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:1.17.3.2 (xanthine oxidase)
8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissues of kuruma shrimp Marsupenaeus japonicus Bate (5.7+/-1.1 g) reared in salinities of 18, 26, 34 and 42 were examined for levels of nucleotide-related compounds, ammonia, urea and uric acid, and activities of xanthine dehydrogenase (XDH), xanthine oxidase (XOD) and uricase. Levels of total nucleotide-related compounds, including xanthine and hypoxanthine, in gill increased directly with salinity, whereas these same levels in hepatopancreas were inversely related with salinity. Hemolymph ammonia, urea and uric acid levels, and epidermal ammonia, urea and uric acid levels increased directly with salinity, whereas hepatopancreas ammonia and uric acid and gill uric acid levels were inversely related to salinity. Activities of XDH and XOD in hepatopancreas increased directly with salinity level, whereas no significant difference of uricase activity in hepatopancreas was observed among the four salinities. It is concluded M. japonicus exhibited uricogenesis and uricolysis, and an increase of uricogenesis occurred for the shrimp under hyper-osmotic conditions (salinity of 42). Uric acid produced in the hepatopancreas was transported and accumulated in the epidermis, and removed along with the spongy connective tissue at the time of molting.
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PMID:Increase of uricogenesis in the kuruma shrimp Marsupenaeus japonicus reared under hyper-osmotic conditions. 1525 73

Kuruma shrimp Marsupenaeus japonicus Bate, under the stress of 0.36 and 1.39 mM nitrite at 30 per thousand (parts per thousand, g kg(-1)) for 48 h, were examined for nucleotide-related compounds, specific activities of xanthine dehydrogenase (XDH), xanthine oxidase (XOD), and uricase. The levels of total nucleotide-related compounds, including xanthine and hypoxanthine, in the gill increased directly with ambient nitrite, whereas the levels of total nucleotide-related compounds, including xanthine and hypoxanthine, in the hepatopancreas were inversely related to ambient nitrite. Specific activity of XOD in the hepatopancreas increased directly with ambient nitrite, whereas no significant difference in uricase activity in the hepatopancreas was observed among three treatments. In another experiment, M. japonicus, following 48 h exposure to 0.36 and 1.39 mM nitrite, were examined for ammonia, urea, and urate levels in tissues. Hemolymph urea and exoskeleton urate levels increased directly with ambient nitrite, whereas hemolymph urate and exoskeleton urea levels were inversely related to ambient nitrite. It is concluded that M. japonicus exhibited uricogenesis and uricolysis, and an increase of uricogenesis occurred for the shrimp under nitrite stress. Urate produced in the hepatopancreas was transported and accumulated in the epidermis, and removed along with the exoskeleton at the time of molting.
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PMID:An increase of uricogenesis in the Kuruma shrimp Marsupenaeus japonicus under nitrite stress. 1577 15

In the presence of 0.5 millimolar allopurinol (4-hydroxypyrazolo [3,4-d]pyrimidine), an inhibitor of NAD:xanthine oxidoreductase (EC 1.2.3.2), intact attached nodules of cowpea (Vigna unguiculata L. Walp. cv Vita 3) formed [(15)N]xanthine from (15)N(2) at rates equivalent to those of ureide synthesis, confirming the direct assimilation of fixed nitrogen into purines. Xanthine accumulated in nodules and was exported in increasing amounts in xylem of allopurinol-treated plants. Other intermediates of purine oxidation, de novo purine synthesis, and ammonia assimilation did not increase and, over the time course of experiments (4 hours), allopurinol had no effect on nitrogenase (EC 1.7.99.2) activity. Negligible (15)N-labeling of asparagine from (15)N(2) was observed, suggesting that the significant pool (up to 14 micromoles per gram of nodule fresh weight) of this amide in cowpea nodules was not formed directly from fixation but may have accumulated as a consequence of phloem delivery.
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PMID:Pathways of Nitrogen Assimilation in Cowpea Nodules Studied using N(2) and Allopurinol. 1666 67

In hyperammonemia, a decrease in brain ATP can be a result of adenine nucleotide catabolism. Xanthine dehydrogenase (XD) and xanthine oxidase (XO) are the end steps in the purine catabolic pathway and directly involved in depletion of the adenylate pool in the cell. Besides, XD can easily be converted to XO to produce reactive oxygen species in the cell. In this study, the effects of acute ammonia intoxication in vivo on brain adenine nucleotide pool and xanthine and hypoxanthine, the end degradation products of adenine nucleotides, during the conversion of XD to XO were studied. Injection of rats with ammonium acetate was shown to lead to the dramatic decrease in the ATP level, adenine nucleotide pool size and adenylate energy charge and to the great increase in hypoxanthine and xanthine 11 min after the lethal dose indicating rapid degradation of adenylates. Conversion of XD to XO in hyperammonemic rat brain was evidenced by elevated XO/XD activity ratio. Injection of MK-801, a NMDA receptor blocker, prevented ammonia-induced catabolism of adenine nucleotides and conversion of XD to XO suggesting that in vivo these processes are mediated by activation of NMDA receptors. The in vitro dose-dependent effects of sodium nitroprusside, a NO donor, on XD and XO activities are indicative of the direct modification of the enzymes by nitric oxide. This is the first report evidencing the increase in brain xanthine and hypoxanthine levels and adenine nucleotide breakdown in acute ammonia intoxication and NMDA receptor-mediated prevention of these alterations.
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PMID:Brain purine metabolism and xanthine dehydrogenase/oxidase conversion in hyperammonemia are under control of NMDA receptors and nitric oxide. 1964 76

Ammonia is considered to be the main agent responsible for hepatic encephalopathy which progressively leads to altered mental status. N-methyl-D-aspartate (NMDA) is an ionotropic glutamate receptor, which is involved in synaptogenesis, memory and neurotoxicity. The aim of this study was to investigate the effects of ammonia intoxication and allopurinol, a xanthine oxidase (XO) inhibitor, on NMDA receptor subunits, NR2A and NR2B, in the hippocampus of rats. Thirty-six male rats were divided into three groups (n = 12/group) as follows: (1)control group (phosphate buffered saline (PBS) solution); (2)ammonia group (ammonium acetate, 2.5 mmol/kg), (3)ammonia + allopurinol group (ammonium acetate, 2.5 mmol/kg, allopurinol, 50 mg/kg). Each rat received intraperitoneal injection for 28 days. Western Blotting technique was used for detecting NR2A and NR2B expressions. Both NR2A and NR2B subunit expressions decreased 27 and 11%, respectively, in ammonia group with respect to the control group. Ammonium acetate decreased significantly in NR2A subunit expressions in the hippocampus (p < 0.01). Administration of ammonia + allopurinol caused statistically significant increases in NR2A subunit expressions compared to the ammonia group (p < 0.001). The down-regulation of NMDA receptors caused by ammonium acetate suggest that these receptors may play role in the process of hepatic encephalopathy and using allopurinol may have some protective effects in ammonia toxicity.
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PMID:Effects of ammonia and allopurinol on rat hippocampal NMDA receptors. 2307 Jul 93

Oxidative stress and antioxidant enzyme activities in liver and white muscle of Nile tilapia (Oreochromis niloticus) juveniles (10+/-1.2g) in chronic exposure to sublethal total ammonia nitrogen (TAN) were studied. The fish were exposed to the TAN concentrations, 5 mg L(-1) (low) or 10 mg L(-1) (high) for consecutive 70 days at 26+/-0.5 degrees C temperature. At the end of experimental period, lipid peroxidation and protein carbonylation levels and the activities of xanthine oxidase (XO), aldehyde oxidase (AO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR), gamma-glutamyl cysteinyl synthetase (gamma-GCS), and gamma-glutamyl transpeptidase (gamma-GT) in liver and white muscle were assayed. The levels of oxidative stress biomarkers and the activities of the enzymes assayed were significantly increased in liver and white muscle of fish exposed to both low and high TAN levels. The changes in these parameters were intensified at high TAN level. The significance of these alterations in enzyme activities is discussed.
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PMID:Oxidative stress and antioxidant enzymes in liver and white muscle of Nile tilapia juveniles in chronic ammonia exposure. 2043 82

Although there have been many studies on this topic, the molecular mechanism of the toxic effects of hyperammonemia on cells has not yet been fully explained. Recent studies have held oxidative stress mechanisms responsible for hyperammonemia-induced cell damage. Kidney functions are affected in diseases associated with an increase in ammonia in the blood. Our study tries to determine whether oxidative stress mechanisms are responsible for kidney damage in chronic hyperammonemia. We also investigated whether kidney damage is dependent on possible reactive oxygen products associated with the xanthine oxidase (XO) enzyme and whether the possible association can be inhibited with allopurinol, an XO enzyme inhibitor. The study took into consideration the enzyme activities of XO, xanthine dehydrogenase (XDH), superoxide dismutase (SOD), glutathione-S-transferase (GST), as well as protein thiol (P-SH) and malondialdehyde (MDA) levels. The data found demonstrated that chronic hyperammonemia had oxidative stress effects on the kidney, and that kidney XO and XDH activity changed. However, it was not possible to inhibit this oxidative stress in the kidney using allopurinol. Thus, we could not conclude that oxidative stress is an XO-dependent mechanism. The outcomes of the study suggested that this oxidative situation arising in hyperammonemia occurred through a mechanism other than the XO enzyme.
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PMID:Investigation of the oxidative effect of chronic hyperammonemia on the kidney and the possible protective effect of allopurinol. 2121 7

There is an increased prevalence of nephrolithiasis and an increase in the incidence of renal colic in patients with diabetes, obesity, hypertension and insulin resistance because of an increased frequency of uric acid crystallization. Uric acid crystallization occurs in the milieu of an acid urine and is not due to hyperuricosuria as with insulin resistance, urinary uric acid levels are generally decreased because of increased renal tubular reabsorption. However, in the presence of insulin resistance, there is decreased renal tubular generation of ammonia and increased sodium absorption leading to acidification of the urine and uric acid crystallization. The presence of a low urine pH should alert the clinician to the increased risk of nephrolithiasis particularly in the obese, diabetic or hypertensive patient. Prevention of nephrolithiasis can be achieved in susceptible individuals either by alkalizing the urine and/or by further decreasing the uric acid content of the urine with a xanthine oxidase inhibitor such as allopurinol.
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PMID:Beware the low urine pH--the major cause of the increased prevalence of nephrolithiasis in the patient with type 2 diabetes. 2199 52

Chronic liver failure leads to hyperammonemia, a central component in the pathogenesis of hepatic encephalopathy (HE); however, a correlation between blood ammonia levels and HE severity remains controversial. It is believed oxidative stress plays a role in modulating the effects of hyperammonemia. This study aimed to determine the relationship between chronic hyperammonemia, oxidative stress, and brain edema (BE) in two rat models of HE: portacaval anastomosis (PCA) and bile-duct ligation (BDL). Ammonia and reactive oxygen species (ROS) levels, BE, oxidant and antioxidant enzyme activities, as well as lipid peroxidation were assessed both systemically and centrally in these two different animal models. Then, the effects of allopurinol (xanthine oxidase inhibitor, 100mg/kg for 10days) on ROS and BE and the temporal resolution of ammonia, ROS, and BE were evaluated only in BDL rats. Similar arterial and cerebrospinal fluid ammonia levels were found in PCA and BDL rats, both significantly higher compared to their respective sham-operated controls (p<0.05). BE was detected in BDL rats (p < 0.05) but not in PCA rats. Evidence of oxidative stress was found systemically but not centrally in BDL rats: increased levels of ROS, increased activity of xanthine oxidase (oxidant enzyme), enhanced oxidative modifications on lipids, as well as decreased antioxidant defense. In PCA rats, a preserved oxidant/antioxidant balance was demonstrated. Treatment with allopurinol in BDL rats attenuated both ROS and BE, suggesting systemic oxidative stress is implicated in the pathogenesis of BE. Analysis of ROS and ammonia temporal resolution in the plasma of BDL rats suggests systemic oxidative stress might be an important "first hit", which, followed by increases in ammonia, leads to BE in chronic liver failure. In conclusion, chronic hyperammonemia and oxidative stress in combination lead to the onset of BE in rats with chronic liver failure.
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PMID:Systemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure. 2230 Jun 46

L-arginine is conditionally essetcial amino acid, required for normal cell growth, protein synthesis, ammonia detoxification, tissue growth and general performance, proposed in the treatment of men sterility and prevention of male impotence. The aim of the present paper was to estimate the activity of the enzymes of adenine nucleotide metabolism: 5'-nucleotidase (5'-NU), adenosine deaminase (ADA), AMP deaminase, and xanthine oxidase (XO), during dietary intake of L-arginine for a period of four weeks of male Wistar rats. Adenosine concentration in tissues is maintained by the relative activities of the adenosine-producing enzyme, 5'-NU and the adenosine-degrading enzyme-ADA adenosine deaminase. Dietary L-arginine intake directed adenine nucleotide metabolism in liver, kidney, and testis tissue toward the activation of adenosine production, by increased 5'-NU activity and decreased ADA activity. Stimulation of adenosine accumulation could be of importance in mediating arginine antiatherosclerotic, vasoactive, immunomodulatory, and antioxidant effects. Assuming that the XO activity reflects the rate of purine catabolism in the cell, while the activity of AMP deaminase is of importance in ATP regeneration, reduced activity of XO, together with the increased AMP-deaminase activity, may suggest that adenine nucleotides are presumably directed to the ATP regenerating process during dietary L-arginine intake.
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PMID:L-arginine intake effect on adenine nucleotide metabolism in rat parenchymal and reproductive tissues. 2262 85


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