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)

Desferrioxamine (DFO) nearly doubles alkaline phosphatase oxidative inactivation by the ascorbate system. The effect is dependent on ascorbate and desferrioxamine concentrations, exhibiting in both cases a saturation mechanism. Conversion of desferrioxamine to ferrioxamine abolishes the prooxidant action. Desferrioxamine also increases ascorbate-dependent oxygen consumption and nitroblue tetrazolium reduction. Superoxide dismutase, which blocks the desferrioxamine enhancing effect on enzyme inactivation, markedly slows down nitroblue tetrazolium reduction as well as oxygen consumption by ascorbate plus desferrioxamine, while it fails to protect against the ascorbate system alone. Therefore, in the presence of desferrioxamine, the metal-catalyzed ascorbate autooxidation becomes superoxide-dependent and thus inhibitable by superoxide dismutase. Catalase, peroxidase, and ascorbate oxidase protect alkaline phosphatase from inactivation by both ascorbate and ascorbate-desferrioxamine systems. Hemin shields the enzyme from ascorbate plus DFO attack but not from ascorbate alone. In air-saturated solution, desferrioxamine seems to mediate one electron transfer from ascorbate to oxygen, generating superoxide anions, which can either trigger a Fenton reaction or produce desferal nitroxide radicals. In the absence of oxygen, ascorbate alone is ineffective, but the ascorbate plus desferrioxamine system still inactivates the enzyme; catalase, peroxidase, and ascorbate oxidase, but not superoxide dismutase, afford protection.
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PMID:Prooxidant action of desferrioxamine: enhancement of alkaline phosphatase inactivation by interaction with ascorbate system. 215 77

Reactive oxygen species have been found to be responsible for the tissue injury caused in experimental pyelonephritis in mice. The extent of lipid peroxidation (as assayed by malondialdehyde formation) was found to be increased significantly (p less than .001) in the infected group as compared to the normal mice. Superoxide dismutase and catalase (oxygen free radical scavengers) showed a significant decrease (p less than .001) in the extent of lipid peroxidation even in the presence of infection. Dimethyl sulfoxide, a hydroxyl ion scavenger, was however found to be effective only at 4 and 7 days postinfection (p less than .001). Allopurinol, an inhibitor of xanthine oxidase, did not significantly (p greater than .05) inhibit the formation of lipid peroxides, even upto 7 days postinfection. There was a significant decrease (p less than .05) in the activities of renal brush border membrane enzymes used as markers of renal tissue damage (i.e. alkaline phosphatase, leucine amino-peptidase and gamma-glutamyl transpeptidase) in the infected group as compared to the normal group. In the presence of superoxide dismutase, dimethylsulfoxide and catalase except allopurinol, the activities of all the enzymes but maltase were found to be increased significantly (p less than .05) as compared to the infected group. There was a significant increase (p less than .01) in the bacterial count in the presence of superoxide dismutase and DMSO in infected mice as compared to the infected control mice. However, no significant difference was observed in the catalase and allopurinol treated groups.
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PMID:Effect of various oxygen free radical scavengers in preventing tissue injury caused by Escherichia coli in pyelonephritic mice. 305 56

The present study was designed to investigate the effect of antioxidant supplementation on the in vitro osmotic fragility of erythrocytes from zinc-deficient rats. Rats were fed either a zinc-adequate diet, zinc-deficient diet or a zinc-deficient diet enriched either with vitamin C or vitamin E or beta-carotene. Components of the primary antioxidant system of erythrocytes, parameters of hemolysis in vivo and indicators of liver injuries were also examined. In order to ensure adequate and identical food intake rats were force-fed by intragastric tube. The supplementation with antioxidants led to a marked improvement of the osmotic fragility without having influenced zinc status of the animals and components of the antioxidant system. The strongest effect was exerted by vitamin E. The rats fed the zinc-adequate diet (control group) showed unusually high values of erythrocytes osmotic fragility. Therefore there was no difference between control group and zinc-deficient group. A possible reason for this is discussed. Zinc deficiency led to a reduction of serum zinc concentration and alkaline phosphatase activity as well as to changes in the antioxidant system of erythrocytes characterized by a decrease of glutathione and an increase of glutathione S-transferase activity. Superoxide dismutase activity in serum decreased. There was no indication for hemolysis in vivo and for liver injuries.
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PMID:Influence of vitamin C, vitamin E and beta-carotene on the osmotic fragility and the primary antioxidant system of erythrocytes in zinc-deficient rats. 927 23

Nitrosoamines such as N-nitrosodiethylamine (NDEA) produce oxidative stress due to generation of reactive oxygen species and may alter antioxidant defence system in the tissues. NDEA was administered ip as a single dose to rats in LD50 or in lower amounts and the animals were sacrificed after 0-48 hr of treatment. The results showed that lipid peroxidation in liver increased, however no significant increase in kidney LPO was observed after NDEA administration. Superoxide dismutase (SOD) and glutathione reductase (GSH-R) activity increased in liver, however, catalase (CAT) activity in liver was inhibited in NDEA treated rats. Kidney showed an increase in SOD activity after an initial decrease along with increase in GSH-R activity in NDEA treated rats. However, kidney CAT activity was not significantly altered in NDEA intoxicated rats. Serum transaminases, serum alkaline phosphatase blood urea nitrogen, serum creatinine and scrum proteins were elevated in NDEA treated rats. The results indicate NDEA-induced oxidative stress and alteration in antioxidant enzymes in liver and kidney to neutralise oxidative stress.
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PMID:Hepatic and renal oxidative stress in acute toxicity of N-nitrosodiethylamine in rats. 1256 51

Ricin a glycoprotein from the Ricinus communis seeds, is known to have diverse toxic effects on cells of different visceral organs. We have studied the hepatotoxicity, nephrotoxicity, and oxidative stress following i.p. administration of ricin (25 microg/kg) in Swiss albino male mice. The results of this study revealed that activities of various enzymes like glutamic pyruvic transaminase (GPT), alkaline phosphatase (ALP), gamma glutamyl transpeptidase (gamma-GT), and lactate dehydrogenase (LDH) were increased in plasma, liver, and kidney tissues indicating damage in liver and kidney. Blood urea level was also increased. However, blood creatinine and bilirubin were not altered. Lipid peroxidation increased to 49 and 25% in hepatic and renal tissue. Total non-protein sulfhydryl content decreased in plasma (12%), hepatic (29%), and renal (16%) tissues. Superoxide dismutase activity decreased significantly in liver (43%) and kidney (37%). The activity of glutatione peroxidase was also decreased. The decrease was more prominent in kidney than liver. A significant increase, 20 to 27% in the activity of catalase was observed in plasma, liver, and kidney. These results indicate that ricin produces hepatoxicity, nephrotoxicity, and oxidative damage at 24 h of post treatment. The hepatotoxicity was more prominent than nephrotoxicity.
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PMID:Oxidative stress associated hepatic and renal toxicity induced by ricin in mice. 1256 56

Sesame oil is regarded as a daily nutritional supplement to increase cell resistance to lipid peroxidation. The aims of this study were to examine the effects of parenteral sesame oil on oxidative stress and hepatic disorder induced by lipopolysaccharide and to determine the defense mechanisms involved in sesame oil-associated anti-oxidative effects in rats. Oxidative stress was induced by lipopolysaccharide (5 mg/kg, intraperitoneally) and assessed by determination of lipid peroxidation. Sesame oil (8 ml/kg, subcutaneously) was given 3 h after lipopolysaccharide, and lipid peroxide levels, hydroxyl radical, superoxide anion, the enzyme activities of superoxide dismutase and catalase as well as the levels of glutathione and nitrite were examined 6 h after lipopolysaccharide. Hepatic function was assessed by determining the activities of serum aspartate aminotransferase and alkaline phosphatase. Sesame oil reduced lipid peroxidation and hydroxyl radical, but failed to affect superoxide anion. Superoxide dismutase and catalase were increased, but glutathione was not affected, and the levels of nitrite were reduced. Further, sesame oil-treated groups showed attenuated hepatic disorder in lipopolysaccharide-treated rats. Thus, parenteral sesame oil can be used to attenuate oxidative stress and relieve hepatic disorder after lipopolysaccharide intoxication in rats.
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PMID:Parenteral sesame oil attenuates oxidative stress after endotoxin intoxication in rats. 1503 64

Enzymes associated with release of iron from internalized ferrated siderophore (ferrisiderophore reductase), with damage to the cell at high iron concentration (superoxide dismutase) and siderophore synthesis (alkaline phosphatase), were examined in 3 test fungi viz., Aspergillus sp. ABp4, Aureobasidium pullulans and Rhizopus sp. Extracellular ferrisiderophore reductase activity was present in all the three fungi, but Aureobasidium pullulans, that showed the highest activity (84.3 microM min(-1)), was the only one to produce intra-cellular ferric reductase (147.9 microM min(-1)). Superoxide dismutase was produced by Aureobasidium pullulans and Rhizopus sp., but not by Aspergillus sp. ABp4, that showed intra-cellular enzyme activity in case of ferric reductase and alkaline phosphatase. Maximum SOD activity was seen in Aureobasidium pullulans both extra-cellularly (93.83 ng ml(-1)) and intra-cellularly (57.14 ng ml(-1)). All the test fungi examined, produced intra-cellular alkaline phosphatase. There was no extracellular alkaline phosphatase. Among the three fungi, Aureobasidium pullulans showed highest alkaline phosphatase activity (129.9 microM min(-1)) and Aspergillus sp. ABp4 the least (76.4 microM min(-1)).
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PMID:Ferric reductase, superoxide dismutase and alkaline phosphatase activities in siderophore producing fungi. 1528 58

Alcohol related disabilities are one of the world's major public health concerns. The effects of alcohol intake include alteration of redox state, acetaldehyde and free radical production, which lead to membrane damage. The damage caused by alcohol is enhanced by polyunsaturated fatty acid ingestion. When alcohol is taken along with thermally oxidized sunflower oil, the toxicity is still more pronounced due to toxic metabolites produced during heating. In our study, we have analysed the effects of a thiol supplier N-acetyl cysteine on alcohol, thermally oxidized sunflower oil and alcohol + thermally oxidized sunflower oil induced toxic effects in male Wistar rats. The activities of liver marker enzymes (alkaline phosphatase and gamma-glutamyl transferase), triglycerides in plasma and lipid peroxidative indices (thiobarbituric acid reactive substances and hydroperoxides) were increased in these groups when compared to normal, which were brought down in N-acetyl cysteine treated groups. The antioxidant status (Superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase) was decreased in tissues of these groups, which were found to be improved in N-acetyl cysteine treated groups. Thus our results show that N-acetyl cysteine regresses the oxidative damage induced by Alcohol, thermally oxidized sunflower oil and alcohol + thermally oxidized sunflower oil.
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PMID:Alcohol and thermally oxidized pufa induced oxidative stress: role of N-acetyl cysteine. 1535 56

The present study was designed to investigate the effects of quercetin on oxidative stress and activation of nuclear factor kappa B (NF-kappaB) in an experimental model of portal hypertensive gastropathy induced by partial portal vein ligation (PPVL). Portal pressure was significantly elevated in PPVL rats. Transaminase and alkaline phosphatase activities were not significantly modified, indicating absence of liver injury. Histological analysis of gastric sections showed a lost of normal architecture, with edema and vasodilatation. The cytosolic concentration of thiobarbituric acid reactive substances and the lipoperoxidation measurement by chemiluminiscence were significantly increased. Superoxide dismutase activity in gastric mucosa was significantly reduced. Portal hypertensive gastropathy induced a marked activation of NF-kappaB, accompanied by a decrease in IkappaB protein levels and a significant induction of nitric oxide synthase (iNOS) protein. Administration of quercetin markedly alleviated histological abnormalities and inhibited oxidative stress and NF-kappaB activation. IkappaB decrease and induction of iNOS protein were partially prevented by quercetin. Quercetin treatment, by abolishing the NF-kappaB signal transduction pathway, may block the production of noxious mediators involved in the pathogenesis of portal hypertensive gastropathy.
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PMID:Quercetin prevents oxidative stress and NF-kappaB activation in gastric mucosa of portal hypertensive rats. 1547 65

Nitrosamine compounds are known hepatic carcinogens. In the metabolism of nitrosamines, such as N-nitrosodiethylamine (NDEA), there is evidence of the formation of reactive oxygen species (ROS) resulting in oxidative stress, which may be one of the factors in the etiology of cancer. The formation of ROS may alter the antioxidant system, while the presence of Vitamin E may counteract NDEA induced oxidative stress. This study was planned to determine whether pre-treatment with Vitamin E (40 mg/kg body weight, i.p., twice a week for 4 weeks) to NDEA induced rats provides protection against oxidative stress in liver caused by the carcinogen. A single necrogenic dose of NDEA (200mg/kg body weight) was administered i.p. to the male albino rats with or without Vitamin E pre-treatment and the animals were sacrificed on Days 7, 14 or 21 after the administration of NDEA. The result showed enhanced levels of hepatic lipid peroxidation (LPO) and conjugated dienes of NDEA treated rats as the indices of oxidative stress, however, Vitamin E pre-treated rats administered NDEA showed decreased LPO and conjugated dienes (Day 21). Superoxide dismutase (SOD) activity in liver was not altered significantly in NDEA treated rats with or without Vitamin E pre-treatment. Catalase (CAT) activity was inhibited with NDEA treatment, however, Vitamin E pre-treatment showed recovery in hepatic CAT activity (Days 14 and 21). Total and Se-glutathione peroxidase (GSH-Px) activities and glutathione-S-transferase (GST) activity in liver increased in NDEA treated rats irrespective of Vitamin E pre-treatment. Glutathione reductase (GSH-R) activity as well as total glutathione (GSH) content in liver decreased in NDEA treated animals, both of which were recovered in Vitamin E pre-treated rats administered NDEA. Activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) were increased significantly following NDEA treatment to rats with or without Vitamin E pre-treatment. The activities of AST and ALT enzymes were significantly reduced on Days 14 and 21 and ALP activity was reduced on Day 21 in NDEA+Vitamin E treated animals when compared to NDEA treated alone. LDH enzyme activity was normalized on Day 14 in Vitamin E pre-treated animals administered NDEA. However, the AST, ALT and ALP enzyme activities remained high in all treatment groups as compared to control group. Normal control and Vitamin E treated alone rats revealed normal histology of liver. On the other hand, NDEA treated animals showed alterations in normal hepatic histoarchitecture, which comprised of necrosis and vacuolization of the cells. However, the rats treated with Vitamin E+NDEA showed that the liver cells were normal, with very little necrosis (Day 21). This study concludes that the pre-treatment with Vitamin E prior to the administration of NDEA, reduced the degree of oxidative stress, although this vitamin produced only slight changes in the hepatic injury, in a time-dependent manner.
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PMID:Protective role of Vitamin E pre-treatment on N-nitrosodiethylamine induced oxidative stress in rat liver. 1614 95


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