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)

A new approach is described for the enzymatic digestion of DNA yielding oligonucleotides ranging from dinucleoside monophosphates to octanucleoside heptaphosphates. DNA was digested by means of the benzon nuclease, an unspecific nuclease, and alkaline phosphatase to remove the terminal phosphate. The mixture of oligonucleotides was separated using capillary-zone electrophoresis with a buffer system, yielding a rather strong electro-osmotic flow. The oligomers are separated into groups with nucleotides of the same chain length. The separation capillary was used as the innermost capillary of an electrospray spraying system. Negative molecular ions of the nucleotides were recorded using a home-built interface and ion source for a sector-field mass spectrometer. This approach allows the facile detection of DNA modifications since they lead not only to differences in mass, but also can possess altered electrophoretic mobility. For modifying reactions which exhibit sequence specificity, the information is retained in the oligomers. Thus, reactions of DNA with electrophiles can be evaluated at different levels, since in longer chains, even complex sequence specificity may be apparent. Results from calf thymus DNA digests and preliminary experiments with DNA adducts with styrene oxide are discussed.
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PMID:A new mass spectrometric approach to detect modifications in DNA. 769 99

Reaction products of calf thymus DNA with (1R,2S,3S)-3-methylcyclohexanediamineplatinum (abbreviated as Pt(RSS-dach)Cl2) were investigated by enzymatic degradation of the platinated DNA and subsequent HPLC analysis. Five platinated adducts involving d(GpG), d(ApG) and (dG)2 residues were identified by HPLC after complete digestion using deoxyribonuclease I, nuclease P1, and alkaline phosphatase. The adducts with d(GpG) and d(ApG) consisted of two geometrical isomers, because Pt(RSS-dach)Cl2 lacks a C2 symmetry element. The d(GpG) and d(ApG) adducts were intrastrand compounds crosslinked between the N7 atoms of the adjacent purine bases. The two d(GpG) adducts were most abundant and comprised more than 65% of all the platinated adducts. The relative ratio of the two d(GpG) isomers was 3:2 for reaction with DNA, whereas the ratio was 1:1 for reaction with a single stranded oligonucleotide. The detailed structure of the two d(GpG) adducts is also described based on NMR spectroscopic data.
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PMID:Reaction of (1R,2S,3S)-3-methylcyclohexanediamineplatinum(II) with DNA: isolation and characterization of the platinum-nucleotide adducts by means of HPLC and NMR spectroscopy. 772 26

Thrombosis of the left subclavian vein occurred in a 44-year-old man. It was found to be caused by an atypical thymus carcinoid of the anterior mediastinum without carcinoid syndrome. Primary resection was not possible, but it was removed after three cycles of neoadjuvant chemotherapy with doxorubicin, cisplatin, vincristine and cyclophosphamide. Increased concentrations of alkaline phosphatase and parathormone were then noted. Subtotal parathyroidectomy revealed hyperplastic parathyroids. A gastrinoma was suspected from a history of peptic ulcer for many years which had persisted despite a Billroth II gastric resection 10 years ago. Serum gastrin, analysis of gastric secretion and a secretin-stimulating test confirmed the diagnosis. Recurrent episodes of weakness and syncope, in the presence of low blood sugar levels and a positive C-peptide suppression test, were interpreted as due to an insulinoma. There was no evidence of increased hypophyseal or adrenal function. Finally, in the absence of a family history, multiple endocrine neoplasia type 1 (MEN 1) was diagnosed with co-existing primary hyperparathyroidism, gastrinoma, insulinoma and thymus carcinoid. Somatostatin-receptor scintigraphy provided localization of the MEN 1 with enrichment in the thorax and abdomen.
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PMID:[Thymus carcinoid in multiple endocrine neoplasms type I]. 790 23

The systemic toxicity of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) following subchronic dietary exposure was investigated in Sprague-Dawley rats. PCB 126 was administered to rats of both sexes at concentrations of 0.1, 1.0, 10, or 100 ppb in their diet for 13 weeks. Another group of rats received a loading dose of 5 micrograms PCB/kg body wt at the start of the feeding period followed by exposure to 10 ppb PCB diet for the same period of time as the other groups. Growth suppression and decreased food consumption were observed in the highest dose groups of both sexes. Increased organ/body weight ratios for the liver occurred in the 10 and 100 ppb groups of both sexes. Rats of both sexes exposed to the highest dose of the PCB also exhibited increased relative kidney, spleen, and brain weights. Hematological and most serum biochemical changes were confined to the 100 ppb groups. These included elevated alkaline phosphatase, bilirubin, cholesterol, and aspartate aminotransferase, and decreased serum glucose, hemoglobin, erythrocytes, hematocrit, and platelets. A dose-dependent increase in liver ethoxyresorufin-O-deethylase activity was observed in rats of both sexes starting at 0.1 ppb. A dose-dependent increase in liver uroporphyrin levels was observed in both sexes and significant changes occurred in the female rats at 1.0 ppb and higher dose groups. Decreased liver vitamin A was observed in the 10 ppb group and higher in both sexes. Kidney vitamin A was elevated in the 100 ppb group. No statistically significant changes were noted in concentrations of brain biogenic amines. PCB 126 residues were 10-fold higher in liver than in fat. Treatment-related histopathological changes were observed in the thymus, thyroid, bone marrow, and liver of rats exposed to the 10 ppb diet, but increased frequency of mild changes was observed in most of these tissues at the 1.0 ppb level. Based on the above data, the no adverse effect level was judged to be 0.1 ppb in the diet or 0.01 micrograms/kg body wt/day.
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PMID:Subchronic toxicity of 3,3',4,4',5-pentachlorobiphenyl in the rat. I. Clinical, biochemical, hematological, and histopathological changes. 805 Jun 40

This study was undertaken to investigate a number of immune parameters which may be compromised with exposure to morphine sulfate. Mice were implanted subcutaneously with 8-, 25-, or 75-mg morphine sulfate pellets. Placebo pellets of identical makeup to the 75-mg morphine pellet (without morphine of course) were used as a control. Twenty-four hours after implantation of a 75-mg morphine pellet, blood levels reached a peak of 1610 ng/ml. Corticosterone increased in parallel with morphine and reached a peak level of 966 ng/ml 24 hr after implantation. The dose response of morphine to increase corticosterone, however, was flat. The weight of the lymphoid organs, spleen and thymus, and the liver were significantly reduced in the morphine-treated groups. Morphine treatment was associated with an increase in serum albumin, SGPT, BUN, and alkaline phosphatase indicative of hepatic damage. In contrast to increased serum proteins, the C3 component of complement was reduced in a dose-dependent manner. Leukocyte number in the peripheral blood was significantly reduced, while erythrocyte number and hematocrit were both increased. The number of B cells and T cells was decreased in morphine-treated animals. However, the percentage of T cells relative to B cells was increased. The primary IgM antibody response to the T-dependent antigen, sheep red blood cells, was decreased. Natural killer cell activity was reduced in response to morphine, as was the phagocytic capacity of Kupffer cells. Host-resistance models of Listeria monocytogenes or Streptococcus pneumoniae showed an increased resistance following administration of morphine. This increased host resistance, however, was not due to an increase in antimicrobial action of sera obtained from mice treated with morphine. The majority of morphine's effects on the immune system exhibited a flat dose response, suggesting that these effects may be mediated secondarily through corticosterone.
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PMID:Immunotoxicological profile of morphine sulfate in B6C3F1 female mice. 805

Five Holstein Friesian calves varying in age from 7 to 9 weeks old, were suspected of suffering from an inherited granulocytopathy known as bovine leucocyte adhesion deficiency (BLAD). Four of them were examined clinically and at necropsy. The most significant clinical findings were fever, depression, weakness, emaciation, diarrhoea, pseudomembranous gingivitis, loose teeth, respiratory infection and occult blood in the faeces. Significant clinicopathological findings were marked leucocytosis, mainly due to a neutrophilia, hypoalbuminemia, hypogammaglobulinemia, increased alpha- and beta-globulins, elevated alkaline phosphatase enzyme activity, hypoglycaemia, and decreased blood urea concentrations. The necropsy revealed emaciated carcasses, granulomatous to necrotising gingivitis, pseudomembranous to necrotising enteritis with perforations, bronchopneumonia, splenic atrophy, and hypoplasia of the thymus. Histopathological examination supported the macroscopic findings.
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PMID:[Suspected inherited granulocytopathy in four Holstein Friesian calves]. 817 99

2,3,7,8-Tetrabromodibenzo-p-dioxin (2,3,7,8-TBDD) was administered daily to male and female rats for 91 days by gavage. Ten male and 10 female rats per group received 0.01, 0.1, 1, 3, or 10 micrograms 2,3,7,8-TBDD/kg body weight per dose per day, solubilised in arachis oil. At 1 microgram/kg per day and above, body weight gain was dose-dependently reduced by treatment. Animals in the 3 and 10 micrograms/kg dose groups showed symptoms of wasting syndrome. Fifty percent of the animals in the 3 micrograms/kg dose-group died and all animals of the highest dose (10 micrograms/kg) died or had to be killed in extremis. Hematological investigations indicated changes--mainly in the 1 and 3 micrograms/kg dose-groups--in hemoglobin content, packed cell volume and number of thrombocytes. The prothrombin-time was markedly prolonged after 3 micrograms/kg in week 13. Clinical chemistry performed at the end of treatment revealed an increase in plasma alkaline phosphatase (APh), aspartate aminotransferase, ASAT and alanine aminotransferase, ALAT (females only) in the highest surviving dose-group (3 micrograms/kg). Marginal changes of APh and ASAT were seen in rats in the 1 microgram/kg dose-group. In the same animals, total bilirubin was elevated. Triglycerides were reduced mainly at 1 and 3 micrograms/kg. Serum thyroxin was reduced, beginning with a marginal change at 0.1 micrograms/kg, triiodothyronine was elevated, starting with a dose of 1 microgram/kg. Thymus weights were reduced in rats of the 1, 3 and 10 micrograms/kg dose-groups. Histopathological analysis showed atrophy of the lymphatic tissue in thymus and spleen. Investigations of the liver indicated peliosis hepatis after treatment with 3 or 10 micrograms/kg. Activities of microsomal enzymes (ethoxyresorufin O-deethylase, ethoxycoumarin O-deethylase, aryl hydrocarbon hydroxylase, UDP-glucuronyltransferase) investigated in liver, lung and kidney were dose-dependently elevated after 13 weeks of treatment. At a dose of 3.0 micrograms/kg, activities were below those of the dose 1.0 microgram/kg, probably due to liver toxicity. The induction ratio of kidney was generally higher than in liver and lung. No signs of treatment-related toxicity were observed in the 0.01 and 0.1 micrograms/kg groups after the subchronic administration of 2,3,7,8-TBDD by gavage.
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PMID:Subchronic toxicity of 2,3,7,8-tetrabromodibenzo-p-dioxin in rats. 824 44

To investigate the relationship of the hematopoietic system to the loss of bone due to ovarian hormone deficiency, we examined the effects of ovariectomy and estrogen administration on the thymus, spleen and the bone marrow, and on the proliferation of marrow progenitors of osteoclasts. We also assessed the effects of daily administration of interleukin-1 receptor antagonist (IL-1ra) on bone loss due to ovarian hormone deficiency. Ovariectomy resulted in decreased cancellous bone volume, increased trabecular osteoblast and osteoclast numbers, and increased serum alkaline phosphatase levels that were prevented by 17 beta-estradiol treatment. Thymus weight, spleen weight, thymus and spleen lymphocytes, and bone marrow monocytes and lymphocytes also increased significantly following ovariectomy, and the increases were suppressed by 17 beta-estradiol. Ovariectomy, in addition, caused a 4-fold increase in the number of tartrate resistant acid phosphatase (TRAP)-positive multinucleated cells formed in cultures of marrow cells and the increase was partially inhibited by 17 beta-estradiol. IL-1ra administration did not prevent the bone loss due to ovariectomy. Our findings indicate that ovariectomy-induced bone loss in the rat is accompanied by marked changes in the hematopoietic system, and that these changes are modulated by estrogen administration. In spite of the negative finding with IL-1ra, the nature of the involvement of the hematopoietic system in the pathogenesis of bone loss due to ovarian hormone deficiency merits continued exploration.
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PMID:Ovariectomy-induced bone loss and the hematopoietic system. 830 79

Groups of rats were treated with graded doses of zineb or aldicarb solely or in association with copper sulphate for nine consecutive weeks. Body weight gain was retarded and thymus gland weight was decreased in all treated groups. A pronounced synergism between copper sulphate and zineb was noticed in lowering the weights of thymus, testes, and adrenal glands. Various degrees of reduction in hemoglobin concentration, red blood cells and platelet counts occurred after treatment with the above-mentioned agrochemical regimen. Copper sulphate synergised the elevation of serum alkaline phosphatase (AP) activity, and bilirubin concentration as well the reduction of hemoglobin concentration by zineb. Alanine aminotransferase (ALT) activity was significantly increased, while cholinesterase (ChE) activity was decreased in all treated groups. Serum triglycerides (TGs) were lowered in rats treated with medium or high doses of zineb or aldicarb.
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PMID:Toxic interactions between copper sulphate and some organic agrochemicals. 831 Apr 52

Human germ cell alkaline phosphatase (GCAP) is developmentally expressed in primordial germ cells and in trace amounts in the testis and thymus. The equivalent mouse isozyme, embryonic alkaline phosphatase (EAP), is similarly expressed in the testis and thymus but also from the 2-cell to blastocyst stage of preimplantation development. EAP has been found to be transiently expressed in M-phase spermatogenic cells in the mouse testis. These alkaline phosphatase isozymes serve as markers of germ cell differentiation and in the management of germ cell tumors. GCAP is expressed in carcinoma-in-situ and seminoma where serum GCAP levels are often elevated and may provide clinically useful information. However, GCAP is a polymorphic enzyme, and monoclonal antibodies to be used in the clinical evaluation of tumor tissues or fluids should be carefully evaluated for their ability to detect all allelic variants of GCAP.
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PMID:Developmental expression of alkaline phosphatase genes; reexpression in germ cell tumours and in vitro immortalized germ cells. 838 57


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