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)

Rats were treated with sennosides (6 x 10, 6 x 40 or 2 x 30 mg/kg weekly) or with danthron (6 x 500 mg/kg weekly) for 6 months. The laxative effect as measured by faecal wet weight during the first 10 h after treatment increased 3- to 4-fold by the higher sennoside doses (daily or intermittently) and 1- to 3-fold by danthron. The low sennoside dose had no measurable effect except on the 1st day (2 fold) compared with the control group. Mean faecal water content increased from 53% (controls) to 66-79% in rats treated with high sennoside doses and to 57 (1st day) -69% in danthron-treated rats. Serum aldosterone levels and mucosal Na(+)-K(+)-ATPase activities in the small intestine and colon did not change with treatment. There were no signs of habituation or secondary hyperaldosteronism due to sennosides or danthron in spite of chronic diarrhoea over 6 months.
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PMID:Chronic sennoside treatment does not cause habituation and secondary hyperaldosteronism in rats. 823 25

An important approach to the major health problem of bacterial infection in young children has been to examine bacterial toxin binding to microvillus membrane receptors, the signal transduction produced by that interaction and the mechanisms of fluid secretion in the developing intestine as a basis for toxigenic diarrhea in the infant population. These studies indicate that receptor binding and effector responses may be subjected to developmental regulation. This regulation process of toxin interaction with the developing intestine may have an enhanced or harmful effect or, under some circumstances, may have a beneficial effect and be protective to the vulnerable child. Specific mechanisms for the developmental control of receptor expression may involve the regulation of individual glycosyltransferases responsible for the addition of receptor sugar sequences to glycolipids and/or glycoproteins, presumably at the transcriptional level. Furthermore, although highly speculative at this point, the differential expression of signal transducers (e.g., guanine nucleotide-regulatory proteins or G proteins) and ion transporters (e.g., Na+,K(+)-stimulated adenosine triphosphatase, the Cl- channels, etc.) during development may also alter the neonatal host's responsiveness. Therefore, the developmental control of microvillus membrane receptors, signal transduction mechanisms, and ion transport systems in the gastro-intestinal tract may in part contribute to the altered host sensitivity in toxigenic diarrhea of infancy.
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PMID:Bacterial toxin interaction with the developing intestine. 838 47

Olsalazine (azodisalicylate) and mesalazine (5-aminosalicylic acid) have recently been developed as new treatment modalities for inflammatory bowel disease to avoid sulfasalazine-related side effects. However, there are reports regarding new and hitherto unexpected side effects in some patients receiving olsalazine or mesalazine, such as watery diarrhea. Since sodium pump activities play an important role in the pathogenesis of water and electrolyte disturbances, we investigated the influence of olsalazine and mesalazine on human ileal and colonic (Na+ + K+)-ATPase and its specific [3H]-ouabain binding. We found a concentration-dependent inhibition of ileal and colonic (Na+ + K+)-ATPase by olsalazine with an IC50 of 4.1 mM and 4.8 mM, respectively. Mesalazine inhibited this enzyme in the ileum with an IC50 of 4.0 mM and in the sigmoid colon with an IC50 3.5 mM. In addition, [3H]-ouabain binding was inhibited by mesalazine with an IC50 of 3.6 mM. The maximal inhibition, however, did not exceed 80% under any conditions (up to 10 mM drug concentration). Olsalazine and mesalazine induce inhibition of the ileal and colonic sodium pump activities that may (in addition to other possible mechanisms) mediate impaired water and electrolyte absorption. This is possibly of clinical relevance in patients with severely damaged mucosa. In patients with milder forms of mucosal inflammation, this inhibition most likely is of minor importance because of the great capacity of the (Na+ + K+)-ATPase and the incomplete inhibition leaving at least 20% of the enzyme activity intact.
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PMID:Effect of olsalazine and mesalazine on human ileal and colonic (Na+ + K+)-ATPase. A possible diarrhogenic factor? 838 34

Erythromycin, an antibiotic used in the treatment of infectious diseases, produces gastrointestinal side effects such as diarrhea. The mechanisms by which erythromycin produces these effects are not known. However, erythromycin has been shown to increase gastrointestinal motor activity and to inhibit intestinal neutral amino acid absorption. Both effects could contribute to the gastrointestinal side effects observed. Because the intestinal systems of amino acid and sugar transport present similar characteristics, the aim of the present work was to determine whether erythromycin also alters D-galactose absorption and sucrase activity in rabbit jejunum. The results show that erythromycin diminishes intestinal D-galactose absorption. This effect seems to be due to an action mainly located on the Na(+)-dependent sugar transport of the mucosal border of the intestinal epithelium. Erythromycin also inhibits the Na(+)-K+ ATPase activity of the enterocyte, which might explain the inhibition of the D-galactose Na(+)-dependent transport. However, a direct action of the erythromycin molecule on the Na(+)-dependent carrier cannot be excluded. Erythromycin did not alter sucrase activity.
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PMID:Effect of erythromycin on D-galactose absorption and sucrase activity in rabbit jejunum. 840 81

The large bowel daily absorbs passively 1500 ml of water down an osmotic gradient created by active electrolyte transports. The system is sustained by the enzyme Na(+)-K+ ATPase, the so called sodium-pump, present on the basolateral membrane of colonocytes. Some pathologic conditions may increase the amount of intraluminal water by inhibiting fluid absorbtion or enhancing fluid secretion. Diarrhoea represents the clinical counterpart of these alterations. Three forms of diarrhoea can be recognized on the basis of pathophysiological alterations. Diarrhoea is due to reduced ionic absorbtion, increased secretion or increased endoluminal osmolality. The drugs used to induce bowel actions or gut lavage increase also intraluminal water content by modifying transmural ionic transports. Laxatives or purges act by increasing either water secretion on endoluminal osmolality and therefore may produce systemic idro-electrolyte imbalance. To avoid this inconvenient an isosmotic electrolyte balanced polyethylene glicol solution (PEG-ELS) has been achieved. In addition orally administred PEG-ELS solution cleans the colon during its intestinal transit without producing relevant transmural water-ionic movements. Aim of this article was to describe the normal ionic transport, and its alterations in pathologic and pharmacologic conditions. Details on PEG-ELS were also given. This solution provides for an effective colon preparation for endoscopic or surgical procedures and resulted to be safe for patients with delicate fluid-electrolyte balance.
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PMID:[Ion transport in the colon]. 866 16

We performed comparative studies to determine an acute toxicity of microsomal Ca(2+)ATPase inhibitor, 2,5-di(tert-butyl)-1,4-hydroquinone (DTBHQ) and its related analog, mono(tert-butyl)-1,4-hydroquinone (MTBHQ), which are both used as antioxodants. Wistar rats, 5 weeks old, male and female, were used. By a single dose of oral administration, DTBHQ-induced LD50 values (obtained by Lorke method) in male and female rats were estimated 295.1 and 234.4 mg/kg BW, respectively, whereas each LD50 value for MTBHQ was 711.6 and 400.0 mg/kg BW, respectively. MTBHQ-induced deaths occurred from 8 to 20 minutes after administration, however, DTBHQ-induced deaths occurred more delayed from 1 to 5 days after administration. The observed toxic signs of DTBHQ included diarrhea (jelly like), prone position, lacrimation, salivation and abnormal gait (such as reluctance to walk, limping). Localized purpura and loss of the tail (perhaps as a result of necrosis) were also observed. In comparison, MTBHQ elicited prone position, panting, staggering gait and spastic gait. Without loss of the tail montioned above, dead and sacrified rats showed no remarkable changes in macroscopic examination due to exposure to both compounds.
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PMID:[Comparative studies on a single dose toxicity of microsomal Ca(2+)ATPase inhibitor, 2,5-di(tert-butyl)-1,4-hydroquinone and its related analog, mono(tert-butyl)-1,4-hydroquinone, in rats]. 871 30

A major advance in transport physiology was H. H. Ussing's development of the voltage-clamp method, and later the Koefoed-Johnsen-Ussing model for Na+ transport. In the same decade, J. C. Skou identified the Na(+)-K(+)-ATPase, which maintains the Na+ and K+ gradients that drive most epithelial transport processes. With this foundation, Danish scientists have pursued the mechanism of ion transport and the resulting solute-linked water flow. Recent contributions have been on isosmotic transport, suggesting solute recycling, and KCl-water cotransport in the basolateral epithelial cell membrane. Efficient small intestinal nutrient absorption is dependent on coupling to the Na+ gradient. Cotransport of Na+ and glucose is quantitatively the most important absorptive mechanism in the small intestine, as illustrated by the success of oral rehydration solutions in diarrhoea. The majority of amino acids are likewise transported by Na+ dependent carriers, but recent experiments have identified a concomitant Cl- dependency for some. Regulation of intestinal secretion, both under normal digestive processes, and in response to enterotoxins, has turned out to be very complex. It involves local and central neuronal regulation through an array of neurotransmitters and local actions of gastrointestinal hormones. Major effectors are the submucosal neurons and the main transmitters serotonin, vasoactive intestinal peptide, acetylcholine, substance P, and neurotensin. Development of antisecretagogues is impeded by the existence of several receptor subtypes and significant species differences. The Na+ and water-conserving properties of the large intestine have been shown to be regulated by adrenocortical hormones, with aldosterone as a potent stimulator of colonic Na+ absorption. A major colonic function is the symbiosis with the anaerobic bacterial population. The fermentation of carbohydrate to short-chain fatty acids, which can be absorbed, supplements small intestinal digestive function.
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PMID:Experimental studies of intestinal ion and water transport. 872 83

Nontoxigenic Escherichia coli strains bearing K88 fimbriae have been associated with diarrhea in piglets. We have used guinea pig erythrocytes as a model of the host cell to study the cellular alterations after adherence of purified K88ab fimbriae. Although Mg2+-dependent ATPase was inhibited (up to 61%), Na/K ATPase was not. Metabolic enzymes were not significantly affected.
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PMID:Adhesion of K88ab to guinea pig erythrocytes: effect on membrane enzyme activities. 875 86

The aim of this work was to compare the effects of colchicine and trimethylcolchicinic acid (TMCA) on liver damage induced by bile duct ligation (BDL) for 2 months in male Wistar rats. Colchicine was evaluated at a dose of 10 micrograms rat-1 day-1, p.o. only, because higher doses produced diarrhoea and death. Trimethylcolchicinic acid showed no toxic effects at 10, 50 or 100 micrograms rat-1 day-1, p.o. Biliary obstruction resulted in a 65% mortality, colchicine decreased it to 46% and TMCA (10 micrograms) to 33.3%. Serum markers of liver damage increased by BDL (P < 0.05), colchicine prevented it partially (P < 0.05) and TMCA did it in a dose-dependent manner. Liver peroxidation increased 10 times by BDL and both drugs prevented it. Hepatic glycogen content decreased 80% by BDL, colchicine TMCA (10 micrograms) failed to preserve it and 50 micrograms of TMCA preserved it completely. Hepatocyte and erythrocyte plasma membrane Na+/K(+)- and Ca(2+)-ATPase activities decreased after BDL (P < 0.05) and 100 micrograms of TMCA preserved normal ATPase activities. It is concluded that TMCA is better than colchicine for protecting the liver from BDL-induced cirrhosis and, due to its lower toxicity, can be used at higher and more effective doses without the common side-effects of colchicine, thus making TMCA a suitable compound to be studied in other hepatic lesions and in humans.
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PMID:Comparative study of colchicine and trimethylcolchicinic acid on prolonged bile duct obstruction in the rat. 881 70

Consumption of oil extracted from accidental or deliberate contamination of argemone seed to mustard seed is known to pose a clinical condition popularly referred to as Epidemic Dropsy. Several outbreaks of Epidemic Dropsy have occurred in the past in India as well as in Mauritius, Fiji Island, and South Africa. Clinico-epidemiological manifestations of argemone oil poisoning include vomiting, diarrhea, nausea, swelling of limbs, erythema, pitting edema, breathlessness, etc. In extreme cases, glaucoma and even death due to cardiac arrest have been encountered. The toxicity of argemone oil has been attributed to two of its physiologically active benzophenanthridine alkaloids, sanguinarine and dihydrosanguinarine. Histopathological studies suggest that liver, lungs, kidney, and heart are the target sites for argemone oil intoxication. Studies have shown to elucidate the cocarcinogenic potential of argemone oil that can be correlated with the binding of sanguinarine with a DNA template. Pharmacological response in intestine revealed immediate stimulation of tone and peristaltic movements of the gut in the sanguinarine-treated animals. Argemone oil/Sanguinarine caused a decrease in hepatic glycogen levels which may be due to the activation of glycogenolysis leading to an accumulation of pyruvate in the blood of Epidemic Dropsy cases. The increase in pyruvate levels causes uncoupling of oxidative phosphorylation leading to breathlessness, as observed in patients. Sanguinarine has been shown to inhibit Na+, K(+)-ATPase activity of different organs such as brain, heart, liver, intestine, and skeletal muscle, which may be due to the interaction with the glycoside receptor site on ATPase enzyme, thereby causing a decrease in the active transport of glucose. Argemone oil/alkaloid showed a Type II binding spectra with hepatic cytochrome P-450 (P-450) protein, thereby causing loss of P-450 content and an impairment of phase I and phase II enzymes. A green fluorescent metabolite of sanguinarine, benzacridine was detected in the milk of grazing animals. The delayed appearance of this metabolite in urine and feces of experimental animals suggests the slow elimination of the alkaloid. Argemone oil enhances hepatic microsomal and mitochondrial lipid peroxidation, indicating that these two organelles are the sites of membrane damage. Furthermore, studies suggest that singlet oxygen and hydroxyl radical are involved in argemone oil toxicity. Several bioantioxidants show protective effect in argemone oil-induced toxicity in experimental animals. The line of treatment in argemone-intoxicated epidemics has so far been only symptomatic, and specific therapeutic measures are still lacking, although it has been suggested that diuretics, bioantioxidants, steroids, vitamins, calcium- and protein-rich diet had some beneficial effects on Epidemic Dropsy cases.
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PMID:Clinicoepidemiological, toxicological, and safety evaluation studies on argemone oil. 918 56


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