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)

The present study further developed primary cultures of rabbit renal proximal tubule cells (RPTC) as an in vitro model to study chemical-induced toxicity by investigating the comparative cytotoxicity of mercuric chloride (HgCl2) and methyl mercury chloride (CH3HgCl) to RPTC. Confluent monolayer cultures of RPTC exposed to HgCl2 and CH3HgCl for 24 hr exhibited a concentration-dependent loss in cell viability at culture medium concentrations greater than 25 and 2.5 microM, respectively. Vital dye exclusion was a more sensitive indicator of cytotoxicity than the amount of lactate dehydrogenase activity, alkaline phosphatase activity, N-acetylglucosaminidase activity, and protein content remaining on the culture dish. On the basis of vital dye exclusion, HgCl2 was less toxic to proximal tubule cells in culture than CH3HgCl after 24 hr of exposure, whether cytotoxicity was based on LC50 values (34.2 microM HgCl2 vs 6.1 microM CH3HgCl) or total cellular mercury uptake (4.6 nmol Hg2+/10(5) cells vs 1.25 nmol CH3Hg+/10(5) cells). Differences in the extent and rate of metal uptake were also evident. Maximum cellular uptake of Hg2+ occurred within 6-24 hr after exposure and was not concentration-dependent, whereas maximum uptake of CH3Hg+ occurred within 3 hr of exposure and was concentration-dependent. The intracellular distribution of both mercurials between acid-soluble and acid-insoluble binding sites also differed. At noncytotoxic concentrations of HgCl2 (0.04-5 microM), intracellular Hg2+ bound increasingly to acid-soluble binding sites as a function of time, from 15-30% after 6 hr of exposure to 40-60% after 72 hr of exposure. However, at subcytotoxic (25 microM) and cytotoxic (34.2 microM) concentrations, Hg2+ binding to acid-soluble binding sites remained constant at approximately 30-40% for 6, 12, 24, and 72 hr after exposure. In contrast, only 20% of total cellular CH3Hg+ was bound to acid-soluble binding sites after exposure to 0.039 to 6.1 microM CH3HgCl for 6, 12, and 24 hr. Total cellular glutathione content was unaffected after exposure to 0.04-5 microM HgCl2 and 0.039-6.1 microM CH3HgCl, but was depleted 6 hr after exposure to 25 and 34.2 microM HgCl2. These results indicate that CH3HgCl was a more potent cytotoxicant to RPTC in primary culture than HgCl2. Furthermore, compared to Hg2+, the low binding of CH3Hg+ to acid-soluble binding sites and the absence of a redistribution of CH3Hg+ from acid-insoluble to acid-soluble binding sites appeared to contribute to its more potent toxicity to cultured cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Primary cultures of rabbit renal proximal tubule cells. III. Comparative cytotoxicity of inorganic and organic mercury. 153 67

Urinary intestinal alkaline phosphatase (EC 3.1.3.1; IAP) is a marker of the S3 segment of the human kidney proximal tubule. An accurate enzyme-antigen immunoassay (EAIA) with a high-affinity specific monoclonal antibody (IAP250) developed for this marker has a detection limit below the lowest IAP activity found in urine samples of normal subjects. The intra- and interassay CVs were less than 5%. Mean analytical recovery of pure IAP added to urine was 102% (SD 6%), and the EAIA results correlated well with immunoreactivity (measured by a sandwich ELISA), suggesting that the EAIA detected all of the IAP in urine. In healthy individuals (ages 20-80 years) the IAP concentrations, expressed as urinary creatinine ratios, ranged from 0.1 to 2.0 U/g (5-95 percentiles) without major differences related to sex and age. Workers exposed to mercury, which affects the S3 segment, showed an increased IAP elimination; abusers of analgesics, which affect more distal parts of the nephron, did not. As opposed to currently measured markers, the EAIA offers easy, accurate, and precise measurement of early alterations in the S3 segment.
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PMID:Immunoassay in urine of a specific marker for proximal tubular S3 segment. 158 13

Male Swiss OF1 mice received a single oral dose of either 80 mg/kg hexachloro-1,3-butadiene (HCBD) or 80 mg/kg methyl mercury (MeHg). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 50% of the proximal tubules after 8 h. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator AT-125 (Acivin, 50 mg/kg i.p., plus 50 mg/kg p.o., reduced the number of damaged tubules by 59 and 58% in mice treated with HCBD and MeHg, respectively. Pretreatment with the two beta-lyase inhibitors, amino-oxyacetic acid (AOAA, 3 x 100 mg/kg p.o.) and DL-propargylglycine (PPG, 300 mg/kg i.p. plus 300 mg/kg p.o.), reduced HCBD nephrotoxicity by 46 and 59%, respectively, but did not protect against MeHg nephrotoxicity. The results support a role for gamma-GT and beta-lyase in the mouse renal toxicity of HCBD and implicate gamma-GT but not beta-lyase in MeHg-induced nephrotoxicity in mice.
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PMID:Role of gamma-glutamyltranspeptidase and beta-lyase in the nephrotoxicity of hexachloro-1,3-butadiene and methyl mercury in mice. 168 80

A feed loading experiment was applied in 2 phases to 45 young cocks over 12 weeks, using 1,2-N,N-bis(methylmercury)-p-toluolsulphamide-dressed wheat (50% of base ration). Investigations were conducted to study the effects of selenium supplementation (0,2 mg Se as sodium selenite/l drinking water) on biochemical and hematological parameters (calcium, phosphorus, total protein, albumin, creatinine, urea, activity of alkaline phosphatase, hematocrit, hemoglobin, leucocyte count) as well as on parameters relating to toxicological residues (selenium and mercury levels in liver, musculature and kidneys). Statistically secured differences were found to exist between the experimental groups with regard to selenium and mercury in the liver and mercury concentrations in kidneys. Possible interrelationships were discussed.
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PMID:[Interrelationships between methylmercury exposure and selenium supplementation in cockerels using selected laboratory diagnostic parameters and toxicological parameters of residues]. 175 6

Plasmids encoding mercury resistance carried by Pseudomonas aeruginosa PAO1161 and PA103 were found to be involved in regulating the secretion of protease, phospholipase C, and alkaline phosphatase. Previously, mutations in Pseudomonas strains that caused pleiotropic effects on the production of extracellular enzymes were mapped to the bacterial chromosome. We show that pleiotropic changes in extracellular enzyme production can also be regulated by plasmids. In this study, the effects on secretion of exoenzymes by two mercury resistance plasmids, FP2 from PAO1161 and pRLW103 from PA103, were assayed in P. aeruginosa PAO1 and PAO18. The introduction of either plasmid into PAO1 resulted in a significant decrease in exoprotease production. Additionally, pRLW103 significantly increased the production of alkaline phosphatase by both strains. Phospholipase C was produced only in strain PAO18 containing the pRLW103 plasmid. FP2 had no effect on alkaline phosphatase or phospholipase C production in either strain and was found to decrease exoprotease secretion only in strain PAO1. The results indicate the P. aeruginosa mercury resistance plasmids vary in their ability to modify exoenzyme expression, and this ability is influenced by the host strain.
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PMID:Effects of FP2 and a mercury resistance plasmid from Pseudomonas aeruginosa PA103 on exoenzyme production. 190 22

Fourteen guinea pigs were injected with sublimate during the period of 3 months. Their urine and blood was examined. In the urine an increase of activity of alkaline phosphatase and lactate dehydrogenase was noted. In the blood plasma an increase of lactate dehydrogenase activity was observed and in the blood serum decrease of gamma-glutamyl-transpeptidase activity. The determination of alkaline phosphatase in urine is a sensitive indicator of renal damage caused by mercury. It has a greater diagnostic value than the determination of this enzyme in the blood serum.
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PMID:The activity of several enzymes in the urine and blood of animals in experimental poisoning with sublimate. Part. II. Chronic poisoning. 198 69

A feed loading experiment was applied in 2 phases to 45 young cocks over 12 weeks, using 1.2 (N, N-bis/methylmercury/-p-toluolsulphamide)-dressed wheat (50% of base ration). The experimental animals were White-Leghorn laying hybrids. Investigations were conducted to study the effects of exclusive exposure to mercury and those of mercury with addition of 0.2 mg of sodium selenite/l drinking water on biochemical parameters (calcium, phosphorus, total protein, albumin, creatinine, urea, activity of alkaline phosphatase, hematocrit, hemoglobin, and leucocyte count) as well as on parameters relating to toxicological residues (selenium and mercury levels in liver, musculature, and kidneys). Statistically secured differences were found to exist between the experimental groups with regard to selenium and mercury in the liver and mercury concentrations in kidneys. These data have shown that the problem of residualisation cannot be solved by selenium supplementation in parallel to methylmercury loading. The results recorded are likely to confirm the need for a general ban on feeding mercury-dressed seed.
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PMID:[Experimental laboratory diagnostic and residual toxicological studies in young cocks after feeding mercury-disinfected seed with and without selenium supplementation]. 261 87

In order to determine the specific action of cadmium on bone metabolism, the effect of cadmium on alkaline phosphatase activity, a marker enzyme of osteoblasts, was compared with that of other divalent heavy metal ions, i.e., zinc, manganese, lead, copper, nickel and mercury (10 microM each), using cloned osteoblast-like cells, MC3T3-E1. Cadmium had the strongest inhibitory effect on alkaline phosphatase activity of the cells among the metals tested. At the same dose, however, cadmium failed to inhibit cellular glucose-6-phosphatase and lactate dehydrogenase activities, suggesting that the inhibitory effect of cadmium on alkaline phosphatase was specific and was not dependent on cell injury. Cadmium treatment caused a significant decrease in cellular zinc level, but mercury treatment had no such effect at the dose inhibiting alkaline phosphatase activity. There was a good correlation between decrease of cellular zinc level and inhibition of alkaline phosphatase activity in cadmium-treated cells. Concomitant treatment of the cells with zinc prevented the cadmium-induced inhibition of alkaline phosphatase activity. However, this was not the case in the mercury-induced inhibition. Cadmium also inhibited the mineralization of osteoblasts. When 10 or 20 microM zinc was concomitantly added to the cultures, the inhibition of mineralization was prevented. These data suggest that the inhibitory effect of cadmium in osteoblasts may be closely related to its influence on the cellular zinc metabolism.
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PMID:Preventive effects of zinc on cadmium-induced inhibition of alkaline phosphatase activity and mineralization activity in osteoblast-like cells, MC3T3-E1. 274 54

Previous experiments indicated that the partial reversal of mercuric chloride-induced renal dysfunction in rats by subsequent dithiothreitol (DTT) administration was not related to increased mercury excretion, decreased renal mercury concentration, a change in renal cortical subcellular mercury distribution, or the formation of a Hg-DTT complex. The present studies investigated whether DTT, a sulfhydryl reducing agent, protected renal cortical sulfhydryl status in general, or the activity of various renal enzymes (Mg- and Na,K-ATPases, alkaline phosphatase, and glutathione peroxidase) in particular. Additionally, the occurrence of conjugated dienes was used to assess the degree of lipid peroxidation. HgCl2 produced significant decreases in renal cortical protein-bound sulfhydryl concentration, alkaline phosphatase activity, and ATPase activity within 2.5 h of administration, with no effect observed on glutathione peroxidase activity or the levels of conjugated dienes in rat renal cortex. Administration of DTT 60 min after mercury neither provided protection from inhibition nor promoted restoration of the affected enzymes or sulfhydryl status. It is concluded that the partial protection of renal function offered by DTT in the early stages of mercury toxicity does not result from maintaining the integrity of renal cortical sulfhydryl status or the activity of the enzymes investigated. Furthermore, the early stages of mercury toxicity did not appear to be related to lipid peroxidation.
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PMID:Enzyme activity and sulfhydryl status in rat renal cortex following mercuric chloride and dithiothreitol administration. 284 77

Alterations in the levels of selected enzymes have been studied in the liver, kidney and brain of mouse following mercuric chloride (1 mg/Kg body wt./d) administration for 10, 20 and 30 d. The activity of acid phosphatase increased in all the tissues, the highest increase was recorded in the kidneys which showed as much as 4.5 fold elevation following mercuric chloride administration for 30 d. Although the alkaline phosphatase activity in the liver and the brain increased following HgCl2 administration, the kidneys experienced a tremendous decline in this enzyme following the same treatment. Mercury-induced changes in ATPase were complex inasmuch as the nature and magnitude of these changes varied with the tissue as well as the duration of the treatment. Whereas the liver ATPase declined after all the treatment intervals, this enzyme increased in the kidney and brain following administration of HgCl2 for 10 d. However, both the kidneys and brain registered a substantial fall in ATPase activity when HgCl2 administration was continued for 30 d. The levels of both glucose-6-phosphatase and succinic dehydrogenase decreased in all the tissues following HgCl2 administration. Invariably, the magnitude of decrease was the highest after 30 d treatment with HgCl2.
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PMID:Enzyme changes in the brain, liver and kidney following repeated administration of mercuric chloride. 302 11


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