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)

Osteoporosis is associated with many etiological causes such as nutrition, cytokines, hormones, and aging. Recently, reactive oxygen species (ROS) are considered to be responsible for the aging process and osteoporosis. We investigated the relationship between ROS and bone metabolism in young female and postmenopausal rats, by using dietary iron overload and several indices including bone metabolic markers, oxidative stress and antioxidant markers, and cytokines. Postmenopausal rats exhibited significant decreases in serum alkaline phosphatase activity and the level of osteocalcin as bone formation markers compared with young female rats; however, urinary excretion of deoxypyridinoline, a bone resorption marker, did not change. On the other hand, a 5% iron lactate diet for 4 weeks in postmenopausal rats led to significantly increased excretion of urinary deoxypyridinoline and 8-hydroxy-2'-deoxyguanosine (8-OHdG) but not serum alkaline phosphatase activity. Interestingly, the diet induced significant increases of serum osteopontin and TGF-beta1, augumenting osteoclast-mediated bone resorption through the RANK/RANKL pathway [J. Clin. Invest. 112 (2003) 181]. TGF-beta1 showed a negative correlation with serum glutathione peroxidase (GPx) activity (r = -0.674, P < 0.003), but a positive correlation with the serum iron level (r = 0.836, P < 0.0001). Taken together, these results suggest for the first time that oxidative stress could be involved in the pathogenesis of metabolic bone diseases such as osteoporosis as demonstrated by analysis of the relationship between bone metabolism and oxidative stress.
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PMID:Bone metabolism and oxidative stress in postmenopausal rats with iron overload. 1500 20

The present study investigated the prophylactic influence of melatonin against cyclophosphamide-induced oxidative stress in mouse tissues. Lipid peroxidation, reduced glutathione (GSH), glutathione disulphide (GSSG), glutathione peroxidase (GSH-Px) and serum phosphatase levels were analyzed in brain, spleen liver, lungs, kidney and testes. Fifteen days oral administration with melatonin (0.1 mg/kg bw per day) before treatment checked the augmentation of the level of lipid peroxidation, blood GSSG and acid phosphatase caused by an acute treatment with a radiomimetic drug, cyclophosphamide (75 mg/kg bw). Cyclophosphamide-induced depletion in the level of GSH, GSH-Px and alkaline phosphatase was made up statistically significant by chronic melatonin administration given orally. The results indicate the antioxidative properties of melatonin resulting into its prophylactic property against the cyclophosphamide-induced biochemical alterations. The finding support the idea that melatonin is a potent free-radical scavenger and antioxidant.
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PMID:Prophylactic action of melatonin against cyclophosphamide-induced oxidative stress in mice. 1501 61

Monolayer primary cultures of thyroid cells produce, in the presence of insulin, a cytosolic inhibitor of thyroid peroxidase (TPO), lacto peroxidase (LPO), horseradish peroxidase (HRPO) and glutathione peroxidase (GPX). The inhibitor, localized in the cytosol, is thermostable and hydrophylic. Its molecular mass is less than 2 kDa. The inhibitory activity, resistant to proteolytic and nucleolytic enzymes, disappears with sodium metaperiodate treatment, as an oxidant of carbohydrates, supporting its oligosaccharide structure. The presence of inositol, mannose, glucose, the specific inhibition of cyclic AMP-dependent protein kinase and the disappearance of peroxidase inhibition by alkaline phosphatase and alpha-mannosidase in purified samples confirms its chemical structure as inositol phosphoglycan-like. Purification by anionic interchange shows that the peroxidase inhibitor elutes like the two subtypes of inositol phosphoglycans (IPG)P and A, characterized as signal transducers of insulin action. Insulin significantly increases the concentration of the peroxidase inhibitor in a thyroid cell culture at 48 h. The addition of both isolated substances to a primary thyroid culture produces, after 30 min, a significant increase in hydrogen peroxide (H2O2) concentration in the medium, concomitantly with the disappearance of the GPX activity in the same conditions. The presence of insulin or anyone of both products, during 48 h, induces cell proliferation of the thyroid cell culture. In conclusion, insulin stimulates thyroid cell division through the effect of a peroxidase inhibitor, as its second messenger. The inhibition of GPX by its action positively modulates the H2O2 level, which would produce, as was demonstrated by other authors, the signal for cell proliferation.
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PMID:Role of peroxidase inhibition by insulin in the bovine thyroid cell proliferation mechanism. 1520 26

We investigated the effect of dehydroepiandrosterone (DHEA) on oxidative injury in obstructive jaundice using three groups of rats: sham-operated group; common bile duct (CBD) group--the CBD was ligated; and DHEA group--DHEA administration followed CBD ligation. Liver function tests were performed using blood samples, and malondialdehyde concentration (MDA), superoxide dismutase activities (SOD), glutathione peroxidase (GPx), and total glutathione (tGSH) concentrations were measured in liver tissue. Serum alkaline phosphatase, gamma-glutamyltransferase and alanine aminotransferase activity were significantly elevated in the CBD group compared with the other groups. Serum aspartate aminotransferase and total bilirubin were highest in the CBD group; the MDA concentration was higher in the CBD group than the sham group. There were no significant differences in GPx activity among the groups. SOD activity and tGSH concentration were significantly lower in the CBD group than the other groups. DHEA may protect hepatic tissue against oxidative injury in obstructive jaundice by decreasing MDA concentration and increasing SOD activity and tGSH concentration.
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PMID:Dehydroepiandrosterone prevents oxidative injury in obstructive jaundice in rats. 1530 71

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 carried out to investigate the effects of copper (Cu) intake on lipid profile, oxidative stress and tissue damage in normal and in diabetic condition. Since diabetes mellitus is a situation of high-risk susceptibility to toxic compounds, we examined potential early markers of Cu excess in diabetic animals. Male Wistar rats, at 60-days-old were divided into six groups of eight rats each. The control(C) received saline from gastric tube, the no-diabetic(Cu-10), treated with 10 mg/kg of Cu(Cu(++)-CuSO4, gastric tube), no-diabetic with Cu-60 mg/kg(Cu-60), diabetic(D), diabetic low-Cu(DCu-10) and diabetic high-Cu(DCu-60). Diabetes was induced by an ip injection of streptozotocin (60 mg/kg). After 30 days of treatments, no changes were observed in serum lactate dehydrogenase, alanine transaminase and alkaline phosphatase, indicating no adverse effects on cardiac and hepatic tissues. D-rats had glucose intolerance and dyslipidemic profile. Cholesterol and LDL-cholesterol were higher in Cu-60 and DCu-60 than in C, Cu-10 and D and DCu-10 groups respectively. Cu-60 rats had higher lipid hydroperoxide (HP) and lower superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) serum activities than C and Cu-10 rats. LH was increased and GSH-Px was decreased, while no alterations were observed in SOD and catalase in serum of DCu-60 animals. DCu-60 rats had increased urinary glucose, creatinine and albumin. In conclusion, Cu intake at high concentration induced adverse effects on lipid profile, associated with oxidative stress and diminished activities of antioxidant enzymes. Diabetic animals were more susceptible to copper toxicity. High Cu intake induced dyslipidemic profile, oxidative stress and kidney dysfunction in diabetic condition. Copper renal toxicity was associated with oxidative stress and reduction at least, one of the antioxidant enzymes.
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PMID:Toxicity of copper intake: lipid profile, oxidative stress and susceptibility to renal dysfunction. 1550 Sep 42

The most important antioxidant aspect of selenium is its function in the active site of selenoenzyme glutathione peroxidase. Glutathione peroxidase not only allows the removal of the toxic radicals but also permits the regeneration of lipid molecules through reacylation in the cellular membrane. Thus, GSHPx may prevent the harmful effects of free radicals and may reduce the formation of the reactive metabolites of carbon tetrachloride. Carbon tetrachloride is a hepatotoxic agent which generates haloalkane radicals during its biotransformation in the liver and is widely used to make the experimental model of hepatic damage. Therefore, the aim of the present study is to investigate the possible protective role of selenium on the experimental liver cirrhosis and some enzyme activities in blood plasma from rats. While the activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased (p < 0.05, p < 0.05 and p < 0.01, respectively), gamma-glutamyle transferase (GGT) activity was not statistically affected (p < 0.05) with carbon tetrachloride-injection. The levels of AST, ALT and GGT in carbon tetrachloride-group decreased to nearly the enzyme values in control-group after the selenium-injection but the ALP was increased (p<0.01). On the other hand, it was noticed that selenium significantly decreased the hepatic injury. In conclusion, our results showed that carbon tetrachloride caused an increase in the activities of liver enzymes in plasma and selenium application decreased the hepatic injury. Plasma levels of the liver enzymes were decreased after selenium-injections. Based upon these results, selenium may play an important role in the preventive indication of hepatic cellular injury inducted by carbon tetrachloride.
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PMID:Effects of selenium on histopathological and enzymatic changes in experimental liver injury of rats. 1558 Dec 76

Ethanol, by its property of generating free radicals during the course of its metabolism, alters redox homeostasis and causes damage to cell structure and function. This study investigated the effect of taurine on ethanol-induced experimental toxicity in rats. Ethanol was administered chronically to rats for 28 days. This resulted in significant increases in the activities of transaminases, alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT) and bilirubin in plasma. The activities of glutathione peroxidase (GPx), glutathione-S-transferase (GST) and the contents of glutathione (GSH) and thiols in plasma and tissues were significantly reduced as compared to control animals. Simultaneous administration of taurine along with ethanol prevented the leakage of enzymes into circulation and restored glutathione and tissue thiols. The activities of antioxidant enzymes were normalized. We propose that taurine may have a bioprotective effect on ethanol-induced toxicity.
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PMID:Protective effects of taurine on glutathione and glutathione-dependent enzymes in ethanol-fed rats. 1558 89

Nicotine, a major toxic component of cigarette smoke has been identified as a major risk factor for lung related diseases. In the present study, we evaluated the protective effects of curcumin on lipid peroxidation and antioxidants status in bronchoalveolar lavage fluid (BALF) and bronchoalveolar lavage (BAL) of nicotine treated Wistar rats. Lung toxicity was induced by subcutaneous injection of nicotine at a dose of 2.5 mg/kg body weight (5 days a week, for 22 weeks) and curcumin (80 mg/kg body weight) was given simultaneously by intragastric intubation for 22 weeks. Measurement of biochemical marker enzymes: alkaline phosphatase, lactate dehydrogenase, lipid peroxidation and antioxidants were used to monitor the antiperoxidative effects of curcumin. The increased biochemical marker enzymes as well as lipid peroxides in BALF and BAL of nicotine treated rats was accompanied by a significant decrease in the levels of glutathione, glutathione peroxidase, superoxide dismutase and catalase. Administration of curcumin significantly lowered the biochemical marker enzymes, lipid peroxidation and enhanced the antioxidant status. The results of the present study suggest that curcumin exert its protective effect against nicotine-induced lung toxicity by modulating the biochemical marker enzymes, lipid peroxidation and augmenting antioxidant defense system.
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PMID:Curcumin ameliorates oxidative stress during nicotine-induced lung toxicity in Wistar rats. 1564 12

The mycotoxin ochratoxin A (OTA) is a widespread contaminant in human and animal food products. It induces a wide range of toxic effects including lipid peroxidation through the generation of free radicals. The aim of this work was to evaluate the antioxidant effects of melatonin against OTA-induced oxidative stress in liver and kidney in rats. Treated animals were fed OTA-contaminated diet (3 mg/kg) for 15 days before, during and after melatonin administration (20 mg/kg bw). The results indicate that OTA caused severe effects typical to those reported in the literature for ochratoxicosis. Melatonin alone was effective in the improving food intake, body weight gain, serum total protein, albumin, the activities of alkaline phosphatase, G-glutamyl transferase and creatinine kinase and liver and kidney glutathione peroxidase, superoxide dismutase and malondialdehyde. Rats fed OTA-contaminated diet before, during or after melatonin administration showed a significant improvement in all tested parameters toward the normal values of the controls. This improvement was most pronounced in the group pretreated with melatonin. It is concluded that melatonin exhibits a preventive effect against OTA-induced oxidative stress through its role in the scavenging of free radicals and/or the prevention of lipid peroxidation.
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PMID:Melatonin counteracts oxidative stress in rats fed an ochratoxin A contaminated diet. 1568 68


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