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)

The influence of wheat bran as a source of dietary fibre on the excretion of ingested cadmium from diet was studied. The cadmium contents in the diets, faeces, urine, liver, kidney and spleen were determined, as well as the weight gains, the relative weights of the cited organs, and the levels of alkaline phosphatase in serum. No evidence is provided that an increasing portion of wheat bran in the diets induced an increase in cadmium excretion. Changes in the studied toxicity parameters were not found.
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PMID:The effect of wheat bran on the excretion of cadmium in rats. 283 May 17

Rats received 0.1% lead acetate in their drinking water for 3 weeks or for 6 weeks, at which time renal brush border fractions were obtained for measurement of enzyme activity. Renal brush border preparations from Pb2+-exposed rats exhibited statistically significant decreases in the activity of gamma-glutamyl transpeptidase and alanine aminopeptidase after 3 or 6 weeks of treatment. There was an increase in the activity of alkaline phosphatase which was statistically significant after 3 weeks of Pb2+ exposure. The (Na+,K+) adenosine triphosphatase activity and urokinase activity, located in the basolateral membrane fractions, were unchanged by Pb2+ exposure, as were the protein and phospholipid contents of the brush border fractions. The results are compared to those following acute exposure to Pb2+ or Cd2+.
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PMID:Rat kidney brush border enzyme activity following subchronic oral lead exposure. 285 32

The effect of cadmium administration on female Bufo regularis was studied. The median lethal doses were 22, 18, 15 and 6.2 mg Cd2+/kg after 24, 48, 72 and 96 hr respectively. After a single intramuscular injection of 6.2 mg Cd2+/kg (representing 96-hr LD50), the results indicated that Cd2+ causes severe physiological abnormalities to this experimental animal. The serums alanine aminotransferase (AlAt), aspartate aminotransferase (AAt), alkaline phosphatase (AlP) and lactic dehydrogenase (LDH) were elevated while the calcium serum was not influenced by Cd2+ throughout the experimental period. On the other hand, phosphorus, total protein and total bilirubin were increased. EDTA treatment (0.2 mmole/kg) protected female toads from mortality up to 20 mg Cd2+/kg. It overcame the physiological alterations that were caused by the Cd2+ injection. This may be due to the fact that Cd2+ is bound to EDTA in a strong complex which is readily excreted via the kidneys.
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PMID:Toxicity of cadmium administration to the toad and the treatment of its poisoning with EDTA. 287 99

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

The administration of sodium N-methyl-N-dithiocarboxy-D-glucamine (NaG) at 500 mg/kg, i.p., or sodium calcium diethylenetriaminepentaacetic acid (DTPA) at 632.5 mg/kg, i.p., reduces the serum enzyme levels characteristic of hepatic damage following the intravenous administration of cadmium chloride (3.5 mg CdCl2.2.5H2O/kg). Some effect on serum enzyme levels was found even when the interval between administration of cadmium chloride and that of the antagonist was as great as 4 h. The enzymes examined included aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), alanine aminotransferase (SGPT), and alkaline phosphatase (AP). A histopathological examination of the livers of such animals also reveals the presence of a significant protective action.
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PMID:Chelating-agent suppression of cadmium-induced hepatotoxicity. 289 Jul 68

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

The described experiments show the influence of a single dose of cadmium chloride (1.5 mg CdCl2/kg body weight applied intraperitoneally) on development of the male gonads from the 1st d of post-fetal life to 1.5 a of life. In the case of the enzymes triggering transportation processes, adenosine triphosphatase stimulated by Mg++ (Mg++-ATP-ase), alkaline phosphatase (AP), and 5'nucleotidase (5'Nt), a considerable damages begin to appear in the 15th d of life whereas in the case of acid phosphatase (AcP) already in the 1st d of life whereas in the case of acid phosphatase (AcP) already in the 1st d of life. These damages increase with age reaching their maximum in the 45th d of life.
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PMID:Evolution of localization of reactions of adenosine triphosphatase (Mg++-ATP-ase), 5'nucleotidase (5'nt), alkaline phosphatase (AP), and acid phosphatase (AcP) in developing rat testis. II. After CdCl2 treatment. 303 15

Detailed biochemical investigations of renal function were made on 75 male workers exposed to cadmium and an equal number of referents matched for age, sex, and employment status. The exposed group consisted of current and retired workers who had been employed in the manufacture of copper-cadmium alloy at a single factory in the United Kingdom for periods of up to 39 years and for whom cumulative cadmium exposure indices could be calculated. In vivo measurements of liver and kidney cadmium burden were made on exposed and referent workers using a transportable neutron activation analysis facility. Significant increases in the urinary excretion of albumin, retinol binding protein, beta 2 microglobulin, N-acetylglucosaminidase (NAG), alkaline phosphatase, gamma-glutamyl transferase and significant decreases in the renal reabsorption of calcium, urate, and phosphate were found in the exposed group compared with the referent group. Measures of glomerular filtration rate (GFR) (creatinine clearance, serum creatinine, and beta 2 microglobulin) indicated a reduction in GFR in the exposed population. Many of these tubular and glomerular function indicators were significantly correlated with both cumulative exposure index and liver cadmium burden. Using cumulative exposure index and liver cadmium as estimates of dose, a two phase linear regression model was applied to identify an inflection point signifying a threshold level above which changes in renal function occur. Many biochemical variables fitted this model; urinary total protein, retinol binding protein, albumin, and beta 2 microglobulin gave similar inflection points at cumulative exposure levels of about 1100 y.micrograms/m3 whereas changes in the tubular reabsorption of urate and phosphate occurred at higher cumulative exposure indices. Measures of GFR, although fitting the threshold model did not give well defined inflection points. Fewer variables fitted the two phase model using liver cadmium; those that did gave threshold levels in the range 20.3-55.1 ppm. When cadmium workers with cumulative exposure indices of less than 1100 y.micrograms/m3 were compared with their respective referents only serum beta 2 microglobulin and urinary NAG were significantly increased in the exposed group and these differences were not related to the degree of cadmium exposure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Relations between liver cadmium, cumulative exposure, and renal function in cadmium alloy workers. 321 4

Zinc, cadmium, lead and copper in sweat from 24 male and 39 female volunteers were determined by anodic stripping voltammetry. Sweating was induced on the forearms by pilocarpine iontophoresis. Average values found for zinc, cadmium, lead and copper in sweat from males were 181 (range 25-863), 1.4 (less than 0.5-10), 41 (6-87) and 103 (less than 5-673) micrograms l-1, respectively. Zinc in sweat from females was significantly higher than in sweat from males (331 micrograms l-1, range 87-836 micrograms l-1), while sweat copper and sweat lead in females were lower (29 micrograms Cu l-1, range less than 5-146 micrograms Cu l-1 and 24 micrograms Pb l-1, range less than 5-66 micrograms Pb l-1). Those taking oral contraceptives showed increased sweat copper concentrations (94 micrograms Cu l-1, range less than 5-480 micrograms Cu l-1) and sweat lead concentrations (36 micrograms Pb l-1, range less than 5-70 micrograms Pb l-1). There was no sex-based difference for copper in sauna-induced sweat. Metal concentrations in sweat were compared with ceruloplasmin, alkaline phosphatase, and total and mobile copper and zinc concentrations in serum in males and females.
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PMID:A comparative study of copper, lead, cadmium and zinc in human sweat and blood. 322 94


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