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)

Vitamin E deficiency was found to stimulate FMLP (N-formyl-L-methionyl-L-leucyl-L-phenylalanine)-induced biosynthesis of PAF (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) in polymorphonuclear leucocytes (PMN) from rat peritoneum. In three separate experiments each, the amounts of PAF synthesized during 6 min and 12 min incubation of PMN cells from control, vitamin E-supplemented, and vitamin E-deficient rats were 129-240, 131-227 and 248-354 pmol/10(6) cells, respectively. The activity of the acetyl-transferase, which transfers the acetyl moiety of [3H]acetyl-CoA to 2-lysoPAF (1-O-alkyl-sn-glycero-3-phosphocholine) to form [3H]PAF, was higher in PMN homogenates from vitamin E-deficient rats (2.28 +/- 0.07 nmol/min/mg protein) than in those from E-supplemented rats (1.06 +/- 0.10 nmol/min/mg protein). However, there was no difference between the two groups in the activity of acetylhydrolase (4.26 +/- 0.71 and 4.26 +/- 0.06 nmol/min/mg protein, respectively), measured as degradation of [3H]PAF to [3H]lysoPAF. In vitro addition of alpha-tocopherol did not inhibit the increased activity of acetyl-transferase in vitamin E-deficient rats, indicating that the enzyme in vitamin E-supplemented rats was not directly inhibited by alpha-tocopherol. The acetyl-transferases of the two groups showed similar Km values for acetyl-CoA, but different Vmax values (225 microM and 6.4 nmol/min/mg protein in vitamin E-deficient rats, and 216 microM and 3.6 nmol/min/mg protein in vitamin E-supplemented rats), suggesting that the enzyme was not activated but increased in amount in vitamin E deficiency.
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PMID:Vitamin E. deficiency increases the synthesis of platelet-activating factor (PAF) in rat polymorphonuclear leucocytes. 276 59

The mnd mouse, a model of neuronal ceroid lipofusinosis (NCL), has a profound vitamin E deficiency in sera and brain, associated with cerebral deterioration characteristic of NCL. In this study, the vitamin E deficiency is corrected using dietary supplementation. However, the histopathological features associated with NCL remained. With use of a bioinformatics approach based on high-resolution solid and solution state 1H-NMR spectroscopy and principal component analysis (PCA), the deficits associated with NCL are defined in terms of a metabolic phenotype. Although vitamin E supplementation reversed some of the metabolic abnormalities, in particular the concentration of phenylalanine in extracts of cerebral tissue, PCA demonstrated that metabolic deficits associated with NCL were greater than any effects produced from vitamin E supplementation. These deficits included increased glutamate and N-acetyl-L-aspartate and decreased creatine and glutamine concentrations in aqueous extracts of the cortex, as well as profound accumulation of lipid in intact cerebral tissue. This is discussed in terms of faulty production of mitochondrial-associated membranes, thought to be central to the deficits in mnd mice.
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PMID:Vitamin E deficiency and metabolic deficits in neuronal ceroid lipofuscinosis described by bioinformatics. 1246 92