eta. The flow activation energy for viscosity, a measure of the degree of order in the hydrophobic portion of the membrane, was decreased from 8.3 kcal/mole in normal red cells to 7.2 kcal/mole in acanthocytes, indicating that acanthocyte membrane lipids are more ordered. Variations in the sphingomyelin/lecithin mole ratio of liposomes prepared from brain sphingomyelin and egg lecithin with equimolar cholesterol caused similar changes in both eta and activation energy. The deformability of acanthocytes, assessed by means of filtration through 3-mum filters, was decreased. These studies indicate that the increased sphingomyelin/lecithin ratio of acanthocytes is responsible for their decreased membrane fluidity. As in spur cells and in red cells enriched with cholesterol in vitro, this decrease in membrane fluidity occurs coincidentally with an abnormality in cell contour and an impairment in cell deformability.
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PMID:Decreased fluidity of red cell membrane lipids in abetalipoproteinemia. 87 76

Vitamin E, a dietary antioxidant, is known to inhibit peroxidation of membrane lipids and to protect the lungs of vitamin E-deficient animals and to a lesser extent vitamin E-sufficient animals from oxidant injury. Since the protective interaction between vitamin E and biological membranes may be related to alterations in composition and physical state of membrane lipids, we evaluated the effect of vitamin E deficiency on lung microsomal lipids and membrane fluidity. Both intact microsomes and lipid vesicles prepared from the total lipid extracts of these microsomes were used. The percentage incorporation of vitamin E and cholesterol, membrane fluidity, and lipid peroxidation were measured in microsomes as well as their lipid vesicles. Fluidity was measured by monitoring changes in fluorescence anisotropy for 1,6-diphenyl-1,3,5-hexatriene (DPH). Lipid peroxidation was measured by thiobarbituric acid reaction. There were significant increases in the phospholipid (p less than 0.01), the total cholesterol (p less than 0.05), and the total saturated fatty acids (p less than 0.05) and decreases in total polyunsaturated fatty acid (p less than 0.01) content of vitamin E-deficient microsomes. There were no detectable peroxidative products in freshly isolated microsomes from either vitamin E-sufficient or -deficient lungs. However, lipids from vitamin E-deficient microsomal membranes were more susceptible to free radical initiated peroxidation than lipids from vitamin E-sufficient microsomes. Fluidity in vitamin E-deficient microsomes or in their lipid vesicles was significantly (p less than 0.05) decreased compared to the respective controls. In vitamin E-deficient microsomes or their lipid vesicles, the incorporation rate of vitamin E was two- to three-fold greater than in vesicles of vitamin E-sufficient microsomes or their lipid vesicles. However, the percentage incorporation of cholesterol was identical in both vitamin E-deficient and vitamin E-sufficient microsomes or in their respective lipid vesicles. As a result of vitamin E incorporation, fluidity was significantly decreased (p less than 0.05) in vitamin E-sufficient vesicles and was further decreased (p less than 0.001) in vitamin E-deficient vesicles. Incorporation of cholesterol also decreased fluidity in both vitamin E-deficient and vitamin E-sufficient vesicles but to the same extent (p less than 0.001). Lipid peroxide formation was two-fold greater in the vitamin E-deficient than in the vitamin E-sufficient vesicles.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vitamin E, membrane order, and antioxidant behavior in lung microsomes and reconstituted lipid vesicles. 318 15