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11.
The effect of neurotensin on submaximally-stimulated hepatobiliary and pancreatic secretion was studied in 6 healthy subjects. An intravenous infusion of neurotensin 1.4 ± 0.3 pmol/kg/min, designed to reproduce plasma neurotensin immunoreactivity levels within the physiological range, produced a significant increase in pancreatic bicarbonate output. Plasma concentrations of pancreatic polypeptide rose by 83 ± 16 pmol/l and were associated with a small reduction in trypsin, but no significant change in bilirubin outputs. 相似文献
12.
Maria P. Abbracchio R. Mark Evans J. Daniel Heck Orazio Cantoni Max Costa 《Biological trace element research》1982,4(4):289-301
The effects of serum components and amino acids on the uptake and cytotoxicity of NiCl2 were examined in cultured Chinese hamster ovary (CHO) cells. CHO cells maintained in a minimal salts/glucose medium accumulated
10-fold more63Ni than did cells maintained in complete medium supplemented with 10% fetal bovine serum. Cell-surface binding of63Ni appeared to account for the majority of this increased accumulation of cell-associated nickel observed in the simple maintenance
medium since such increases were reduced 70% by trypsin treatment. The addition of the Ni2+-binding amino acids cysteine or histidine to the salts/glucose medium markedly decreased63Ni accumulations, an effect not observed following addition of any of several amino acids that do not bind Ni2+. Supplementation of the salts/glucose medium with fetal bovine serum decreased in a concentration dependent fashion both
the63Ni2+ uptake and cell detachment caused by Ni2+, while dialyzed (amino acid-free) serum was 3–5-fold less effective than undialyzed serum at reducing63Ni2+ uptake and similarly exhibited only a slight protective effect against nickel-induced cytotoxicity. Supplementation of dialyzed
serum with cysteine at levels approximating those in whole serum partially restored its inhibitory activity toward nickel
uptake by cells and restored completely its inhibition of nickel's cytotoxicity, indicating the predominant role of specific
amino acids over serum proteins in regulating the uptake and subsequent cytotoxicity of Ni2+. Addition of cysteine to the salts/glucose medium during a 2 h exposure of cells to either 100 μM HgCl2 or 1 mM NiCl2 masked the cytotoxic effects of these metal ions. These results demonstrate the importance of extracellular small molecular
weight metal ion chelators in altering the biological effects of metal ions at the level of metal uptake. 相似文献
13.
Anti-viral activity of 3-deazaadenosine and 5'-deoxy-5'-isobutylthio-3-deazaadenosine (3-deaza-SIBA) 总被引:1,自引:0,他引:1
A J Bodner G L Cantoni P K Chiang 《Biochemical and biophysical research communications》1981,98(2):476-481
3-Deazaadenosine and 5′-deoxy-5′-isobutylthio-3-deazaadenosine (3-deaza-SIBA) inhibits replication of both herpes simplex type 1 virus and the RNA type C virus, HL-23. Oncogenic transformation caused by SV40 and HL-23 are also blocked by either compound. Both compounds exhibit relatively low cytotoxicity at the anti-viral concentrations. 相似文献
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Guanidoacetate methyltransferase has been purified about 140-fold from pig liver. Polyacrylamide gel electrophoresis of the purified enzyme showed four protein bands, each of which is associated with guanidoacetate methyltransferase activity. During gel electrophoresis at pH 3 in 8 M urea, guanidoacetate methyltransferase migrated as a single component. The molecular weight of the purified guanidoacetate methyltransferase was estimated to be 31,000 by sodium dodecyl sulfate-gel electrophoresis, which also showed only one protein component with guanidoacetate methyltransferase activity. This molecular weight is in agreement with that estimated by Sephadex G-75 chromatography. Guanidoacetate methyltransferase is inhibited by adenosylhomocysteine, 3-deazaadenosylhomocysteine, and sinefungin with Ki values of 16 microM, 39 microM, and 18 microM, respectively. 相似文献
16.
Edward J. Leonard Alison Skeel Peter K. Chiang Giulio L. Cantoni 《Biochemical and biophysical research communications》1978,84(1):102-109
An inhibitor of adenosylhomocysteine hydrolase, 3-deazaadenosine, caused profound inhibition of phagocytosis of opsonized erythrocytes by mouse resident peritoneal macrophages . The inhibition was evident at concentrations as low as 2×10?7M, and increased with increasing concentration and time of exposure to the analogue. It was not associated with detachment of the macrophage monolayers or with loss of cell viability. Although the inhibition was not reversible, progression of the functional impairment was interrupted by washing out the analogue. In striking contrast, phagocytic function of human blood monocytes was unaffected by 3-deazaadenosine. 相似文献
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