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)

Imbalance of zinc and copper status has been hypothesized in human hypertension. A case-control study was carried out to elucidate the possible relationship between zinc and copper status and essential hypertension. Thirty-one subjects affected by mild stable hypertension, pharmacologically untreated, were investigated together with 31 normotensive controls individually matched for sex, age, and smoking habits. Zinc and copper in serum and urine wee measured, and serum activities of alkaline phosphatase (AP), lactic dehydrogenase (LDH), copper-zinc superoxide dismutase (Cu-Zn SOD), lysyl oxidase (LOX), and monoamine oxidase (MAO) were evaluated. No significant difference in serum and urine zinc and copper content as far as in serum activity of zinc (AP and LDH) or copper (Cu-Zn SOD, LOX, and MAO)-dependent enzymes was found between hypertensives and normotensives. Positive relationships were found in normotensives between serum and urine levels of zinc (r = 0.577; p = 0.001) and copper (r = 0.394; p = 0.028), and between serum copper and Cu-Zn SOD (r = 0.534; p = 0.002). In normotensives, diastolic blood pressure and serum zinc were positively related (r = 0.370; p = 0.041). In hypertensives, inverse correlations were observed between diastolic blood pressure and AP (r = -0.498; p = 0.004) and Cu-Zn SOD (r = 0.452; p = 0.011), and between systolic blood pressure and LOX (r = -0.385; p = 0.033). Diastolic blood pressure was related to LDH inversely in hypertensives (r = -0.357; p = 0.049) and positively in normotensives (r = 0.457; p = 0.010). In normotensives, diastolic blood pressure was inversely related with MAO (r = -0.360; p = 0.046). These findings support the hypothesis that an imbalance of zinc and copper status might be involved in human hypertension.
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PMID:Zinc, copper, and zinc- or copper-dependent enzymes in human hypertension. 856 90

Superoxide radical (O2-) is a free radical that may be involved in various toxic processes. Cu-Zn superoxide dismutase catalyzes the dismutation of the superoxide free radical and protects cells from oxidative damage. A rat bioassay validated for the identification of the toxic effects of azomethine H revealed increased serum activities of amylase, alanine transaminase, and alkaline phosphatase. The lipoperoxide and bilirubin concentrations were also increased in animals that received azomethine H (1 g/kg) from ascorbic or hydrochloric acid solutions. Azomethine H increased Cu-Zn superoxide dismutase activity. This elevation of Cu-Zn superoxide dismutase activity was highest on the 7th day and was at levels comparable with those of control rats from day 60 onwards. Superoxide is an important intermediate in the action and toxicity of azomethine H.
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PMID:Reactive oxygen generation by azomethine H: a new antimalarial drug. 856 88

Terbium (Tb) is a rare earth metal that finds use in several emerging technologies. However, little is known about the biological effects of Tb. Thus, in this study the pulmonary toxicity of systemic Tb in mice was investigated. Mice were treated intravenously with a single dose of 20 or 200 mumol Tb/kg, as TbCly and killed at 3, 6, 12, 24, 48, or 72 h later. Administration of Tb at a dose of 200 mumol/kg increased pulmonary weight, lipid peroxidation, and protein content but decreased pulmonary glutathione content. Pulmonary gamma-glutamyl transpeptidase (gamma-GTP) activity was increased after Tb administration at a dose of 200 mumol/kg. Pulmonary alkaline phosphatase (ALP) activity was also increased after Tb administration at a dose of 200 mumol/kg. Investigation of the defense system against oxidative damage in the lung showed that superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were all decreased after Tb administration at the higher dose. The concentrations of Tb, Ca, and P in lung was increased by the dose of 200 mumol/kg. These results suggest that pulmonary lipid peroxidation may be an early and sensitive consequence of Tb exposure and that SOD, CAT, and GSH-Px might be considered as potential modulators of Tb-induced lipid peroxidation. The mechanisms involved in Tb-induced pulmonary lipid peroxidation deserve further study.
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PMID:Pulmonary toxicity of systemic terbium chloride in mice. 863 60

To evaluate the specificity of some functional indices in assessment of body zinc nutrition status, we used experimental rat model to observe the effects of some factors, such as forced swimming, starvation, trauma and alcohol intoxication on zinc the status. Plasma zinc levels of rats significantly decreased after trauma increased after starvation. Liver zinc content showed a rising tendency in trauma and starvation rats. Activities of superoxide dismutase in red blood cells and alkaline phosphatase, mannosidase, 5'-nucleotidase in plasma of rats with alcohol intoxication declined significantly. Starvation led to decreased activities of alkaline phosphatase and angiotensin-converting enzyme, but increased activities of mannosidase. Trauma and forced swimming could cause increase of angiotensin-converting enzyme activity and decrease of 5'-nucleotidase activity, respectively. These results indicate that physiological and pathological effects should be excluded from of the above indices as plasma zinc index, in the assessment of body zinc nutrition status.
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PMID:[Effects of stress on indices for assessing zinc nutrition status]. 875 64

The adoption of cell culture models to screen putative neurotoxicants is recognized in view of the consequences of nerve damage by environmental chemicals. Developing cell culture models that mimic certain properties of the blood-brain barrier (BBB) would be especially useful in view of the barrier's strategic role in the neurotoxic process. The present study evaluates a kidney epithelial cell line for its functional and enzymatic resemblance to cerebral endothelial cells. Madin-Darby canine kidney (i.e., MDCK) cells display morphological (i.e., ultrastructurally defined tight junctions), enzymatic (acetylcholinesterase, butyrylcholinesterase, gamma-glutamyl transpeptidase, superoxide dismutase, alkaline phosphatase, lactate dehydrogenase), and antigenic cell markers (i.e., Factor VIII), also found in cerebral endothelial cells. In addition, MDCK cells develop electrical resistance which is increased in response to conditioned media from astroglial cell lines (i.e., C6). These results suggest that the MDCK cell line might be useful for identifying neurotoxic chemicals that affect BBB integrity through similar endpoints.
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PMID:Characterization of the MDCK cell line for screening neurotoxicants. 885 39

The effect of administration of superoxide dismutase (SOD) on gentamicin nephrotoxicity was examined in rats. SOD was administered at a dose of 2000 i.u/kg or 8000 i.u/kg for 10 consecutive days, and nephrotoxicity was induced by daily i.m. injections of gentamicin at a dose of 80 mg/kg during the last 6 days of the experimental period. Gentamicin induced significant increases in plasma creatinine and urea and protein urinary concentrations, and significant decreases in creatinine clearance and kidney cortical alkaline phosphatase activity and reduced glutathione (GSH) concentrations. The antibiotic also produced marked necrosis of the renal proximal tubules. SOD treatment (8000 i.u/kg) reversed most of these variables, indicating that it was effective in ameliorating gentamicin nephrotoxicity. However, at a dose of 2000 i.u./kg it was mostly ineffective.
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PMID:Effect of superoxide dismutase treatment on gentamicin nephrotoxicity in rats. 891 55

A mouse embryo culture model was used to determine whether embryonic prostaglandin H synthase (PHS)-catalyzed bioactivation and resultant oxidative damage to embryonic protein and DNA may constitute a molecular mechanism mediating phenytoin and benzo[a]pyrene teratogenesis. Embryos were explanted from CD-1 mouse dams on gestational day 9.5 (vaginal plug = day 1) and incubated for either 4 h (biochemistry) or 24 h (embryotoxicity) at 37 degrees C in medium containing either phenytoin (20 micrograms/ml, 80 microM), benzo[a]pyrene (10 microM), or their respective vehicles. As previously observed with phenytoin (Mol. Pharmacol.48: 112-120, 1995), embryos incubated with benzo[a]pyrene showed decreases in anterior neuropore closure, turning, yolk sac diameter, and somite development (p < .05). Addition of the antioxidative enzyme superoxide dismutase (SOD) substantially enhanced embryonic SOD activity (p < .05) and completely inhibited benzo[a]pyrene embryotoxicity (p < .05). Substantial PHS was detected in day 9.5 embryos using SDS/PAGE, anti-PHS antibody, and alkaline phosphatase-conjugated donkey anti-goat IgG. Embryonic protein oxidation was detected by the reaction of 0.5 mM 2,4-dinitrophenylhydrazine with protein carbonyl groups. This method was first validated by using a known hydroxyl radical-generating system consisting of vanadyl sulfate and H2O2, with bovine serum albumin or embryonic protein as the target. Embryonic proteins were characterized by SDS/PAGE, anti-dinitrophenyl antisera, and peroxidase-labeled goat anti-donkey IgG. Using enhanced chemiluminescence, the number and content of oxidized protein bands detected between 25 and 200 kDa were substantially increased by both phenytoin and benzo[a]pyrene. Addition of the reducing agent dithiothreitol, or SOD or catalase, decreased protein oxidation in phenytoin-exposed embryos. Both phenytoin (Mol. Pharmacol.48: 112-120, 1995) and benzo[a]pyrene enhanced embryonic DNA oxidation, determined by the formation of 8-hydroxy-2'-deoxyguanosine, as measured by high-performance liquid chromatography (HPLC) (p < .05). Phenytoin also enhanced the oxidation of embryonic glutathione (GSH) to its GSSG disulfide, as measured by HPLC (p < .05). These results provide direct evidence that, in the absence of maternal or placental processes, embryonic PHS-catalyzed bioactivation and reactive oxygen species-mediated oxidation of embryonic protein, thiols, and DNA may constitute a molecular mechanism mediating phenytoin and benzo[a]pyrene teratogenesis.
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PMID:Evidence for embryonic prostaglandin H synthase-catalyzed bioactivation and reactive oxygen species-mediated oxidation of cellular macromolecules in phenytoin and benzo[a]pyrene teratogenesis. 901 24

Oxygen free radicals have been implicated as mediators of tissue injury in a variety of diseases. We investigated the role of oxidative injury and oxygen free radical scavengers in liver cell injury associated with obstructive jaundice in Wistar rats. Bile duct ligation for 4 or 7 days led to a decrease in both vitamin E and A in the plasma and liver of male Wistar rats, indicating the malabsorption of lipid-soluble vitamins. Serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase activities were increased in the bile-duct-ligated rats. Furthermore, marked increases in lipid peroxide and oxidized glutathione levels indicated cholestatic liver injury. The antioxidant defense system was impaired, as shown by decreases in reduced glutathione and in the activities of glutathione peroxidase (GSH-Px) and superoxide dismutase. Moreover, these high lipid peroxide levels and low levels of antioxidants correlated with the severity of jaundice. After releasing the bile duct ligation, levels of bilirubin, lipid peroxide and oxidized glutathione declined, while the levels of vitamin E and A, reduced glutathione, and the activities of GSH-Px increased, indicating an improvement in liver function. These findings suggest that lipid peroxidation is associated with the pathogenesis of liver damage in animals with bile duct ligation. Meanwhile, free oxygen radical scavengers are reduced in the bile-duct-ligated rats, thereby increasing the susceptibility of the liver to injury by oxygen-derived free radicals.
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PMID:Biochemical events associated with ligation of the common bile duct in Wistar rats. 903 77

In a group of patients with endometriosis and in a control group of healthy women, the polymorphism of the following systems were studied: ABO and RH blood-group systems; serum proteins haptoglobin (HP), transferrin (TF), vitamin D-transporting protein (GC), protease inhibitor (PI), and the third component of the complement (C3); serum enzymes-amylase of the loci 1 and 2 (AMY1 and AMY2), pseudocholinesterase (E2), and alkaline phosphatase (PP); erythrocytic enzymes-acid phosphatase (ACP1), phosphoglucomutase (PGM1), superoxide dismutase (SOD-A), esterase D (ESD), and glyoxalase (GLO1). Statistically significant differences between the groups compared were established for five genetic systems: ABO, E2, C3, TF, and PGM1. Among patient with endometriosis, the rare alleles of the locus ESD-ESD5 and ESD7-were found, along with ESD 5-5 homozygotes. Several genetic loci can be involved in the pathogenesis of endometriosis; their products can be specifically realized due to peculiarities of biochemical reactions in the organisms of people predisposed to this pathology.
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PMID:[Genetic aspects of endometriosis: features of the distribution of polymorphic gene frequencies]. 910 63

A reciprocal type of the relationship between superoxide dismutase (SOD) and hepatic ceruloplasmin levels in the liver and plasma has been demonstrated. This acts as an integrating mechanism of antioxidant resistance in hepatobiliary diseases. The value of SOD/ceruloplasmin ratio is presented which was low in primary biliary cirrhosis and chronic cholestatic hepatitis. A statistical significance for the differences between biochemical indices of cholestasis (bilirubin, cholesterol, alkaline phosphatase) was less than for SOD/ceruloplasmin ratio. The latter proved more informative in the diagnosis of cholestasis.
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PMID:[A new approach to the diagnosis of cholestasis by the activity of copper-containing enzymes]. 913 6


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