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)

Changes in oxidative metabolism were studied in hepatopancreas, muscle, and hemolymph of the edible crab Scylla serrata, exposed to a sublethal concentration (2.5 ppm) of cadmium chloride. A significant decrease in glycogen, total carbohydrates, and pyruvate and an increase in lactate levels in hepatopancreas and muscle were observed. Hemolymph sugar levels were increased in experimental crabs. An increase in phosphorylase suggested increased glycogenolysis during cadmium toxicity. The decrease in lactate dehydrogenase activity and the increase in lactate content indicated reduced mobilization of pyruvate into the citric acid cycle. Krebs cycle enzymes such as succinate dehydrogenase and malate dehydrogenase were found to be decreased, suggesting impairment of mitochondrial oxidative metabolism as a consequence of cadmium toxicity. Glucose-6-phosphate dehydrogenase activity was increased, suggesting enhanced oxidation of glucose by the HMP pathway. Cytochrome-c oxidase and Mg2+ ATPase activity levels decreased, indicating impaired energy synthesis during cadmium stress. Acid and alkaline phosphatase activities increased, suggesting enhanced breakdown of phosphates to release energy in view of impaired ATPase system during cadmium exposure. A significant decrease in protein and free amino acid and an increase in ammonia, urea, and glutamine levels were observed in the tissues during exposure. An increase in protease, alanine aminotransaminase, and aspartate aminotransaminase suggested increased proteolysis and transamination of amino acids. The increase in glutamate dehydrogenase, AMP deaminase, and adenosine deaminase indicated increased ammonia production. The increased arginase and glutamine synthetase suggested the detoxification or mobilization of ammonia toward the production of urea and glutamine. These results suggest that cadmium affects oxidative metabolism and induces hyperammonemia, and crabs switch over their metabolic profiles toward compensatory mechanisms for the survivability in cadmium-polluted habitats.
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PMID:Changes in oxidative metabolism in selected tissues of the crab (Scylla serrata) in response to cadmium toxicity. 753 86

The effect of cadmium (Cd) in drinking water on repair of bone at a site of hole injury to the tibia of young rats was followed using quantitative methods. The rats (3-4 wk old) were given 20 ppm and 200 ppm Cd for 5 wk and compared to a control group. A slight reduction (about 10%) in body weight and water and food consumption was observed in cadmium-exposed rats as compared to control rats. Clinical chemistry tests in the blood and histology of kidney, liver, and bone did not indicate changes related to Cd toxicity. A significant reduction (43%) in alkaline phosphatase (ALP) and tartarate-resistant acid phosphatase (TRAP) (46%) enzymatic activity was observed at 4 and 7 d postinjury respectively, in the site of injury in the rats receiving 200 ppm Cd in drinking water as compared to control rats. Calcium accumulation in the newly formed repair tissue at the site of injury was also significantly reduced (53%) at 13 d postinjury in the Cd-treated (200 ppm) rats as compared to control rats. It is concluded that Cd probably exhibits an effect on the bone repair process as reflected by reduction in ALP activity (osteoblastic cells) and mineralization at the site of injury in the tibia of young rats.
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PMID:Effect of cadmium on bone repair in young rats. 760 1

In this study, we compared results obtained in protein calorie malnourished (PCM) monkeys and controls given Cd2+ (5 mg Cd2+/kg body wt./day) orally for 24 weeks. After 16 weeks of Cd2+ exposure, an indolent renal failure develops in PCM monkeys which resulted in significant increase in urinary excretion of total protein, Cd2+, Zn2+ and Ca2+ as compared to corresponding to Cd(2+)-treated control group. In isolated proximal tubule brush border membrane vesicles (BBMV), Cd2+, Zn2+ and Ca2+ transport were significantly impaired in Cd(2+)-exposed PCM monkeys as compared to Cd(2+)-treated controls. The mechanism of higher urinary excretion of Cd2+, Zn2+ and Ca2+ was examined by analyzing the kinetic parameters of transport systems. The kinetic studies of Cd2+, Zn2+ and Ca2+ transport systems in the BBMV preparations of Cd(2+)-exposed PCM monkeys exhibited a significant decrease in Vmax and an appreciable increase in Km as compared to Cd(2+)-treated controls. These findings suggested that Cd2+ treatment of PCM monkeys caused either a decrease in the number of transporters in the brush border membrane or an increase in the number of less active transporters for Cd2+, Zn2+ and Ca2+. Furthermore, brush border membrane-bound enzymes, viz. alkaline phosphatase and leucine aminopeptidase, activities were significantly impaired in Cd(2+)-exposed PCM monkeys. Cadmium content in kidney cortex of Cd(2+)-exposed PCM monkeys was 3.34-fold higher than Cd(2+)-exposed controls. These findings also established that Cd2+ not bound to metallothionein (MT) was significantly higher in Cd-exposed PCM monkeys, which may be an important determinant in renal toxicity by interacting with sensitive sites in the renal cells and causing renal damage in Cd-exposed PCM monkeys.
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PMID:Cadmium-induced nephrotoxicity in rhesus monkeys (Macaca mulatta) in relation to protein calorie malnutrition. 762 86

The effects of N-benzyl-D-glucamine dithiocarbamate (BGD), diethyldithiocarbamate (DDTC), and N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD) on the enzymatic activities in mice were studied. The mice were given i.v. injections of these chelating agents (1 mmol/kg) and 3 h later the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (gamma-GTP), alkaline phosphatase (ALP), leucine aminopeptidase (LAP), and cholinesterase (ChE) in the liver, kidney, and blood were determined. These enzymatic activities were little changed by treatment with these chelating agents. Cadmium (Cd) administration markedly decreased the activities of AST and ALT in the liver and kidney and greatly increased these enzymatic activities in blood. The changes in the enzymatic activities by treatment with Cd were prevented by injection of BGD (1 mmol/kg). These results indicate that BGD, DDTC, and HBGD were not toxic to the liver or kidney of mice and that BGD treatment protected against the acute hepatic and renal toxicity induced by Cd.
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PMID:Effects of dithiocarbamates and cadmium on the enzymatic activities in liver, kidney and blood of mice. 762 88

We tested the diagnostic sensitivity of various urinary analytes for detecting cadmium-induced nephropathy at an early stage. We investigated 73 healthy persons (control group 1) and individuals exposed to cadmium, either environmentally (n = 36, risk group 2) or occupationally (n = 62, exposed group 3). All data were related to limits of the central 95% reference intervals of the control group. The serum creatinine and ribonuclease values, indicators of the glomerular filtration rate, were not different in the three groups. In the exposed persons (group 3), proximal tubular indicators (low-M(r) proteins lysozyme, ribonuclease, retinol-binding protein, and alpha 1-microglobulin) were more often increased than the glomerular indices (higher-M(r) proteins transferrin, IgG, and albumin). Both the low-M(r) proteins and tubular enzymes were differently altered in their excretion rates. Alanine aminopeptidase, alkaline phosphatase, and N-acetyl-beta-D-glucosaminidase increased even in the risk group 2. alpha 1-Microglobulin was increased in the exposed persons whose cadmium excretion was < 5 mumol/mol creatinine. The combined determination of alpha 1-microglobulin and N-acetyl-beta-D-glucosaminidase exceeded the corresponding upper reference limits in 30% of group 2 and 39% of group 3. We recommend screening for these two analytes to detect cadmium-induced renal dysfunction at an early stage.
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PMID:Urinary proteins and enzymes as early indicators of renal dysfunction in chronic exposure to cadmium. 848 64

The reaction of alkaline phosphatase (APase) with the complexes of myo-inositol hexakisphosphate (IHP) and various cations at pH 7.2 results in a decrease in activity. Singly, neither IHP nor metal ions induce such changes. IHP-Mn(II) complexes were the least effective. Using the ions of nickel or cadmium, activity was reduced by > 95%. A similar large decrease (> 99%) was seen previously in the reaction of APase with IHP-Cu(II) complexes. With Co(II) and IHP as reactants, the activity was reduced to 10-12% of that of the native enzyme. When the apoprotein, prepared by reaction of the enzyme with either EDTA or 1,10-phenanthroline, was titrated with Co(II), the activity was equal to that resulting from the reaction of the enzyme with IHP-Co(II) complexes. Titration with zinc restored 95% of the original activity. The products are metal-substituted derivatives in which the resident catalytic (A-site) zinc ions, at least, are replaced by the cation of the IHP complex that was used. The rates of such reactions were fastest with the complexes of Cu(II) and Cd(II) (0.12 min-1), less so with Co(II) as the ion (0.056 min-1), and slowest with complexes of nickel and manganese (0.01 min-1). In every case, the rate of reaction, but not its extent of change, was inhibited by zinc ions that reduced rate constants to 0.0014-0.0054 min-1. Magnesium ions had no effect. Likewise, Mn(II), with but one exception, did not affect the reactions. When present along with IHP-Ni(II) complexes, the rate was increased and the enzyme activity further decreased. If Zn(II) was also present, this enhancement was eliminated. All changes in enzyme activity were reversible by treatment with EDTA followed by reconstitution with zinc. Approximately 95% conversion to the original activity could be attained. Reactivation of modified APase preparation also could be attained, in some cases, by pre-incubation with Zn(II) at pH 8. For example, conversion of the Cd(II)-substituted APase to the zinc enzyme was rapid and complete in 15 min. With the Cu(II)-substituted derivative, reactivation was much slower. Incubation with zinc ions had little or no effect on other Me(II)-substituted APase preparations. Co-APase and Cu-APase, prepared from the apoprotein, behaved similarly to their respective "counterpart product" of the appropriate metal ion-exchange reaction. In contrast, Co-APase, but not Cu-APase, could be converted to the zinc enzyme by incubation with IHP-Zn(II) complexes at pH 7.2. The reaction rate of the various metal-substituted APase preparations with EDTA varied with the IHP-Me(II) used in its formation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reaction of the coordinate complexes of inositol hexaphosphate with first row transition series cations and Cd(II) with calf intestinal alkaline phosphatase. 776 85

There is a clear lack of information on the toxicological risk of dietary intake of cadmium-metallothionein (CdMt). The present study aimed at establishing dose-dependent cadmium (Cd) disposition and to investigate differences in renal toxicity after long-term dietary exposure to CdMt or cadmium chloride (CdCl2) in rats. Male Wistar rats were fed diets containing 0.3, 3, 30, or 90 mg Cd/kg either as CdMt or as CdCl2 for 10 months. In rats fed 30 and 90 mg/kg Cd as CdCl2 the Cd concentrations in intestine, liver, and kidneys were all higher than in rats fed the same doses in the form of CdMt. The kidney/liver Cd concentration ratio was higher with CdMt than with CdCl2. At the lower Cd concentrations (0.3 and 3 mg/kg), no differences in Cd accumulation between CdMt and CdCl2 groups were observed and the kidney/liver Cd ratio was also similar. When based on the amount of CdMt per milligram Cd in the tissue, rats fed CdMt and those fed CdCl2 had a similar relative CdMt concentration in liver and kidney. First signs of renal injury, indicated by an increase of urinary lactate dehydrogenase (LDH) activity, were seen 4 months after exposure to 90 mg/kg Cd as CdCl2. After 8 and 10 months the renal effect of 90 mg/kg Cd as CdCl2 became more pronounced and urinary enzyme activities of LDH, N-acetyl-beta-D-glucosaminidase and alkaline phosphatase were all elevated. The only clinical effect of CdMt at the dose level of 90 mg/kg was a slight increase in urinary gamma-glutamyl transpeptidase activity at 8 and 10 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of renal toxicity after long-term oral administration of cadmium chloride and cadmium-metallothionein in rats. 786 6

We demonstrated that polyamines, such as spermine and spermidine, can enhance the pyrophosphatase (PPase) activity of alkaline phosphatase (ALP). Bisphosphonates such as disodium-1-hydroxy-1-aminopropylidine-1,1-diphosphonate (APD) and ethane-1-hydroxy-1,1'-diphosphonate (HEDP) inhibited ALP phosphate ester hydrolysis activity more than PPase activity at the same concentrations. This indicated that PPase activity of ALP was available in the presence of pyrophosphate analogues and possibly organic pyrophosphates as well. Vanadate and cadmium inhibited ALP and PPase activity more than ALP phosphate ester hydrolysis activity at the same concentrations. Calcium inhibited ALP PPase activity, though it did not inhibit ALP phosphate ester hydrolysis activity. At high concentrations, ascorbic acid slightly inhibited ALP PPase activity, though it did not inhibit ALP phosphate ester hydrolysis activity. ALP PPase activity appeared to have ubiquitous intracellular existence, broad substrate specificity and extensive interaction with calcium, vanadium and polyamines-substances which are important for cell metabolism and cell growth. These findings suggested that intracellular ALP modulated cell metabolism and cell growth by its PPase activity.
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PMID:[Implications of alkaline phosphatase pyrophosphatase activity: intracellular functions of alkaline phosphatase]. 807 80

To clarify the significance of elevated serum total alkaline phosphatase activity (t-ALP) in persons exposed to environmental cadmium (Cd), the fraction of ALP originating from bone (b-ALP) was assayed using a wheat-germ agglutinin method in 23 men and 20 women in a Cd-polluted area who showed excessive urinary beta 2-microglobulin excretion, and in 21 men and 44 women in a non-polluted area, in addition to 7 patients with itai-itai disease. The fraction of b-ALP increased linearly with the increase in t-ALP in the women, irrespective of Cd-exposure. Elevations of both t-ALP and b-ALP in the Cd-exposed women, including inhabitants of the Cd-polluted area and patients with itai-itai disease, were found with decreases in serum calcium and bone density. It is concluded that elevated serum ALP levels found in Cd-exposed persons reflect the development of Cd-induced bone damage.
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PMID:Serum bone-type alkaline phosphatase activity in women living in a cadmium-polluted area. 816 Feb 9

The toxic effects of environmental factors at work places on the hematopoietic and immune systems are of basic importance due to the time of exposure, lasting on average 8 hours daily during one week. Porphyrinurias and porphyrias have been observed after exposure to hexachlorobenzene, chlorinated dibenzodioxins, polychlorinated biphenyls, polybrominated biphenyls, vinyl chloride and lead. Aplastic anemia may occur after exposure to benzene, pesticides, arsenic, cadmium and copper compounds. Megaloblastic anemia has been noted in subjects exposed to arsenic, chlordane, benzene and nitrous oxide. Methemoglobinemia is induced by aromatic nitro and amino compounds. Hemolytic reactions caused by arsenic, methyl chloride, naphthalene, lead, cadmium and mercury compounds represent a separate problem. Immunodeficiencies resulting in decreased antitumor and antiinfectious immunity have been reported in subjects exposed to asbestos, ozone, dimethylsulphoxide, vinilidene chloride, and benzene homologues. Lymphocytopenia may be induced by manganese, lead, toluene and industrial noise. Neutropenia was marked after exposure to carbon disulphide, arsenic compounds, benzene and electromagnetic fields. Only a few reports concern the lymphocyte T3, T4 and T8 subpopulations. Electromagnetic fields (microwaves) cause an imbalance of that subpopulation, consisting of a decrease in the T8 cell count. The neutrophil enzymes, such as myeloperoxidase and alkaline phosphatase, decrease in their activity after exposure to polychlorinated biphenyls, carbon disulphide, chlorobenzene and DDT. A majority of agents cited include genotoxic effects reflected in chromosome aberrations and increased sister chromatid exchange and abnormal unscheduled DNA synthesis. Leukemia or lymphoma risk is increased after exposure to pesticides, electromagnetic fields, benzene and irradiation.
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PMID:Immunotoxic and hematotoxic effects of occupational exposures. 817 62


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