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)

Mouse L929 cells were used to study the mechanism of cAMP induction of alkaline phosphatase (AP) activity. Following treatment with 200 microM 8-chlorophenylthio-cAMP (CPT-cAMP), alkaline phosphatase enzyme activity was observed to increase 80-fold after 24 h. The CPT-cAMP dose response of the alkaline phosphatase enzyme activity correlated well with the CPT-cAMP activation of cAMP-dependent protein kinase in L cells. A cDNA clone for the alkaline phosphatase was isolated and used to demonstrate a 10-fold increase in alkaline phosphatase mRNA levels after a 24-h treatment of L cells with CPT-cAMP. Increased mRNA levels were first detected 4-6 h, after CPT-cAMP treatment, and the level of alkaline phosphatase mRNA decreased rapidly after removal of CPT-cAMP. In vitro nuclear transcription studies showed that a 3-fold increase in alkaline phosphatase gene transcription was detectable 6 h after CPT treatment, and this increase was blocked by cycloheximide. In order to determine if the catalytic (C) subunit of cAMP-dependent protein kinase was able to mediate the induction of AP, L cells were transfected with expression vectors containing the metallothionein promoter and coding for the C alpha isoform of the catalytic subunit of cAMP-dependent protein kinase or for a catalytic subunit in which lysine 72 had been mutated to methionine (C alpha K72M). Zinc treatment of stably transfected cells expressing the wild-type C subunit showed an increase in protein kinase activity and an increase in AP activity. Zinc treatment of cells containing the mutant C subunit expression vector produced an increase in the amount of a protein which was recognized by C subunit antibodies on Western blots, but these cells showed no increase in protein kinase activity or in AP activity. We conclude that the C subunit is sufficient for transcriptional induction of the AP gene and that the phosphotransferase activity of the C subunit is required for this induction.
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PMID:Induction of alkaline phosphatase in mouse L cells by overexpression of the catalytic subunit of cAMP-dependent protein kinase. 216 96

Inadequate vitamin D intake is an important cofactor in clinical and experimental bone disease induced by chronic cadmium exposure. The interaction was investigated by culture of rat osteoblastic osteosarcoma cells (ROS 17/2.8) in a serum-free medium with equimolar concentrations of cadmium chloride and 1 alpha,25-(OH)2 vitamin D3. After addition of cadmium alone to culture medium, the unstimulated secretion of osteocalcin and cellular alkaline phosphatase activity were inhibited at 10 pM, and of DNA synthesis and proline incorporation into collagen at 500 nM. In the presence of equimolar amounts of cadmium and 1 alpha,25-(OH)2 vitamin D3, all four responses paralleled those of 1 alpha,25-(OH)2 vitamin D3 alone up to the inhibitory concentration of 500 nM cadmium. Neither 10 nM 1 alpha,25-(OH)2 vitamin D3 nor 1 microM cadmium induced synthesis of metallothionein in these cells indicating that the protective effect of D3 was not related to the induction of a metallothionein-like protein in ROS 17/2.8 cells. In the presence or absence of D3, cadmium inhibited osteoblastic function at concentrations below the whole-organ concentration of cadmium in bone as reported in experimental and clinical cadmium-induced osteotoxicity. The extreme sensitivity of ROS 17/2.8 cells to cadmium may relate to the absence of metallothionein synthesis.
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PMID:Toxicity of cadmium to rat osteosarcoma cells (ROS 17/2.8): protective effect of 1 alpha,25-dihydroxyvitamin D3. 231 24

The purpose of this 2 factorial designed study was to investigate the influence of citric acid on the availability of zinc from diets containing 140 g corn germs as a native phytate source (0.5% phytate in diet). Growing male rats with an average initial weight of 42 g were divided into 8 groups of 8 animals each. After a 7 d depletion period (2.4 micrograms Zn/g diet) the animals were fed ad libitum for 21 d a diet on the basis of egg white solid and corn germs. The diets were supplemented with zinc in order to obtain phytate:zinc molar ratios of 31, 20, 14, and 0 (control without corn germs, 11 micrograms Zn/g diet). Each diet was fed with and without a supplementation of 1% citric acid. A phytate:Zn molar ratio of 31:1 resulted in typical symptoms of zinc-deficiency like anorexia, alopecia and a significant depression of growth. These effects were apparently reduced by citric acid. The zinc concentration in serum and organs followed the graded levels of phytate:zinc molar ratios. Primary significant effects of the phytate:Zn molar ratio but also effects of citric acid and interactions between the 2 factors phytate:Zn and citric acid could be detected. Only total liver zinc but not liver zinc based on fresh matter was affected by the phytate:Zn molar ratio. In serum and tissues the activity of alkaline phosphatase showed a significant response to the phytate:zinc molar ratio. Furthermore the supplementation with citric acid increased the femur alkaline phosphatase and slightly reduced it in the liver. The concentrations of metallothionein in liver duodenum, jejunum and ileum were significantly affected by the phytate:Zn molar ratio.
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PMID:[The effect of a supplement of citric acid on the bioavailability of zinc from corn germ]. 233 19

The promoters of murine hepatocarcinogenesis phenobarbital (PB) and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) given to adult C3Hf female mice increased the content of total liver DNA by 1.6-1.8-fold each week after the beginning of treatment. Both compounds increased the aminopyrine-N-demethylase activity, decreased the glucose 6-phosphatase (G6Pase), alkaline phosphodiesterase I and alkaline phosphatase specific activities, but did not modify the gamma-glutamyltransferase levels. Both compounds decreased the abundance of tyrosine aminotransferase- and metallothionein I-related RNA transcripts. These findings confirmed the PB-like activity of TCPOBOP and showed that both chemicals had a pleiotropic effect on mouse liver, that was not limited to stimulation of drug metabolism, but also affected other hepatocyte functions.
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PMID:Effects of phenobarbital and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene on differentiated functions in mouse liver. 244 87

Renal functions were damaged at the reabsorptive site by the injection of cadmium-metallothionein (Cd-MT) and its effect on discrimination of chemically similar elements was examined for the two alkaline-earth elements, calcium (Ca) and strontium (Sr). Tubular damage was induced in female Wistar rats, 7 wk old, body wt 145.1 +/- 3.5 g (mean +/- S.D.), by an intraperitoneal injection of Cd-MT (400 micrograms Cd/kg body wt). The Cd-MT injection caused increases in urinary enzymes (lactate dehydrogenase; alkaline phosphatase), glucose, and total protein. Urinary Ca and Sr increased and urinary Sr/Ca ratio decreased rapidly after the Cd-MT injection. Both changes remained at significant levels throughout the experiment. On the other hand, renal Ca and Sr levels increased with time after 18 or 24 h and changed similarly. Although plasma levels of Ca and Sr slightly increased after 30 or 36 h post-injections, the plasma Sr/Ca level remained constant. A close exponential relationship formed between the relative clearances of Ca and Sr. There was no significant difference between the exponent of the following equation (K) for the Cd-MT-injected group and that for the control group. Sr clearance/creatinine clearance = (Ca clearance/creatinine clearance)K where K = 0.408 from experimental data for the two groups. This suggests that the discrimination mechanism between Sr and Ca during the reabsorptive step in the kidney is strictly regulated.
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PMID:Renal discrimination between strontium and calcium in rats. Effects of renal damage caused by cadmium-metallothionein. 248 30

The mechanism of cadmium metallothionein (Cd-MT)-induced renal toxicity was studied in rats using urinary enzyme excretion as a marker for cellular damage. Animals were injected with either saline or Zn (20 mg of Zn as ZnSO4/kg b.wt.) at 0.5, 4 or 24 hr before injection of Cd-MT (0.3 mg of Cd as Cd-MT/kg b.wt. i.p.). Activities of two brush border enzymes, alkaline phosphatase (ALP) and gamma-glutamyl-transpeptidase (GGT), and a lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG), were measured in 24-hr urine collections. Urinary excretion of all three enzymes was increased significantly after Cd-MT injection. Both ALP and GGT excretions reached a maximum at 24 hr whereas NAG excretion reached peak values at 48 hr after Cd-MT injection. The excretion of all three enzymes decreased to the control level by the 3rd day. Zn pretreatment alone had no effect on urinary enzyme excretion. Pretreatment with Zn salts at 0.5 and 2 hr before Cd-MT injection did not show any difference in the urinary excretion of the enzymes as compared with the saline-treated controls. However, injection of Zn salts at 24 hr before Cd-MT injection resulted in a significant decrease in the excretion of the lysosomal enzyme NAG whereas both ALP and GGT excretions were unchanged. Extensive proximal tubular damage was observed morphologically in all the rats injected with Cd-MT, but the cellular damage was less in rats pretreated with Zn sulfate 24 hr before Cd-MT injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal toxicity of cadmium-metallothionein and enzymuria in rats. 287 4

Time dependent changes in urinary biochemical indicators for renal tubular injury and dysfunction were determined in female Wistar rats after an intraperitoneal injection of cadmium-metallothionein (Cd-MT) (50, 150 or 300 micrograms Cd/kg body wt) to further characterize the tubular damage caused by Cd. The Cd-MT injection caused dose-dependent increases in urinary activities of the enzymes (alkaline phosphatase; gamma-glutamyl transpeptidase; lactate dehydrogenase, LDH; N-acetyl-beta-D-glucosaminidase) on day 1, which appeared to reflect the tubular injury. The rate of increase in LDH, a cytosolic enzyme, was the largest among those of the enzymes. This result coincided with the data reported for repeated administration of ionic Cd to rats, suggesting that the feature of tubular injury caused by an injection of Cd-MT is similar to that by chronic exposure to ionic Cd. Changes in urinary glucose and total protein, indicators of tubular dysfunction, and metals (Cd, zinc and copper) were accompanied with those in urinary enzymes. Hydrocarbons in breath of rats injected with Cd-MT at a dose of 300 micrograms Cd/kg body weight were also determined as an indicator of in vivo lipid peroxidation. The levels of ethane and propane were significantly increased at 12 h after injection, which suggests that lipid peroxidation is partly involved in the tubular damage reflected by the increases in urinary enzymes.
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PMID:Renal damage induced by cadmium-metallothionein: effects on biochemical indicators. 288 22

A monkey model has been set up for protein calorie malnutrition and calcium deficiency. Oral exposure of 5ppm Cd/kg body wt./day for 24 weeks led to increased excretion of Cd, metallothionein (MT) and zinc. Rehabilitation of PCM monkeys for one year resulted in gradual reduction and finally complete disappearance of urinary metallothionein. During Cd exposure, the accumulation of Cd and induction of MT was significantly higher in liver, kidney and intestine. MT was also induced in heart, lung and testis of Cd exposed PCM and calcium deficient monkeys. Metallothionein from liver has been resolved into three isoforms, viz MTa, MTb and MTc on DEAE-Sephadex A 25 ion exchange column. MTc is the major isoform in Cd-treated, normal and protein calorie malnourished monkeys whereas MTb is the major isoprotein in the cadmium treated calcium deficient monkeys. The iso-metallothioneins varied in their metal composition in the nutritional stress conditions and showed different capacities to reactivate apo-enzymes viz. alkaline phosphatase, ceruloplasmin, superoxide dismutase and glutathione peroxidase. Thus, metallothionein plays a key role in metal metabolism during cadmium toxicity under nutritional stress conditions.
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PMID:Role of metallothionein in metal detoxification and metal tolerance in protein calorie malnutrition and calcium deficient monkeys (Macaca mulatta). 295 56

A rapid automatic method of synthesis of deoxypolynucleotides from 5'-O-dimethoxytritylnucleoside-3'-H-phosphonates is described. An improved construction of synthesizer "Gene-2" adapted for this method has been developed. The modified scheme of synthesis included detritylation with trifluoroacetic acids in dichloromethane, washing with acetonitrile instead of pyridine--acetonitrile mixture and one-step oxidation with iodine solution in acetic acid and pyridine instead of two-step oxidation in the presence of amines. By means of this method, more then 160 polynucleotides containing 8 to 83 monomers were prepared for various biochemical goals including synthesis of promotor 9(260 bp) of the mouse metallothionein-I gene and of promotor and leader sequence (120 bp) of gene of the E. coli alkaline phosphatase.
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PMID:[Rapid automated synthesis of polydeoxynucleotides]. 338 38

To evaluate a critical concentration concept of cadmium (Cd) toxicity on the kidney, relationships of renal Cd level with urinary excretion of various substances--i.e., metallothionein, alkaline phosphatase, lactate dehydrogenase, N-acetyl-beta-D-glucosaminidase, total protein, Cd, copper, and zinc--were studied in Cd-injected rats. At the renal Cd concentration of 100-200 micrograms/g tissue, a dramatic increase of all these substances in urine was observed, supporting the idea of the critical concentration proposed by Friberg and co-workers (1974). The significance of increase of urinary metallothionein below this level is also discussed.
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PMID:Critical concentration of cadmium for renal toxicity in rats. 368 16


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