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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endotoxin-induced peroxynitrite formation has been demonstrated in plasma. The aim of this study is to evaluate whether this has an effect on erythrocytes. For this purpose erythrocyte 3-nitrotyrosine (3-NT) level, Na+-K+ ATPase and glutathione peroxidase activities were measured both in vivo and in vitro. In vivo peroxynitrite formation was induced in rats by intraperitoneal Escherichia coli (E.coli) injection. Erythrocytes were directly incubated with peroxynitrite in the in vitro experiment. 3-NT levels were measured by reverse-phase HPLC, glutathione peroxidase, and Na+-K+ ATPase activities were measured by spectrophotometric techniques. There was a marked increase in the 3-NT levels in both experiments. However, glutathione peroxidase activity was significantly increased in in vivo experiments, while decreasing in in vitro conditions. Although Na+-K+ ATPase activities were significantly reduced by peroxynitrite in vitro, Na+-K+ ATPase activities were similar in control and E.coli-injected rat erythrocytes. Although nitrating effect of peroxynitrite does not seem to be preventable by endogenous antioxidants, this effect of peroxynitrite may not endanger erythrocytes if the oxidative damage of peroxynitrite is prevented.
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PMID:The effects of peroxynitrite on erythrocytes. 1179 88

In this study, we examined the modulatory effects of kolaviron, a biflavonoid from Garcinia kola seeds on the antioxidant defense mechanisms, cellular redox status and oxidative stress in the kidney and liver of rats pretreated with potassium bromate (KBrO(3)) intragastrically as a single dose of 300 mg kg(-1)weight for 4 weeks. Treatment of rats with KBrO(3)resulted in an insignificant difference (P> 0.05) in body weight compared to controls. However, a significant increase in kidney/body weight ratio (P< 0.001) was observed in rats treated with KBrO(3)while liver/body weight ratio was not affected. KBrO(3)depressed the activities of superoxide dismutase, glutathione peroxidase and catalase (P< 0.001) in the kidney but not in the liver. Kolaviron (200 mg kg(-1)body weight) administered three times a week for 4 weeks inhibited the decrease mediated by KBrO(3)of these enzymes in the kidney by 29, 88 and 45%, respectively. Similarly, kolaviron reduced the KBrO(3)-induced decrease in the activities of gamma -glutamyltransferase and microsomal Ca(2+)ATPase by 73 and 63% in the kidney. In addition, the extract elicited a 27 and 25% decrease in the KBrO(3)-induced increase in malondialdehyde and lipid hydroperoxide formation in the kidney. Kolaviron also attenuated the KBrO(3)-decreased activities of glucose 6-phosphatase, 5 prime prime or minute nucleotidase and alkaline phosphatase (membrane enzymes) by 72, 57 and 25% respectively. The results of the present investigation indicate the antioxidative effect of kolaviron, a natural antioxidant, on drug-induced kidney toxicity. Kolaviron may therefore intervene in the cellular redox status and depression of membrane protein activities caused by KBrO(3)and other environmental carcinogens in the kidney.
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PMID:Kolaviron modulates cellular redox status and impairment of membrane protein activities induced by potassium bromate (KBrO(3)) in rats. 1182 Aug 64

Membrane injury facilitated the fixation of calcium oxalate crystals and subsequent growth into kidney stones. Oxalate-induced membrane injury was mediated by lipid peroxidation reaction through the generation of oxygen free radicals. In urolithic rat kidney or oxalate exposed cultured cells, both superoxide anion and hydroxyl radicals were generated in excess, causing cellular injury. In hyperoxaluric rat kidney, both superoxide and H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine oxidase (XO) were increased, and hydroxyl radical and transition metal ions, iron, and copper were accumulated. The lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were excessively released in tissues of urolithic rats and in plasma of rats as well as stone patients. The accumulation of these products was concomitant with the decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione (GSH), and protein thiol. All the above parameters were decreased in urolithic condition, irrespective of the agents used for the induction of urolithiasis. Oxalate binding activity and calcium oxalate crystal deposition were markedly pronounced, along with decreased adenosine triphosphatase (ATPase) activity. Lipid peroxidation positively correlated with cellular oxalate, oxalate binding, gamma-glutamyl carboxylase, and calcium level and negatively correlated with GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid, or fish oil normalised the cellular antioxidant system, enzymes and scavengers, and interrupted membrane lipid and protein peroxidation reaction, ATPase inactivation, and its associated calcium accumulation. Antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients. Similarly, calcium oxalate crystal deposition in vitro to urothelium was prevented by free radical scavengers such as phytic acid and mannitol by protecting the membrane from free radical-mediated damage. All these observations were suggestive of the active involvement of free radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis of calcium oxalate crystal deposition and retention.
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PMID:Calcium oxalate stone disease: role of lipid peroxidation and antioxidants. 1194 24

To identify genes whose alterations lead to gastric cancer, gene expression profiles have been obtained from 22 gastric cancer tissues and their surrounding gastric mucosa tissues. A total of 16 genes were differentially expressed in more than 50% of gastric cancer tissues compared with surrounding gastric mucosa tissues. Genes such as HMG-Y, fibroblast collagenase inhibitor, and osteopontin are among those that are overexpressed in over 50% of the gastric cancer tissues. Dihydrodiol dehydrogenase, ribonuclease A, and glutathione peroxidase are among those genes that are underexpressed in over 50% of the gastric cancer tissues. We identified genes that are associated with clinical phenotypes of patients with gastric cancers. Alpha-II spectrin, Na/K-ATPase and KIAA0111 are those that are enhanced in intestinal type of gastric cancer. Gene such as platelet-endothelial tetraspan antigen 3 was enhanced in highly metastatic gastric cancer tissues.
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PMID:Identification of genes differentially expressed between gastric cancers and normal gastric mucosa with cDNA microarrays. 1212 92

This study evaluated the antioxidant defense system of the rat kidney following chronic exposure to red wine rich in flavonols. Both ethanol and antioxidant non-alcoholic wine components, mainly polyphenols, could contribute to the antioxidant status of kidney. Adult rats were given separately, water, ethanol (12.5%), red wine or alcohol-free red wine. After ten weeks of treatment, blood samples were obtained to determine plasma antioxidant capacity (FRAP, ferric reducing ability of plasma), uric acid and ethanol levels. Kidney tissues (cortex and papilla) were separated to perform measurements of reduced glutathione (GSH), glutathione disulfide (GSSG), lipid peroxidation (malondialdehyde, MDA) and the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The activity of (Na + K)-ATPase, a membrane-bound enzyme, was also assessed. Red wine in plasma, elevated the FRAP without changing the concentration of uric acid; in kidney, it diminished the MDA production and elevated the GSH/GSSG ratio and the activity of CAT and GSH-Px. The activity of SOD did not change. Despite the finding that renal (Na + K)-ATPase activity was upregulated by ethanol, it was not altered by either red wine or alcohol-free red wine. The effects on the antioxidant enzymes could be attributed to ethanol, but the increase in the FRAP and GSH/GSSG ratio is attributed to the non-alcoholic components of red wine. These data suggest that there is an enhancement of the antioxidant defense potential in kidney and plasma, after chronic red wine consumption. Both ethanol and the non-alcoholic antioxidant constituents of red wine could be responsible for these effects.
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PMID:Rat kidney antioxidant response to long-term exposure to flavonol rich red wine. 1237 69

Cellular energetics and redox status were evaluated in NRK-52E cells, a stable cell line derived from rat proximal tubules. To assess toxicological implications of these properties, susceptibility to apoptosis induced by S-(1,2-dichlorovinyl)-L-cysteine (DCVC), a well-known mitochondrial and renal cytotoxicant, was studied. Cells exhibited high activities of several glutathione (GSH)-dependent enzymes, including gamma-glutamylcysteine synthetase, GSH peroxidase, glutathione disulfide reductase, and GSH S-transferase, but very low activities of gamma-glutamyltransferase and alkaline phosphatase, consistent with a low content of brush-border microvilli. Uptake and total cellular accumulation of [14C]alpha-methylglucose was significantly higher when cells were exposed at the basolateral as compared to the brush-border membrane. Similarly, uptake of GSH was nearly 2-fold higher across the basolateral than the brush-border membrane. High activities of (Na(+)+K(+))-ATPase and malic dehydrogenase, but low activities of other mitochondrial enzymes, respiration, and transport of GSH and dicarboxylates into mitochondria were observed. Examination of mitochondrial density by confocal microscopy, using a fluorescent marker (MitoTracker Orange), indicated that NRK-52E cells contain a much lower content of mitochondria than rat renal proximal tubules in vivo. Incubation of cells with DCVC caused time- and concentration-dependent ATP depletion that was largely dependent on transport and bioactivation, as observed in the rat, on induction of apoptosis, and on morphological damage. Comparison with primary cultures of rat and human proximal tubular cells suggests that the NRK-52E cells are modestly less sensitive to DCVC. In most respects, however, NRK-52E cells exhibited functions similar to those of the rat renal proximal tubule in vivo.
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PMID:Cellular energetics and glutathione status in NRK-52E cells: toxicological implications. 1241 66

In the present study we evaluated the effect of acute homocysteine (Hcy) administration on Na(+),K(+)-ATPase activity, as well as on some parameters of oxidative stress such as total radical-trapping antioxidant potential (TRAP) and on activities of antioxidant enzymes catalase (CAT), superoxide dismutase and glutathione peroxidase in rat hippocampus. Results showed that Hcy significantly decreased TRAP, Na(+),K(+)-ATPase and CAT activities, without affecting the activities of superoxide dismutase and glutathione peroxidase. We also verified the effect of chronic pretreatment with vitamins E and C on the reduction of TRAP, Na(+),K(+)-ATPase and CAT activities caused by Hcy. Vitamins E and C per se did not alter these parameters, but prevented the reduction of TRAP, Na(+),K(+)-ATPase and CAT activities caused by Hcy. Our results indicate that oxidative stress is probably involved in the pathogenesis of homocystinuria and that reduction of Na(+),K(+)-ATPase activity may be related to the neuronal dysfunction found in homocystinuric patients.
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PMID:Inhibition of Na(+),K(+)-ATPase activity in hippocampus of rats subjected to acute administration of homocysteine is prevented by vitamins E and C treatment. 1251 23

The present study assessed the biochemical differences of free radical metabolism and mitochondrial function between right hemispheric dominant and left hemispheric dominant individuals. The following parameters were measured: (1) plasma HMG CoA reductase activity, (2) isoprenoid metabolites--digoxin and ubiquinone, (3) plasma magnesium and RBC membrane Na(+)-K+ ATPase activity; (4) lipid peroxidation products--malondialdehyde, hydroperoxides and conjugated dienes, and NO, (5) reduced glutathione, and (6) activity of superoxide dismutase, catalase, GSH peroxidase, and GSH reductase. The results showed that right hemispheric dominant individuals had (i) increased plasma HMG CoA reductase activity and elevated digoxin levels, (ii) decreased plasma magnesium and RBC membrane Na(+)-K+ ATPase activity, (iii) reduced ubiquinone levels, (iv) with increased levels of lipid peroxidation products and NO, (v) decreased levels of reduced glutathione and free radical scavenging enzymes, and (vi) increased tryptophan and reduced tyrosine levels. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition and increased lipid peroxidation. Left hemispheric dominance represents the reverse pattern with hypodigoxinemic/membrane sodium-potassium ATPase stimulation and decreased lipid peroxidation. Cerebral dominance can regulate mitochondrial function and free radical metabolism.
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PMID:Hypothalamic digoxin, cerebral dominance, and mitochondrial function/free radical metabolism. 1265 94

One of the most intriguing phenomenon observed during lead toxicity has been attributed to lead-induced oxidative stress. The combined effect of DL-alpha-lipoic acid (LA) and meso-2,3-dimercaptosuccinic acid (DMSA) on lead-induced alterations in selected parameters, which are indicators of oxidative stress in erythrocytes, have been studied. Lead acetate (Pb, 0.2%) was administered in drinking water for 5 weeks to induce toxicity. LA (25 mg/ kg body weight per day i.p.) and DMSA (20 mg/kg body weight per day i.p.) were administered individually and also in combination during week 6. Clinical evidence of toxic exposure was evident from the elevated blood lead levels (BPb) along with lowered levels of haemoglobin (Hb) and haematocrit (Ht). Lead-exposed animals showed enhanced membrane lipid peroxidation (LPO) in the erythrocytes. Damage to the erythrocyte membrane was evident from the decline in the activities of the transmembrane enzymes, viz., Na+, K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase. Lead-exposed rats also suffered an onslaught on the antioxidant defence system witnessed by lowered activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH). Serum glutamic-oxoloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) were also elevated in lead-exposed rats. Treatment with either LA or DMSA reversed the lead-induced biochemical disturbances encountered by the erythrocytes, but combined treatment with LA and DMSA was very effective in mitigating all the parameters indicative of oxidative stress.
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PMID:Combined efficacies of lipoic acid and meso-2,3-dimercaptosuccinic acid on lead-induced erythrocyte membrane lipid peroxidation and antioxidant status in rats. 1275 69

This study investigated the influence of chronically administered L-deprenyl on normal ageing-related parameters: multiple unit action potentials, the activities of the enzymes Na(+),K(+)-adenosine triphosphatase, glutathione-s-transferase and glutathione peroxidase, and the levels of lipid peroxidation products and lipofuscin contents in the brain regions (cerebral cortex, hippocampus, striatum and thalamus) of 24-month-old rats. The drug increased the activity of Na(+),K(+)-ATPase and glutathione-s-transferase. The activity of glutathione peroxidase remained unaffected. The drug also increased the multiple unit action potentials activity. The levels of lipid peroxidation products were, however, decreased, and lipofuscin accumulation was diminished by the drug. The results essentially indicated that chronic treatment of rats with L-deprenyl significantly influenced the ageing-related alterations in: multiple unit action potentials, Na(+),K(+)-adenosine triphosphatase, glutathione-s-transferase, lipid peroxidation products and lipofuscin accumulation. These novel data on the effect of L-deprenyl on parameters of normal ageing provide new additional evidence concerning the anti-ageing therapeutic potential of L-deprenyl.
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PMID:Neurostimulatory and antioxidative effects of L-deprenyl in aged rat brain regions. 1276 35


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