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)

Incubation of primary cultures of rat hepatocytes with K2Cr2O7 plus the pineal hormone melatonin resulted in a marked decrease in cellular levels of DNA single-strand breaks caused by K2Cr2O7. Cellular treatment with melatonin also suppressed both dichromate-induced cytotoxicity, as evaluated by the leakage of lactate dehydrogenase, and lipid peroxidation, as monitored by malondialdehyde formation. In addition, treatment with melatonin attenuated the suppression of the levels of vitamins E and C as well as the inhibition of catalase activity attributed to K2Cr2O7. However, melatonin had no influence on cellular level of glutathione and the activity of glutathione reductase, glutathione peroxidase, superoxide dismutase, and alkaline phosphatase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of Cr were not affected by melatonin. Electron spin resonance (ESR) studies showed that melatonin did not affect the formation of Cr(V) complexes in the reaction of K2Cr2O7 with reduced glutathione; however, melatonin caused a 25% decrease in the levels of Cr(V)-related hydroxyl radicals in vitro. These results indicate that melatonin protects cells from Cr(VI)-induced DNA strand breaks, cytotoxicity, and lipid peroxidation, possibly through its ability to increase cellular levels of vitamins E and C as well as catalase activity and/or to directly scavenge toxic hydroxyl radicals in cells.
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PMID:Potent protective effect of melatonin on chromium(VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes. 919 22

The protective mechanisms operating in the gastrointestinal (GI) tract to counteract the potential oxidizing effects of excess free iron, was tested in rats fed with excess iron. The activities of some antioxidant enzymes, the levels of GSH and the extent of lipid peroxidation at the site of iron absorption were measured. Based on the amount of thiobarbituric acid reactive substances (TBARS) produced, it could be deduced that the duodenal segment of GI tract is resistant to iron mediated lipid peroxidation. The duodenal function as judged from the activities of marker enzymes, namely, alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase was normal. There was depletion of GSH possibly due to the increased activities of Cu, Zn SOD and catalase. However, the activity of Gpx was decreased in the Fe fed group. It was also observed that the ratios of SOD/Gpx and Cat/Gpx had significantly increased in the treated group whereas SOD/Cat remained constant suggesting that antioxidative enzymes play a key role in rendering the intestinal mucosal cells resistant to iron induced oxidative damage in rats.
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PMID:Protective effects of antioxidant enzymes and GSH in vivo on iron mediated lipid peroxidation in gastrointestinal tract of rat. 949 52

Cadmium induced lipid peroxidation (LPO) and the activity of antioxidant enzymes after the administration of a single dose of CdCl2 (0.4 mg kg-1 body wt, i.p.) was studied in rat erythrocytes. Cd intoxication increased erythrocyte LPO along with a decrease in superoxide dismutase (SOD) up to three days of Cd treatment. The decrease in erythrocyte catalase (CAT) activity was marked within 9 h of Cd intoxication. After three days of Cd treatment, LPO decreased towards normal, along with an increase in erythrocyte SOC and CAT activity. Blood glutathione (GSH) decreased significantly within 24 h of Cd treatment, followed by an increase towards normal. Erythrocyte glutathione S-transferase (GST) activity increased up to 10 days of Cd intoxication, probably in an attempt to reduce Cd toxicity. Serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (SALP) and serum bilirubin increased up to 10 days of Cd intoxication. Blood urea increased significantly up to three days, followed by a decrease towards normal. The results show that Cd induced LPO was associated with a decrease in antioxidant enzymes and GSH in erythrocytes; as these antioxidants increase in erythrocytes with recovery from Cd intoxication, the Cd induced LPO reversed towards normal. The increase in the SGPT, SALP and serum bilirubin correlated with LPO. The results suggest that Cd intoxication induces oxidative stress and alters the antioxidant system, resulting in oxidative damage to rat erythrocytes.
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PMID:Lipid peroxidative damage on cadmium exposure and alterations in antioxidant system in rat erythrocytes: a study with relation to time. 954 68

A Gram-negative, motile bacterium with bipolar sheathed flagella (one at each end) was isolated from the stomach of house musk shrews (Suncus murinus) with chronic gastritis. The isolates grew at 37 degrees C under microaerophilic conditions, but not under aerobic conditions; rapidly hydrolyzed urea; were catalase, oxidase, alkaline phosphatase, and arginine aminopeptidase positive; reduced nitrate to nitrite; and were resistant to cephalothin and nalidixic acid, but sensitive to tetracycline, erythromycin, and chloramphenicol. This bacterium was found on gastric epithelial cells by electron microscopy. In addition, a coccoid form of the bacteria was found in vacuoles formed in the epithelial cells of some of the house musk shrews tested. These results, including 16S rRNA gene sequence analysis, strongly suggested that this bacterium should be classified as a novel Helicobacter species. It is proposed that this bacterium should be called "Helicobacter suncus."
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PMID:Isolation and characterization of Helicobacter species from the stomach of the house musk shrew (Suncus murinus) with chronic gastritis. 962 89

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease of unknown aetiology. Recent studies have shown that genetic factors and both cellular and humoral immunological abnormalities are important in the pathogenesis of PSC. The most prominent autoantibodies in PSC are anti-neutrophil cytoplasmic antibodies (ANCA). The autoepitopes of ANCA in PSC are not well defined. The aim of this study was to identify corresponding ANCA autoantigens in patients with PSC. A biochemical approach with enrichment and partial purification of soluble neutrophil proteins, detection of autoantibodies by Western blot and partial amino acid sequencing were used. Two new autoantigen/autoantibody systems in patients with PSC were detected: catalase and alpha-enolase. The presence of catalase autoantibodies in 9/15 (60%) and alpha-enolase autoantibodies in 4/15 (27%) was confirmed by ELISA and Western blot. Furthermore, we showed immunoreactions of PSC sera with human biliary epithelial cells, showed the reduction of fluorescence in anti-catalase absorption experiments and observed partial co-localization of anti-catalase antibodies and PSC sera in double-staining experiments on biliary epithelial cells. The anti-catalase antibody-positive PSC patients had a more severe course of disease with a significantly higher alkaline phosphatase compared with the anti-catalase-negative PSC patients (P < 0.06). All ulcerative colitis control sera were anti-catalase antibody-negative. The identified antigens catalase and alpha-enolase can partly explain the ANCA fluorescence on ethanol-fixed and formaldehyde-fixed granulocytes in patients with PSC. Catalase is an important anti-oxidant enzyme and prevents cell damage from highly reactive oxygen-derived free radicals. Catalase autoantibodies might play a pathogenic role in patients with PSC. Our findings support the hypothesis that oxidative stress is one of the pathogenic mechanisms in patients with PSC.
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PMID:Identification and characterization of autoantibodies against catalase and alpha-enolase in patients with primary sclerosing cholangitis. 964 23

The lower levels of serum alkaline phosphatase (AP) activity found in patients with diabetes mellitus apparently originate from the selective disappearance or decrease in bone AP activity in the circulation. Hence, we investigated in vitro the effect of glycation on the activities of five AP isozymes. Aseptic incubation with 25 mmol/L of D-glucose and APs rapidly reduced bone and placental AP activities before those of liver, kidney and intestinal enzymes. The resulting bone and placental AP molecules were clearly glycated, according to the result of aminophenylboronic acid affinity chromatography. Furthermore, Western blotting analysis revealed that the placental AP molecule was fragmented, and its partial cleavage took place at Ala154 on the AP molecule. Since glycation of serum proteins causes the generation of reactive oxygen species, the effects of reactive oxygen species on placental AP activity were assayed, and the results indicated that hydroxyl radicals might be a major factor for the specific inactivation of AP activities. The reduction in AP activity by incubation with glucose in vitro was reversed by the further addition of catalase. Furthermore, ferrous ion with hydrogen peroxide, which generates hydroxyl radicals, had an inhibitory effect on AP activities. These findings suggest that the reduced AP activity in diabetic patients might result from partial cleavage of the bone AP molecule by reactive oxygen species induced by glycation.
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PMID:Partial breakdown of glycated alkaline phosphatases mediated by reactive oxygen species. 970 41

Ultrastructural studies of rare and small cellular lesions in pathologically altered tissue are difficult to perform by applying conventional electron microscopic preparation. The search for lesions, often consisting of only a few cells in randomly obtained small specimen blocks, is time consuming and often without success. The methodological requirements for comparative enzyme cytochemical and morphological studies, i.e., preservation of both enzyme activity and ultrastructure, are divergent. By processing large native cryostat sections for electron microscopy, small preneoplastic focal lesions were successfully targeted in liver and kidney. Glucose-6-phosphatase, alkaline phosphatase, acid phosphatase, catalase, and cytochrome c oxidase activities were distinctly localized to endoplasmic reticulum, canalicular membrane, lysosomes, peroxisomes, and mitochondria, respectively, in the morphologically altered cells. Fixation of serial cryostat sections and enzyme reactions were both carried out through a semipermeable membrane except those for cytochrome c oxidase, which was demonstrated after fixation through the membrane by floating the section in incubation medium containing cytochrome c. Thereafter, the sections were flat embedded and polymerized between epoxy resin disks and aluminum dishes fitting exactly together. The objects of interest were identified in the light microscope, cut out, and reembedded in reversed gelatine capsules. By using this technique an ultrastructural preservation was achieved similar to that seen after immersion fixation. The enzyme activities were clearly localized without diffusion of the reaction product or unspecific deposits. The procedure permits precise targeting and complex studies of rare and small lesions, and opens new perspectives for the use of cryo-preserved tissue.
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PMID:A new method for flat-embedding large native cryostat sections for targeting small preneoplastic lesions in comparative ultrastructural and ultracytochemical investigations. 974 66

Severe iron deficiency results in complex systemic disorders e.g., including metabolism of energy and minerals. To investigate whether also moderate iron depletion may alter the activities of citric cycle enzymes and the cytochrome oxidase, the trace element status, and serum enzymes indicative of cell damage, this experiment was carried out with rats supplied with sub-optimal iron (9, 13 and 18 mg iron per kg diet) over a total of 5 weeks. The study included 3 pair-fed groups and an ad libitum group, fed with 50 mg iron/kg diet. All iron-restricted rats were classified as iron-deficient on the basis of reduced iron concentrations in body and iron-depending blood parameters. Body weight gain and catalase activity in kidney were lowered in rats receiving the lowest dietary iron level, exclusively. Rats fed 9 and 13 mg iron per kg diet had nearly 6- and 3-fold, respectively higher platelet counts in blood than their corresponding pair-fed controls. The activities of transaminases ASAT and ALAT, alkaline phosphatase, glutamate dehydrogenase and lactate dehydrogenase in serum which are indicative of cell damage were also markedly influenced by moderate dietary iron restriction, in which the enzyme levels in serum increased with intensifying iron depletion. Although, moderate iron restriction to young male rats was associated with marked alterations in iron status and serum enzymes, the activities of tricarboxylic acid cycle enzymes including malic dehydrogenase, fumarase, and isocitric dehydrogenase as well as cytochrome oxidase in liver remained largely unaffected. Only hepatic aconitase showed a somewhat reduction with iron depletion. Moreover, iron restriction was also accompanied with an accumulation of copper in liver which was significant for rats fed 9 and 13 mg iron per kg diet, whereas zinc status remained completely unaffected by moderate iron deficiency. It can be concluded, that a short-term moderate iron deficiency with ranging hemoglobin concentrations from 66 and 121 g/L, was accompanied with altered platelet counts, serum enzyme activities indicative of cell damage, and hepatic copper concentrations, but the activities of the tricarboxylic acid cycle enzymes and cytochrome oxidase in liver remained largely unaffected.
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PMID:Effect of different degrees of moderate iron deficiency on the activities of tricarboxylic acid cycle enzymes, and the cytochrome oxidase, and the iron, copper, and zinc concentrations in rat tissues. 980 Mar 17

Redox-active forms of iron are known to catalyze free radical mediated peroxidative reactions. There is scanty information on such effects at the sites of iron absorption. This was tested in iron-deficient WKY female rats supplemented for 15 days with FeSO4 equivalent to 8 mg of iron (D+) and compared with iron deficient (D) and iron adequate (C) rats. The levels of intestinal MDA and protein carbonyls and the activities of various antioxidant enzymes were estimated. As markers of functional integrity, the activities of alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were evaluated. In addition, we measured the concentrations of ferritin, transferrin, and ceruloplasmin levels in serum and in intestinal mucosa. It was observed that correction of iron deficiency resulted in significant increase in MDA and protein carbonyl formation. Activities of both alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were significantly decreased in D+ compared to C. The increase in catalase and decrease in Gpx was found to be sensitive to iron administration. Neither iron deficiency nor its correction had any effect on the activity of SOD and GSH levels. Iron supplementation has resulted in decreased mobilization of stored iron as reflected by increased mucosal ferritin level and decreased serum ceruloplasmin ferroxidase activity contributing to greater peroxidative stress in the intestine. These results suggest that iron-deficient intestine of rat is more susceptible to iron-mediated peroxidative damage and functional impairment during correction of deficiency with iron.
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PMID:Iron-deficient intestine is more susceptible to peroxidative damage during iron supplementation in rats. 980 Oct 65

Vascular invasion of calcified cartilage, during endochondral ossification, is initiated and sustained by invasive cells (endothelial cells and macrophages) which degrade the tissue by releasing lytic enzymes. Concurrently, reactive oxygen species (ROS) are also released by these cells and we hypothesize that ROS also contribute to the degradation of the tissue. As a preliminary approach to this problem, the antioxidant activities and the effect of ROS on hypertrophic cartilage and chondrocytes (HCs) were investigated. Compared to resting or articular chondrocytes, HCs exhibited higher catalase but lower SOD specific activities and lower PHGPx concentration, thus revealing a defence activity specific against H2O2. Moreover, dose-dependent depletion of ATP occurred after few minutes of exposure to ROS, and a long-term treatment (16 h incubation with ROS) promoted the release of LDH activity and a significant variation of the poly- to mono-unsaturated fatty acid ratio. Finally, the incubation of HCs with low ROS doses induced the release of sedimentable alkaline phosphatase activity (matrix vesicles). How the obtained results fit the in vivo occurring events is discussed.
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PMID:Sensitivity of chondrocytes of growing cartilage to reactive oxygen species. 981 64


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