Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis of a defect in GH-receptor interaction, which could explain the growth failure of thalassemic children, the binding of [125I]human (h) GH to membrane fractions prepared from liver biopsies was studied. Small amounts of liver were obtained from 6 girls and 11 boys with homozygous beta-thalassemia, aged 3-15 yr, all prepubertal, at the time of splenectomy. Specific binding of [125I]hGH ranged from 0.37-5.11% of the added radioactivity/100 micrograms liver membrane protein, with variations in both receptor number and binding affinity. This 14-fold variation in hGH binding to liver membranes of thalassemic children was comparable to that in membrane fractions of livers obtained from normal donors at the time of liver transplant. The binding of insulin to liver membranes from the thalassemic patients ranged from 9.8-17.9% of the added radioactivity/100 micrograms membrane protein and from 2.8-15.0%/100 micrograms membrane protein in the normal donors. Insulin and GH binding to liver membranes did not vary in a consistent way. A 3-fold difference was found in 5'-nucleotidase activity of the membrane fractions. Histological hepatic modifications were assessed with respect to siderosis and fibrosis. No correlation was found between these parameters and GH binding. These results suggest that possible membrane alterations are not the only reason for the variations in hGH binding. All patients had retarded growth, and all but 2 had low plasma insulin-like growth factor I levels. No relationship was found between the level of GH binding to liver membranes and the growth failure. Thus, a defect in GH binding to liver membranes is probably not the cause of the growth retardation of thalassemic children.
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PMID:No evidence for a defect in growth hormone binding to liver membranes in thalassemia major. 264 90

Theoretically, zinc can exert a number of indirect antioxidant functions. Researchers at our laboratory have found evidence to support this concept by studying mild zinc deficiency in rats. This state produces low resistance to chemically induced liver oxidant injury, and it produces high vulnerability of lipoproteins to oxidation. We are building on this work in rats to test a hypothesis in humans that increased zinc intake will protect against oxidant stress in persons with tendencies for both moderate zinc deficiency and high oxidant stress. This hypothesis has been tested in postmenopausal, type 2 diabetic women. A 3-wk supplementation with zinc (30 mg/d as glycine-chelate) raised initially low plasma zinc values to above normal values and increased plasma activities of 5'-nucleotidase. However, the latter values were still well below normal. Lipoprotein oxidation tendencies, a measure of oxidant stress, were not altered by the zinc treatment. A new project has been initiated to determine whether both a higher dose and longer duration of zinc treatment will normalize 5'-nucleotidase activities and affect the indices of oxidant stress. The latter will be considered in terms of both zinc supplementation and supplementation of zinc plus vitamin C, another problem nutrient for diabetic persons.
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PMID:Zinc in relation to diabetes and oxidative disease. 1080 67