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)

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

The present study assessed the biochemical differences in membrane composition/function between right hemispheric dominant and left hemispheric dominant individuals. The HMG CoA reductase activity, serum isoprenoid metabolite--digoxin--serum magnesium, and the RBC membrane composition/Na(+)-K+ ATPase activity were studied. The results showed that right hemispheric dominant individuals had (i) increased HMG CoA reductase activity and elevated digoxin levels, (ii) decreased RBC membrane Na(+)-K+ ATPase activity and serum magnesium levels, and (iii) increased cholesterol:phospholipid ratio of RBC membranes with reduced membrane glycoconjugates. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition. Left hemispheric dominance represents the reverse pattern with hypodigoxinemia and membrane sodium-potassium ATPase stimulation. Cerebral dominance can regulate membrane structure/function.
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PMID:Hypothalamic digoxin, cerebral dominance, and membrane biochemistry. 1265 96

The present study assessed the biochemical differences in lipid metabolism between right hemispheric dominant and left hemispheric dominant individuals. The HMG CoA reductase activity and the serum isoprenoidal metabolities--digoxin, dolichol, and ubiquinone--were studied. The results showed that right hemispheric dominant individuals had (i) increased HMG CoA reductase activity, (ii) elevated serum digoxin levels, (iii) reduced serum ubiquinone levels, (iv) increased serum tryptophan and reduced tyrosine, (v) increased serum dolichol levels, and (vi) decreased RBC membrane Na(+)-K+ ATPase activity and serum magnesium levels. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition and an upregulated isoprenoid pathway. Left hemispheric dominance represents the reverse pattern with hypodigoxinemia/membrane sodium-potassium ATPase stimulation and a downregulated isoprenoid pathway. Cerebral dominance can regulate lipid metabolism.
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PMID:Hypothalamic digoxin, cerebral dominance, and lipid metabolism. 1269 Oct 3

The present study assessed the neurochemical differences between right hemispheric dominant and left hemispheric dominant individuals. The HMG CoA reductase activity, serum digoxin, magnesium, tryptophan catabolites, tyrosine catabolites, and RBC membrane (Na+)-K+ ATPase activity were measured in individuals of differing hemispheric dominance. The results showed that right hemispheric dominant individuals had elevated digoxin synthesis, increased tryptophan catabolites, and reduced tyrosine catabolites and membrane (Na+)-K+ ATPase with hypomagnesemia. Left hemispheric dominant individuals had the opposite patterns. Right hemispheric dominance represents a hyperdigoxinemic state with membrane sodium-potassium ATPase inhibition. Left hemispheric dominance represents the reverse pattern with hypodigoxinemia and membrane sodium-potassium ATPase stimulation.
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PMID:Hypothalamic digoxin, regulation of neuronal transmission, and cerebral dominance. 1277 46

The isoprenoid pathway produces three key metabolites: i) digoxin (a membrane sodium-potassium ATPase inhibitor which can regulate intracellular calcium/magnesium ratios), ii) dolichol (which regulates N-glycosylation of proteins), and iii) ubiquinone (a free radical scavenger), all of which are important in bone and joint metabolism. The pathway was assessed in senile osteoporosis, spondylosis, and osteoarthritis. Digoxin could possibly play a role in the genesis of cerebral dominance because it can regulate multiple neurotransmitter systems. The pathway was also assessed in individuals of differing hemispheric dominance for comparison and to find out the role of cerebral dominance in the pathogenesis of these diseases. The plasma/serum-activity of HMG CoA reductase, magnesium, digoxin, dolichol, ubiquinone, and tryptophan/tyrosine catabolic patterns, as well as RBC Na(+)-K+ ATPase activity, were measured in the above mentioned groups. The glycoconjugate metabolism, free radical metabolism, and membrane composition were also studied. The pathway was upregulated with increased digoxin synthesis in patients with spondylosis and osteoarthritis. In this group of patients, the glycoconjugate levels and dolichol levels were increased and lysosomal stability reduced. The ubiquinone levels were low and free radicals increased in spondylosis and osteoarthritis. On the other hand, in senile osteoporosis, the isoprenoid pathway was downregulated and digoxin synthesis reduced. The glycoconjugate and dolichol levels were low and lysosomal stability increased. The ubiquinone levels were increased and free radical production increased in senile osteoporosis. The significance of these changes in the pathogenesis of osteoarthritis, spondylosis, and osteoporosis is discussed. The hyperdigoxinemic state is seen in osteoarthritis and spondylosis and in right hemispheric dominance. The hypodigoxinemic state is seen in left hemispheric dominance and senile osteoporosis. Hemispheric dominance plays a crucial role in deciding the predisposition to bone and joint diseases. Right hemispheric chemical dominance predisposes to spondylosis and osteoarthritis. Left hemispheric chemical dominance predisposes to osteoporosis.
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PMID:Hypothalamic digoxin and hemispheric chemical dominance--relation to the pathogenesis of senile osteoporosis, degenerative osteoarthritis, and spondylosis. 1280 38

The study assessed the biochemical differences between right hemispheric dominant and left hemispheric dominant individuals. The HMG CoA reductase activity, isoprenoid metabolites--serum digoxin--serum magnesium, and RBC membrane Na+-K+ ATPase activity were also studied. The results showed that right hemispheric chemically dominant individuals had increased (i) HMG CoA reductase activity, elevated digoxin levels, (ii) reduced RBC membrane Na+-K+ ATPase activity and serum magnesium levels. Left hemispheric chemically dominant individuals had the opposite patterns. Right hemispheric chemical dominance represents a hyperdigoxinemic/hypomagnesemic state with membrane sodium-potassium ATPase inhibition. Left hemispheric chemical dominance represents the reverse pattern with hypodigoxinemia/hypermagnesemia and membrane sodium-potassium ATPase stimulation. Cerebral chemical dominance can regulate calcium/magnesium metabolism.
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PMID:Hypothalamic digoxin, cerebral chemical dominance, and calcium/magnesium metabolism. 1288 Nov 91

The protective effects of glutathione monoester (GME) on buthionine sulfoximine (BSO)-induced glutathione (GSH) depletion and its sequel were evaluated in rat erythrocyte/erythrocyte membrane. Animals were divided into three groups (n=6 in each): control, BSO and BSO+GME group. Administration of BSO, at a concentration of 4 mmol/kg bw, to the albino rats resulted in depletion of blood GSH level to about 59%. GSH was elevated several folds in the GME group as compared to the control (P<0.05) and BSO (P<0.001) groups. Decreased concentration of vitamin E was found in the erythrocyte membrane isolated from BSO-administered animals. Antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX) were also found to be altered due to BSO-induced GSH depletion in blood erythrocytes. The SOD and CAT activities in BSO group were significantly lower (P<0.001) than the other groups. Lipid peroxidation index and malondialdehyde (MDA) levels in erythrocytes and their membranes were increased to about 45% and 40%, respectively. The activities of Ca2+ ATPase, Mg2+ ATPase and Na+K+ ATPase were lower than those of control group (P<0.05), whereas the activities of these enzymes were found to be restored to normal followed by GME therapy (P<0.05). Cholesterol, phospholipid and C/P ratio and some of the phospholipid classes like phosphatidylcholine (PC), lysophosphatidylcholine (LPC) and sphingomyelin were significantly (P<0.05) altered in the erythrocyte membranes of BSO-administered rats compared with those of control group. These parameters were restored to control group levels in GME-treated group. Oxidative stress may play a major role in the BSO-mediated gamma glutamyl cysteine synthetase (gamma-GCS) inhibition and hence the depletion of GSH. In conclusion, our findings have shown that antioxidant status decreased and lipid peroxidation increased in BSO-treated rats. GME potentiates the RBC and blood antioxidant defense mechanisms and decreases lipid peroxidation.
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PMID:Modulation of rat erythrocyte antioxidant defense system by buthionine sulfoximine and its reversal by glutathione monoester therapy. 1499 Mar 42

Molecular investigations of deep-level relationships within and among the animal phyla have been hampered by a lack of slowly evolving genes that are amenable to study by molecular systematists. To provide new data for use in deep-level metazoan phylogenetic studies, primers were developed to amplify a 1.3-kb region of the alpha subunit of the nuclear-encoded sodium-potassium ATPase gene from 31 bilaterians representing several phyla. Maximum parsimony, maximum likelihood, and Bayesian analyses of these sequences (combined with ATPase sequences for 23 taxa downloaded from GenBank) yield congruent trees that corroborate recent findings based on analyses of other data sets (e.g., the 18S ribosomal RNA gene). The ATPase-based trees support monophyly for several clades (including Lophotrochozoa, a form of Ecdysozoa, Vertebrata, Mollusca, Bivalvia, Gastropoda, Arachnida, Hexapoda, Coleoptera, and Diptera) but do not support monophyly for Deuterostomia, Arthropoda, or Nemertea. Parametric bootstrapping tests reject monophyly for Arthropoda and Nemertea but are unable to reject deuterostome monophyly. Overall, the sodium-potassium ATPase alpha-subunit gene appears to be useful for deep-level studies of metazoan phylogeny.
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PMID:Bilaterian phylogeny based on analyses of a region of the sodium-potassium ATPase beta-subunit gene. 1504 81

DHC-1, a multiherbal formulation, was tested for its antioxidant activity in rats. DHC-1 was investigated at dose levels of 100 mg/kg, p.o. and 200 mg/kg, p.o., once daily, for 30 days in normal rats. The levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), lipid peroxidation, membrane bound enzymes like Ca2+ ATPase, Mg2+ ATPase, Na+K+ ATPase, lipids like phospholipid, cholesterol, triglyceride and total proteins were estimated in liver, kidneys and heart. Liver glucose-6-phosphate-dehydrogenase (G-6-P-D) was also determined. The serum levels of GOT, GPT, alkaline phosphatase, lactate dehydrogenase and bilirubin were also estimated. The decrease in the serum enzymes may be due to the membrane stabilising action of DHC-1. The inhibition of lipid peroxidation and enhancement of antioxidant enzymes (SOD and CAT) along with reduced GSH by DHC-1 may be attributed to the antioxidant potential of various ingredients present in the formulation. Thus, it can be concluded that DHC-1 exhibits an antioxidant activity and could prove beneficial in the treatment of various disorders associated with the involvement of reactive oxygen species.
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PMID:Antioxidant activity of DHC-1--a herbal formulation. 1526 74

Effect of various doses (125, 250, 500 and 1000 mg/kg, po) of Normacid was studied on gastric secretion and gastric ulcers in pylorus-ligation and on ethanol-induced gastric mucosal injury in rats. The reduction in ulcer index in both the models along with the reduction in total acidity and an increase in the pH of gastric fluid in pylorus-ligated rats proved the anti-ulcer activity of Normacid. The increase in the levels of superoxide dismutase, catalase, reduced glutathione and membrane bound enzymes like Ca2+ ATPase, Mg2+ ATPase and Na+K+ ATPase and decrease in lipid peroxidation in both the models showed the antioxidant activity of the formulation. Thus it can be concluded that the anti-ulcer activity shown by Normacid may be due to the modulation of defensive factors by improvenent in gastric cytoprotection and partly due to antioxidant property.
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PMID:Anti-ulcer and antioxidant activity of Normacid, a herbomineral formulation. 1533 31


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