Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty 100 g male rats were fed, in groups of eight, either 0, 5, or 25 ppm cadmium in a purified diet for 14 wk. Three groups were fed each of the levels of cadmium on an ad libitum basis. Two other groups were fed either 0 or 5 ppm cadmium in amounts that were equalized to that consumed by the 25 ppm group fed ad libitum. Cadmium ingestion decreased daily diet consumption, weight gain, and terminal body weight. These parameters were not significantly different in rats whose diet consumption was equalized. Packed cell volume and serum iron as well as serum zinc were decreased in the rats fed 25 ppm cadmium. These effects were not related to diet intake. No major differences were observed in serum ceruloplasmin, glucose, protein, leucine aminopeptidase activity, or copper in any of the groups. Blood urea nitrogen and renal leucine aminopeptidase activity were decreased by cadmium ingestion in the rats fed ad libitum only. In contrast, serum alkaline phosphatase activity was elevated by cadmium in the equalized-intake groups only. Cadmium and zinc concentrations were elevated and the iron concentration was decreased in the kidney, liver, and intestinal mucosa of the cadmium-fed rats irrespective of level of diet consumption. The increased uptake of cadmium in these tissues was coincident with the increased content of the cadmium-binding protein, metallothionein, in the cytosol fraction. The results indicate that some parameters of chronic cadmium toxicity are associated with diet consumption whereas others are not.
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PMID:Biomedical responses of rats to chronic exposure to dietary cadmium fed in ad libitum and equalized regimes. 85 45

An improved ELISA combined with linear sweep voltammetry detection of p-nitrophenol generated by an enzyme has been investigated in this study. p-nitrophenol, produced from alkaline phosphatase catalysing p-nitrophenyl phosphate, yielded an oxidative peak at 1.06 V (vs. Ag/AgCl) with a wax-impregnated tubular graphite anode. Without separation, the small three-electrode system was directly inserted in the well of an ELISA plate for detection. The detection limit for p-nitrophenol was 1 x 10(-6) M, lower than that obtained by measuring the absorbance of p-nitrophenol. The feasibility of utilizing linear sweep voltammetry as a detection scheme was demonstrated by determining metallothionein, granulocyte-colony stimulating factor and Xenopus laevis keratin using the above new system. The method was simple, reproducible and much more sensitive than traditional spectrophotometry.
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PMID:An improved ELISA with linear sweep voltammetry detection. 137 75

The influence of 12-O-Tetradecanoylphorbol-13-acetate, an activator of proteinkinase C and A 23187, a calcium ionophore increasing cytosolic free calcium concentration on zinc metabolism was investigated in a study with 24 eight-week old rats. Twenty-four hours before killing, the rats (235 g body weight, 8 per group) were either injected intraperitoneally with TPA (1.6 x 10(-7) mol/kg body weight) or A 23187 (1.6 x 10(-6) mol/kg body weight). Control rats received the solvent dimethylsulfoxide. The application of TPA and A 23187 provoked a marked decline in feed intake accompanied by a reduction in body weight and liver mass. Serum concentrations of zinc were reduced significantly after A 23187 injections. TPA and A 23187 increased liver zinc levels by 20 and 30% respectively, if based on fresh and dry weight. The injections, however, did not alter total liver zinc. Liver metallothionein (MT) concentration was elevated 2.4-fold after TPA administration. The increase in response to A 23187 was only 1.5-fold and not significant. Mucosa MT levels were not altered. Serum activity of alkaline phosphatase was significantly reduced (TPA: -23%, A 23187: -31%). There was no change in serum glucose after injections. However, serum creatinine and urea were increased in response to A 23187. In conclusion, TPA and A 23187 had an effect on zinc metabolism of the rat, most marked in the case of MT induction in the liver. There is evidence that the reduced feed intake caused by TPA and A 23187 resulted in effects indistinguishable from those caused by fasting. Further experiments are needed to clarify whether proteinkinase C and cytosolic free calcium are directly involved in the regulation of zinc metabolism.
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PMID:[Influence of an activator of protein kinase C (TPA) and a calcium-mobilizing agonist (A 23187) on zinc metabolism in the rat]. 149 28

Pregnant Sprague-Dawley rats were intraperitoneally injected with physiological saline solution (vehicle) or cadmium chloride (CdCl2) at 2.5 mg kg-1 body wt. on days 8, 10, 12 and 14 of gestation. Offspring were examined for renal alkaline phosphatase activity (ALP) on postnatal days (PND) 3 and 12, and for kidney metallothionein (MTh) and for liver, kidney and entire gastrointestinal tract 109Cd content at birth and on PND 3 and 12. No effects were observed on neonatal survival or on body, liver and kidney weights of pups up to PND 12. Newborns born and fed by mothers exposed to CdCl2 during pregnancy exhibited a significant decrease in ALP activity on PND 3. Conversely, no significant changes were observed in newborns lactated by surrogate non-treated mothers. Renal MTh increased with age but was not influenced by maternal treatment. Traces of 109Cd were present in the liver at birth (5-7 ng). Thereafter, 109Cd was mainly found in the gastrointestinal tract of newborns lactated by their biological mothers (610-690 ng on PND 12), with a marginal uptake in the liver (10-12 ng on PND 12). 109Cd was not detectable in the kidneys at any age (less than 4 ng). These results show that prenatal exposure to Cd cannot be the sole aetiological agent in the induction of the subtle and transitory changes in renal biochemistry observed in offspring born and fed by female rats intraperitoneally injected with 2.5 mg CdCl2 kg-1 body wt. on days 8, 10, 12 and 14 of gestation. The results also contradict the role of a direct effect on the kidney.
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PMID:Indirect and lactation-associated changes in renal alkaline phosphatase of newborn rats prenatally exposed to cadmium chloride. 162 16

We have established mutant SaOS-2 cell lines that express a cyclic AMP (cAMP)-resistant phenotype to investigate the regulation and functional importance of orthophosphoric-monoester phosphohydrolase alkaline optimum (ALPase) in the action of parathyroid hormone (PTH). Cells were stably transfected with a plasmid that directs the synthesis of a mutant form of the type I regulatory subunit of protein kinase A (PKA) under the control of the metallothionein promotor. There was no significant difference between parental SaOS-2 cells and the mutant lines in the affinity or number of receptors for 125I-Nle8,18Tyr34bPTH1-34NH2, either in the absence or presence of Zn2+. When cAMP-dependent gene transcription was examined using transient transfection with a somatostatin promoter-chloramphenicol acetyl transferase (CAT) reporter plasmid, CAT activity stimulated by human PTH and dibutyryl cAMP (DBcAMP) was inhibited by greater than 90% in the presence of Zn2+ in the mutant cell lines. In contrast, activation by a phorbol ester of a pentameric collagenase promoter/CAT construct containing five tandem copies of the AP-1 response element (5x-TRE-CAT) was unaffected in Zn(2+)-treated mutant cells. The inhibitory actions of PTH and DBcAMP on ALPase release were blunted by up to 80-90% in the mutant cell lines in the presence of Zn2+; there were no significant differences in the magnitude of inhibitory effects between these agonists. We conclude that the inhibitory action of PTH on ALPase release in SaOS-2 cells is mediated via activation of PKA. These cAMP-resistant cell lines will be especially useful in elucidating signal transduction mechanism(s) for PTH in human osteoblastic cells.
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PMID:Protein kinase A-dependent inhibition of alkaline phosphatase release by SaOS-2 human osteoblastic cells: studies in new mutant cell lines that express a cyclic AMP-resistant phenotype. 166 91

Pregnant Sprague-Dawley rats were injected intraperitoneally with physiological saline solution (vehicle) or cadmium chloride (CdCl2) at 2.0 or 2.5 mg kg-1 on days 8, 10, 12 and 14 of gestation. On postnatal day (PND) 3, 12 or 49, the offspring were examined for 8- or 24-h urinary excretion of beta 2-microglobulin (beta 2-m), metallothionein (MT) and urinary activity of three proximal tubular enzymes: gammaglutamyl transferase (GGT), alkaline phosphatase (ALP) and N-acetyl-beta-glucosaminidase (NAG). Treatment with CdCl2 did not affect growth or survival of offspring. Significant decreases in the urinary excretion of GGT, ALP and NAG were observed on PND 3, at both doses. Exposure to 4 x 2.5 mg kg-1 resulted in functional deficit of the proximal tubule on PND 3, as evidenced by the significant increase in beta 2-m. Except for a slight but significant increase of beta 2-m in 49-day-old males, all the other urinary parameters returned to control values on PND 12. There was no effect on MT. Results from this study show that prenatal exposure to CdCl2 can induce significant changes in the kidney biochemistry of rats in the early postnatal period.
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PMID:Changes in urinary proximal tubule parameters in neonatal rats exposed to cadmium chloride during pregnancy. 167 94

Dose- and time-related effects of Cd (II) (0.5 or 1.0 mg/kg, Cd as CdCl2.H2O, subcutaneously, daily for 48 h, 1, 3, or 6 wk) were investigated in rats. A dose-related increase in the activity of plasma alkaline phosphatase (ALP), lactate dehydrogenase (LDH), aspartate aminotransferase (GOT), and alanine aminotransferase (GPT) was evident only at 6 wk, whereas an early rise in ALP and LDH was seen at 3 wk in 1.0 mg Cd group only. The hepatic and renal metallothionein (MT) induction displayed a dose- as well as time-related increase with Cd accumulation. A significant increase in hepatic Zn and renal Cu, no change in hepatic Cu, and a slight increase in renal Zn was observed. Urinary ALP and leucine aminopeptidase (LAP) showed an initial increase at 48 h, thereafter returned to near normal. A second phase of enzymuria (ALP, LAP, GOT, GPT, gamma-glutamyl transpeptidase), proteinuria, and aminoaciduria occurred at 6 wk in a dose-related manner. The urinary excretion of specific renal enzymes appeared closely related to the MT induction and organ Cd levels.
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PMID:Biochemical response to cadmium. Dose-time effect. 171 72

To clarify the effects of dexamethasone (Dex) on metallothionein (MT) synthesis and calcification in osteoblastic cells, a clonal osteogenic cell line (MC3T3-E1) was used in the present study. Under culture conditions designed not to cause calcification, MT synthesis of cells at 3 days after inoculation increased with increasing concentration of Dex (2.5-50 nM) for a 24-h culture period. Cells at 6 or 9 days after inoculation also synthesized MT by a 24-h exposure to Dex. These show that undifferentiated osteoblasts have the ability to synthesize MT by Dex. Under culture conditions designed to cause calcification, cells at 6 days after inoculation were cultured with 50 nM Dex in the presence of 7 mM beta-glycerophosphate (beta-GP) for 7 days. Ca content of Dex-treated cells was about 7.5 times as high as that of untreated cells. Dex-treated cells showed a high activity of alkaline phosphatase (ALP). The Zn content of the MT fraction in Dex-treated cells was about 8 times as high as that of untreated cells. These results show that Dex has the ability to induce MT synthesis in osteoblastic cells and to cause a high calcification which is due at least partly to an enhanced activity of ALP.
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PMID:Induction of metallothionein and stimulation of calcification by dexamethasone in cultured clonal osteogenic cells, MC3T3-E1. 188 87

An animal model of marginal zinc deficiency was tested in mice, and salt taste threshold and salt preference were investigated in the state of marginal zinc deficiency. Two experiments were conducted. In Experiment 1, four-week-old male ICR mice were fed diets of three different levels of zinc content (3.17, 9.27, or 48.13 micrograms Zn/g) for 60 days. Food intake, growth, zinc levels in tissues, hepatic metallothionein (MT) content, and activities of selected enzymes (hepatic and RBC delta-amino-levulinic acid dehydratase (ALAD) and plasma alkaline phosphatase (ALP] did not differ among the groups throughout the experiment, and no overt signs of zinc deficiency were manifested in any group. In Experiment 2, four-week-old male ICR mice were fed a zinc-deficient diet (1.98 micrograms Zn/g) or a zinc-adequate diet (49.14 micrograms Zn/g) for 56 days. Food intake and growth did not differ between the two groups, and no overt signs of zinc deficiency were observed throughout the experiment. Zinc levels in the plasma and femur--but not those in the brain, kidneys, liver, and red blood cell (RBC)--and plasma ALP activities were significantly lower on Day 42 and Day 56 of the experiment in the mice fed the zinc-deficient diet (ZnD group) than in those fed the zinc-adequate diet (ZnA group). Hepatic MT contents were lower in the ZnD group than in the ZnA group on Day 56 only. Salt taste threshold was 0.05% in the ZnA group, while it was 0.1% in the ZnD group, between Day 30 and Day 38, and between Day 44 and Day 52 of the experiment. Preference for 0.9% NaCl solution was no different in the two groups when tested between Day 38 and Day 40 or between Day 52 and Day 54, but that for 1.6% NaCl solution was significantly higher in the ZnD group than in the ZnA group between Day 40 and Day 42, and between Day 54 and Day 56.
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PMID:Marginal zinc deficiency and changes in behavioral salt taste threshold and salt preference in mice. 191 5

The involvement of metallothionein (MT) in the nephrotoxicity of cis-diamminedichloroplatinum (c-DDP) was investigated in rats using enzyme excretion and histology as indicators of renal damage. In addition, the effects of renal glutathione (GSH) depletion on the nephrotoxicity of c-DDP was assessed by organic anion transport in renal cortical slices. A dose of 6.0 mg c-DDP/kg body wt, i.p. was administered to rats either as a single injection of 6.0 mg/kg or as six daily injections of 1.0 mg/kg. Concentrations of platinum (Pt) after c-DDP injection in both dosing regimens were approximately 12 micrograms/g in kidney and 2 micrograms/g in liver. However, there were no increases in either hepatic or renal concentrations of MT after both series of c-DDP injections. Fractionation of kidney cytosols from c-DDP injected rats on Sephadex G-75 columns revealed that 60-70% of cytosolic Pt was associated with proteins of high molecular weight and 15-20% of the Pt associated with the low molecular weight ligands. No discernable Pt peak was detected in the elution volume of MT. Pretreatment of rats with ZnSO4 increased both hepatic and renal concentrations of MT, but there was no Pt associated with the MT fraction after a subsequent injection of c-DDP. Small increases in the urinary excretion of the lysosomal enzyme, N-acetyl-beta-D-glucosaminidase and two brush border enzymes, alkaline phosphatase and gamma-glutamyltranspeptidase were observed 2 and 3 days after a single injection of c-DDP (6.0 mg/kg body wt, i.p.). Urinary creatinine excretion decreased by 50% 1 day after c-DDP injection and continued to decrease for the next 2 days. On the third day after c-DDP treatment, a small but significant decrease in body weight was also observed in the c-DDP injected animals. Pretreatment with Zn did not alter the c-DDP-induced enzymuria or renal tubular damage but slightly attenuated both the decrease in creatinine excretion and the loss in body weight. Uptake of the organic anion, p-aminohippuric acid (PAH) was reduced at 12 and 24 h after c-DDP injection. Reduction of tissue GSH concentrations by pretreatment with buthionine sulfoxime (BSO), resulted in only a slight increase in the c-DDP-induced inhibition of PAH uptake at 24 h after c-DDP injection. These results suggest that, in rats, neither MT nor GSH appear to play major roles in the binding or nephrotoxicity of c-DDP.
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PMID:The interactions of cis-diamminedichloroplatinum with metallothionein and glutathione in rat liver and kidney. 197 10


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