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

This article reports correlations among gamma-glutamyltransferase (GGT), fetal haemoglobin (fH), alpha-fetoprotein, 5'-nucleotidase, ceruloplasmin, and direct, indirect, and total bilirubin in the serum of blood taken from the umbilical cords of 128 newborns delivered after 37-42 weeks of gestation. GGT was significantly correlated with alpha-fetoprotein, but not with direct bilirubin, indirect bilirubin, total bilirubin, fH, or %fH. Neither fH nor %fH were correlated with alpha-fetoprotein, but there was highly significant negative correlation between both fH and %fH on the one hand, and gestational age and weight at birth on the other. The %fH was also correlated negatively with ceruloplasmin, which in turn exhibited negative correlation with alpha-fetoprotein. The predominant forms of GGT in umbilical cord and adult sera were, respectively, those with alpha 1 and alpha 2 mobility. In cord sera, delipidation with n-butanol brought about loss of GGT activity and a shift from an alpha 1 to an alpha 2 position, whereas no significant effect of this kind was observed in adult sera. Affinity chromatography through Concanavalin A-Sepharose showed cord sera to contain a proportion of bound-GGT (68.5 +/- 5.5%) that was significantly greater (p less than 0.001) than that found in adult sera (59.8 +/- 10.2%). It is concluded that the high GGT activity of cord sera is probably due to hepatic immaturity rather than maternal sources, enzymatic induction or microsomal lesions; that the predominant form of GGT in cord serum may be a complex with HDL and less sialized than the adult enzyme; and that, of the factors examined, the best indicator of neonatal maturity is fetal haemoglobin.
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PMID:Cord serum gamma glutamyltransferase in newborns. 244 3

Twelve serum analytes [triglycerides, cholesterol, total and conjugated bilirubin, high-density-lipoprotein cholesterol (HDL-C), alkaline phosphatase (AP), gammaglutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), beta-glucuronidase (beta-glu), alanine aminopeptidase (AAP), and 5'-nucleotidase (5'nuc)] were measured to investigate their correlation with exposure to polychlorinated biphenyls (PCBs) and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT). The relationship between serum lipids, lipophilic toxicants, and the analytes was also evaluated. The beta-glu, 5'nuc, triglycerides, cholesterol, and total bilirubin correlated positively and significantly with log concentrations of serum total PCBs and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), a metabolite of DDT. The more highly chlorinated PCBs (Aroclor 1260) had significant, positive correlations with several serum analytes, but the less chlorinated PCBs (Aroclor 1242) correlated significantly and negatively only with HDL-cholesterol. Triglyceride- and cholesterol-rich lipoproteins were added to serum to determine the effects of lipids on these assays. Several were spuriously elevated. AP and beta-glu were not affected by lipoprotein addition with the methods used in this study. AAP was increased significantly only at triglyceride concentrations exceeding 400 mg/dl. Lipoproteins may be elevated because of deranged lipid metabolism in response to PCBs, or PCBs may be elevated because elevated lipoproteins are present, as in familial triglyceridemia, a relatively common dyslipoproteinemia. Because this relationship is not well understood with respect to cause and effect, we propose the further use in epidemiological investigations of assay methods that are little affected by blood lipids yet are correlated with PCB concentrations. Congener-specific quantification of PCBs would help elucidate the effects of PCBs on assays used to monitor health effects.
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PMID:Effects of polychlorinated biphenyls and lipemia on serum analytes. 302 64

The subcellular distribution of 125I-labelled HDL taken up by rat hepatocytes in vivo and in vitro has been studied with subcellular fractionation techniques: differential centrifugation and isopycnic centrifugation in sucrose gradients. 125I-labelled HDL bind to plasma membranes both in vivo and in vitro and part of the membrane-bound 125I-labelled HDL can be dissociated by the addition of unlabelled HDL. The hepatocytes also internalize 125I-labelled HDL. The 125I-labelled HDL accumulate, however, at different intracellular sites in the in vivo and in vitro situation. The subcellular distribution pattern of 125I-labelled HDL taken up by the cells in vivo is similar to that of the lysosomal marker enzyme acid phosphatase. Peak activity was found at a density of 1.20 g/ml. In vitro 125I-labelled HDL accumulate in an organelle with a medium density of about 1.13 g/ml. This distribution was similar to that of the plasma membrane marker 5'-nucleotidase. The subcellular distribution of radioactivity taken up in vivo was changed to lower density by incubating the cells with chloroquine, a drug known to render the lysosomes more boyant. Chloroquine had no effect on the distribution of 125I-labelled HDL taken up by hepatocytes in vitro.
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PMID:The intracellular distribution of high density lipoproteins taken up by isolated rat hepatocytes. 625 95

The binding of human 125I-labeled HDL3 to purified rat liver and testis plasma membranes was studied. About 50-65% of the total HDL binding in these membranes was abolished by 1% bovine serum albumin in the incubation medium. The remaining albumin-insensitive binding sites, determined in the presence of albumin were associated with plasma membranes; a good correlation was found between the 125I-labeled HDL3 binding and the 5'-nucleotidase activities of the membrane fractions. The binding sites in these tissues were saturable, specific for HDL (not competed for by LDL) and had similar affinities for 125I-labeled HDL3 (Kd, 11.8 micrograms protein/ml for liver and 12.7 micrograms protein/ml for testis membranes); the maximum binding capacity of the testis membranes was higher (1.3 vs. 0.7 microgram protein/mg membrane protein). Egg phosphatidylcholine complexes of both human apolipoprotein A-I and apolipoprotein C's competed for the HDL-binding sites, but phosphatidylcholine vesicles alone did not. Chemical modification of the lysine and arginine residues of apolipoproteins did not affect the interaction of HDL3 with its binding sites. Despite the fact that the HDL-binding sites in these tissues are not specific for apolipoprotein A-I, they may have important physiological roles in lipid transport, as they appear to recognize apolipoprotein-phospholipid complexes.
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PMID:Characterization of high-density lipoprotein binding sites in rat liver and testis membranes. 647 54

Water-suppressed proton nuclear magnetic resonance spectroscopy of plasma had been proposed as a technique for detecting malignant tumors although its general diagnostic value is widely contested. To assess its diagnostic value in screening for breast cancer, we collected and analyzed 108 plasma samples from healthy women and women with breast disorders, mainly adenocarcinomas. No significant differences were found between controls and patients when average methylene-methyl linewidths were compared. Significant differences, however, were observed when methylene linewidths were compared. Unfortunately, the marked overlapping of both groups greatly reduced the possible diagnostic value of the technique. Among the various biochemical parameters analyzed for each plasma sample--triglyceride, total cholesterol and HDL cholesterol concentration, altered levels of carcinoembryonic antigen, phosphohexose isomerase, 5'-nucleotidase and phosphatase alkaline in patient samples, and estrogen and progesterone receptors of tumors--only triglyceride concentrations presented a clear inverse linear correlation with methylene linewidths.
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PMID:Study of the ability of proton nuclear magnetic resonance spectroscopy of human plasma to differentiate between controls and breast cancer patients. 838 28