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 intravenous injection of zinc chloride immediately before and 15 minutes after alloxan or dithizone prevented the usual hyperglycaemia observed 24 hours after induction of diabetes. The intravenous injection of manganese chloride prevented any marked rise of blood glucose, while chromium and cobalt chlorides lowered the blood glucose level to a certain extent. In alloxan diabetic rats, serum GOT and GPT levels were significantly higher than normal. The serum GOT levels were higher in animals injected with chromium than cobalt, zinc and manganese; while serum GPT levels were higher in cobalt than in chromium, zinc and manganese. In dithizone diabetes, serum GOT and GPT were increased in animals injected with cobalt than chromium, zinc and manganese. Alloxan diabetic rats showed lower serum alkaline phosphatase levels and higher in animals injected with cobalt than chromium, zinc and manganese. For dithizone, there are statistically significant differences in all cases. In alloxan diabetes, coeruloplasmin was higher than normal, while intravenous injection of dithizone was without effect on serum coeruloplasmin.
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PMID:Serum enzyme changes due to trace amounts of some transition metal ions on the induction of experimental diabetes. 742 63

Effect of seven-day enteral administration of clinkers, cement and dust sedimented on electric filters on DNA and RNA, total protein levels, adenylate desaminase (AD) and alkaline phosphatase (AP) activities in thymus und spleen was shown in rats. Harmful effect of industrial dust on the lymphatic organs was maximal in thymus: diminished lymphatic tissue, decreased DNA, RNA and total protein levels, increased AD and AP activities. Compounds of chromium with lead, copper and mercury appeared to have maximal harmful effect on the lymphatic tissue.
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PMID:[Effect of chrome compounds and other chemicals in the content of cement and clincker dust on metabolic parameters++ of lymphoid organs in rats]. 752 Dec 63

Urinary biochemical indicators of renal injury were examined in 84 male and 38 female ferrochromium-producing workers exposed to water-soluble chromium compounds [Cr(VI)]. The indicators examined included urinary chromium (U-Cr), alkaline phosphatase (ALP), gamma-glutamyl transferase (gamma-GT), glutamic-oxalacetic and glutamic-pyruvic transaminases (GOT & GPT), lactate dehydrogenase (LDH), N-acetyl-beta-D-glucosaminidase (NAG), total protein (TPr) and beta 2-microglobulin (beta 2-MG). The U-Cr levels in the exposed group were approximately 1.8 times that of the control group. Compared to controls, the activities of gamma-GT, NAG, ALP, GOT and LDH in the urine of workers were significantly increased whenever U-Cr concentration exceeded 45 microgram/g creatinine. The activities of gamma-GT, GOT and NAG were elevated in workers employed for longer than ten years. However, no clear dose-response relationships nor time-effect relationships were found. The present results suggest that long-term exposure to water-soluble chromium [Cr(VI)] produces chronic renal injury. The site of the injury appears to mainly involve the proximal tubule. U-Cr concentrations of > 15 microgram/g creatinine can be proposed as a threshold dosage for nephrotoxicity, and gamma-GT, NAG and ALP are early sensitive indicators of the most valuable for evaluating the renal injury.
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PMID:Chromium-induced early changes in renal function among ferrochromium-producing workers. 791 62

For the first time, otosclerotic stapes have been distinguished from unafflicted controls at a high level of significance by using a spectrum of elements measured by energy-dispersive spectrometer-electron probe microanalyses (EDS/EPMA). Discriminant analyses of the maximum concentration of 13 elements measured at several sites within each of 32 stapes differentiated otosclerotic from unafflicted individuals well above the 95% confidence level. Eight of the 9 control (unafflicted) and 21 of the 23 afflicted stapes were correctly classified. In descending order of contribution to the discriminant function, the elements are Zn > Cr > K > Ca > Si > Mn > Na > Al > Mg > P > Fe > S > Ti. Zinc and chromium account for much of the difference, but discriminant analyses excluding them still distinguish the two groups at the 95% confidence level. These results are consistent with previous reports of high levels of alkaline phosphatase, a zinc-containing enzyme, in afflicted stapes. But the broad spectrum of elements capable of distinguishing otosclerotic stapes warrants study of additional zinc-containing and other metal-containing or metal-activated moieties.
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PMID:Composition of the otosclerotic stapes: electron microprobe analyses. 848 64

Certain chromium compounds are known to be nephrotoxic, but renal damage from long-term environmental or occupational exposure to chromium has not been documented. To detect possible preclinical renal damage, we tested the urine of 55 lifelong residents of an area contaminated with chromium landfill. The levels of four proteins were determined in urine samples: (1) human intestinal alkaline phosphatase, (2) tissue nonspecific alkaline phosphatase, (3) N-acetyl-beta-D-glucosaminidase, and (4) microalbumin. No elevated levels of proteins were found, and there were no significant correlations between urine protein and urine chromium concentrations. We concluded that long-term environmental exposure to chromium dust did not lead to tubular proteinuria.
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PMID:Absence of tubular proteinuria following environmental exposure to chromium. 875 13

The toxicity of nickel, chromium (III) and (VI), vanadium and aluminium was compared in an immortalized neonatal rat osteoblast cell line using the MTT assay and a novel index of cytotoxicity, alkaline phosphatase (ALP) activity. Where toxicity was observed, ALP was a consistently more sensitive detection method than the MTT assay. The toxicity of the metals increased in the order aluminium < chromium (III) < vanadium < nickel < chromium (VI). alpha-Tocopherol partially prevented nickel-induced toxicity (as assessed by ALP activity), whereas ascorbic acid had no protective effect. Chromium (VI) was more toxic than (III), with significant toxicity observed at 0.5 microM. It is thought that Cr (III) cannot readily penetrate the cell membrane and this may account for the lower toxicity. Aluminium had a stimulatory effect on cell growth at low concentrations (0.5 microM). The combination of immortalized rat osteoblasts and the ALP activity test provides a powerful tool for in vitro testing of orthopaedic materials.
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PMID:Interactions of orthopaedic metals with an immortalized rat osteoblast cell line. 880 83

Particulate wear debris can induce the release of bone-resorbing cytokines from cultured macrophages and fibroblasts in vitro, and these mediators are believed to be the cause of the periprosthetic bone resorption which leads to aseptic loosening in vivo. Much less is known about the effects of particulate debris on the growth and metabolism of osteoblastic cells. We exposed two human osteoblast-like cell lines (SaOS-2 and MG-63) to particulate cobalt, chromium and cobalt-chromium alloy at concentrations of 0, 0.01, 0.1 and 1.0 mg/ml. Cobalt was toxic to both cell lines and inhibited the production of type-I collagen, osteocalcin and alkaline phosphatase. Chromium and cobalt-chromium were well tolerated by both cell lines, producing no cytotoxicity and no inhibition of type-I collagen synthesis. At the highest concentration tested (1.0 mg/ml), however, chromium inhibited alkaline phosphatase activity, and both chromium and cobalt-chromium alloy inhibited osteocalcin expression. Our results clearly show that particulate metal debris can modulate the growth and metabolism of osteoblastic cells in vitro. Reduced osteoblastic activity at the bone-implant interface may be an important mechanism by which particulate wear debris influences the pathogenesis of aseptic loosening in vivo.
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PMID:The effects of particulate cobalt, chromium and cobalt-chromium alloy on human osteoblast-like cells in vitro. 976 14

Incubation of primary cultures of rat hepatocytes with K2CR2O7 and deferoxamine (DFO), an iron chelator, resulted in a marked decrease in cellular levels of DNA single-strand breaks caused by K2Cr2O7. Cellular treatment with DFO also suppressed both dichromate-induced cytotoxicity--evaluated by the leakage of lactate dehydrogenase, and lipid peroxidation--as monitored by malondialdehyde formation. In addition, treatment with DFO attenuated the suppression of the levels of vitamin E and C as well as the inhibition of alkaline phosphatase and glutathione peroxidase activity attributed to K2Cr2O7. However, DFO had no influence on the cellular level of glutathione or the activity of glutathione reductase and superoxide dismutase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of chromium were not affected by DFO. These results indicate that DFO protects cells from chromium (VI)-induced DNA strand breaks, cytotoxicity, lipid peroxidation, vitamin E and C depression, and glutathione peroxidase inhibition The role of antioxidants in chromium (VI)-induced cytotoxicity, DNA breaks, and lipid peroxidation is discussed.
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PMID:Protective effect of deferoxamine on chromium (VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes. 919 15

Hepatotoxic effects of chromium have been studied on the liver function enzymes of male New Zealand white rabbits, Oryctolagus cuniculus, with and without pretreatment with phenobarbitone (PB) and promethazine (PM). The total body weight was decreased under all experimental conditions. After PB administration (5 mg/kg body wt/day for 5 days), the serum glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), lactate dehydrogenase (LDH), and isocitrate dehydrogenase (ICDH) activities decreased 21%, 65%, 25%, and 37%, respectively, whereas the alkaline phosphatase (AP) activity increased 70%. After PM treatment (5 mg/kg body wt/day for 5 days) the serum GPT was inhibited 73%, whereas LDH activity was increased 37%. The hepatic GPT and AP activities decreased after PB (52% and 31%, respectively), and PM (48% and 44%, respectively) treatments, whereas the activities of LDH and ICDH increased (after PB: 817% and 109%, respectively, and after PM: 136% and 44%, respectively). Potassium dichromate, administered at a dose of 8 mg/kg body wt/day for 5 days, decreased serum GOT (44%), GPT (61%), LDH (63%), and AP (44%) activities. The hepatic GOT, GPT and AP activities were likewise decreased (86%, 51%, and 46%, respectively), whereas hepatic LDH and ICDH activities increased 667% and 193%, respectively. When administered to PB-pretreated animals, the serum GOT and AP activities were decreased (50% and 68%), whereas ICDH was increased (29%). The hepatic GOT, LDH, and ICDH activities increased 79%, 221%, and 130%, respectively. In the PM-pretreated animals, the chromium treatment inhibited the activities of serum GOT (48%), GPT (44%), and LDH (43%). The hepatic GPT, LDH, and ICDH activities increased 90%, 133%, and 52%, respectively.
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PMID:Sublethal effects of hexavalent chromium on the body growth rate and liver function enzymes of phenobarbitone-pretreated and promethazine-pretreated rabbits. 925 33

Pretreatment of primary cultures of rat hepatocytes with sodium diethyldithiocarbamate (DDTC) for 15 min prior to exposure to K2Cr2O7 resulted in a marked decrease in dichromate-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, and in lipid peroxidation, as monitored by malondialdehyde formation. In addition, pretreatment with DDTC attenuated the suppression of the level of vitamin E attributed to K2Cr2O7. However, DDTC pretreatment had no effect on the cellular levels of glutathione or vitamin C or on the activity of the glutathione reductase, glutathione peroxidase, superoxide dismutase or alkaline phosphatase suppressed by dichromate. Under the same experimental conditions, cellular uptake or distribution of chromium was not affected by DDTC. These results indicate that the protective effect of DDTC on chromium (VI)-induced cytotoxicity as well as lipid peroxidation may be associated with the level of nonenzymatic antioxidants such as vitamin E.
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PMID:Protective effect of diethyldithiocarbamate pretreatment on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat hepatocytes. 949 63


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