Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of cimetidine on the dynamic transmucosal potential difference (PD) of the normal human gastric fundus was studied, to quantitate the influence of the hydrogen ion on measurements. PD was measured between an intravenous flowing bridge of isotonic NaCl and a perfused intragastric probe by means of two calomel half-cells. The probe was used for luminal infusion of different electrolyte solutions, which at the same time functioned as the mucosal measuring electrode. Cimetidine increased PD -12 mV during NaCl infusion. When gastric acidity was neutralized with isotonic NaHCO3, this change of PD decreased to -5 mV. We conclude that 60% of the PD increase seen after H2 blockade may be explained by the mere disappearance of H+ from the gastric juice, and the other 40% by changes in the gastric mucous membrane. PD decreased progressively as luminal NaCl content was lowered, but this reaction was reversed after cimetidine. These findings may be explained by a twofold decrease of transmucosal permeability to Na+ during H2 blockade.
 ...
PMID:The potential difference response of the human gastric mucosa to cimetidine. 239 81

Regulation of the acidity of osteoclasts was determined in situ on the endocranial surfaces of mouse calvaria using acridine orange, a fluorescent weak base. Osteoclasts could be identified by large size, multiple nuclei, relatively small numbers of cells, and the way and the extent to which they took up the dye. Nonosteoclastic cells were stained mainly in their nuclei and occasionally in a few lysosomes surrounding their nuclei, which were uniformly single in nonosteoclasts. Nuclei in osteoclasts were also stained, but the staining of the nuclei was partially masked by the intensity and completeness of the staining of the cytoplasm. In some cells the cytoplasmic staining appeared to be in discrete granules, giving the cytoplasm a bright, frothy appearance. This fluorescence was present in both treated and untreated cells and aided in identifying the osteoclasts. Acridine orange fluorescence at 624 nm intensity, and hence, osteoclast acidity, was increased by parathyroid hormone and prostaglandin E2. Parathyroid hormone-induced increases in acidity were inhibited by calcitonin, cortisol, sodium fluoride, and prostaglandin E2. Furthermore, osteoclast acidity was dependent largely or partially on maintenance of K+ and Na+ gradients, patent Na+ channels, chloride-bicarbonate exchange, and H+, K+-ATPase. These findings demonstrate that osteoclasts become acidified by mechanisms similar to those occurring in gastric parietal cells.
 ...
PMID:Humoral and ionic regulation of osteoclast acidity. 243 48

Ammonia production increases in several models of renal hypertrophy in vivo. The present study was designed to determine whether ammonia can directly modulate the growth of renal cells in the absence of a change in extracellular acidity. In serum-free media NH4Cl (0-20 mM) caused JTC cells and a primary culture of rabbit proximal tubule cells to hypertrophy (increase in cell protein content) in a dose-dependent fashion without a change in DNA synthesis. Studies in JTC cells revealed that the cell protein content increased as a result of both an increase in protein synthesis and a decrease in protein degradation. Total cell RNA content and ribosome number increased after NH4Cl exposure and the cell content of the lysosomal enzymes cathepsin B and L decreased. Inhibition of the Na+/H+ antiporter with amiloride did not prevent the hypertrophic response induced by NH4Cl. The results indicate that ammonia is an important modulator of renal cell growth and that hypertrophy can occur in the absence of functioning Na+/H+ antiport activity.
 ...
PMID:Induction of hypertrophy in cultured proximal tubule cells by extracellular NH4Cl. 248 Mar 66

Induced physiologic changes in the gastric mucosa was investigated both in the presence of normal gastric acidity and after parietal cell vagotomy (PCV), in dogs. Cholecystogastrostomy and common bile duct ligation was performed in eleven and PCV was added to this procedure in five dogs. During histopathological examination, 70 days after the procedure, both groups proved to have superficial gastritis. The most prominent changes occurred at the anastomotic site and at the gastric antrum. Bile had broken down the gastric mucosal barrier and the Na+ flux roughly paralleled the H+ back diffusion. Potassium had taken part in the bi-directional movement of ions in the gastric mucosa, as well as the sodium flux, and in the late phase it accompanied the action of sodium ions. The destruction of the K+-H+ pump, possibly located in the plasma membrane, may be the responsible mechanism of this flux.
 ...
PMID:The effect of bile on the gastric mucosal barrier in the presence and after blockade of normal gastric acidity. 251 46

Measurement of pH in tissue has shown that the microenvironment in tumors is generally more acidic than in normal tissues. Major mechanisms which lead to tumor acidity probably include the production of lactic acid and hydrolysis of ATP in hypoxic regions of tumors. Further reduction in pH may be achieved in some tumors by administration of glucose (+/- insulin) and by drugs such as hydralazine which modify the relative blood flow to tumors and normal tissues. Cells have evolved mechanisms for regulating their intracellular pH. The amiloride-sensitive Na+/H+ antiport and the DIDS-sensitive Na+-dependent HCO3-/Cl- exchanger appear to be the major mechanisms for regulating pHi under conditions of acid loading, although additional mechanisms may contribute to acid extrusion. Mitogen-induced initiation of proliferation in some cells is preceded by cytoplasmic alkalinization, usually triggered by stimulation of Na+/H+ exchange; proliferation of other cells can be induced without prior alkalinization. Mutant cells which lack Na+/H+ exchange activity have reduced or absent ability to generate solid tumors; a plausible explanation is the failure of such mutant cells to withstand acidic conditions that are generated during tumor growth. Studies in tissue culture have demonstrated that the combination of hypoxia and acid pHe is toxic to mammalian cells, whereas short exposures to either factor alone are not very toxic. This interaction may contribute to cell death and necrosis in solid tumors. Acidic pH may influence the outcome of tumor therapy. There are rather small effects of pHe on the response of cells to ionizing radiation but acute exposure to acid pHe causes a marked increase in response to hyperthermia; this effect is decreased in cells that are adapted to low pHe. Acidity may have varying effects on the response of cells to conventional anticancer drugs. Ionophores such as nigericin or CCCP cause acid loading of cells in culture and are toxic only at low pHc; this toxicity is enhanced by agents such as amiloride or DIDS which impair mechanisms involved in regulation of pHi. It is suggested that acid conditions in tumors might allow the development of new and relatively specific types of therapy which are directed against mechanisms which regulate pHi under acid conditions.
 ...
PMID:Acid pH in tumors and its potential for therapeutic exploitation. 254 40

The bioavailability of sulpiride taken in film-coated tablet form with sodium bicarbonate or cimetidine or with natural orange juice or diluted hydrochloric acid was studied. A commercial sulpiride film-coated tablet (100 mg/T) treated with polyvinylacetal diethylaminoacetate (AEA), which remain undissolved at pH above 4-5, was given to four healthy volunteers who had fasted overnight. The subjects were divided into two groups, those showing high and low bioavailability of sulpiride from an AEA film-coated tablet. The two high bioavailability subjects took one tablet (100 mg) with 100 ml of water (1) alone, (2) together with 1 g of sodium bicarbonate or (3) during concurrent dosing with cimetidine, 200 mg three times a day. The two low bioavailability subjects swallowed one tablet with 100 ml of (1) water, (2) natural orange juice, or (3) diluted hydrochloric acid. Urine samples were collected over a 48-h period following sulpiride administration to determine sulpiride concentrations by HPLC. The bioavailability was estimated from the cumulative amount excreted unchanged in urine over 48 h (Du48). In the high bioavailability subjects, the bioavailability of sulpiride markedly decreased with the coadministration of sodium bicarbonate or cimetidine compared to when the tablet was taken alone. In the low bioavailability subjects, the bioavailability remarkably increased with the concomitant intake of orange juice or diluted hydrochloric acid over that with only water. These results suggest that the bioavailability of sulpiride from AEA film-coated tablet is influenced by the individual's gastric acidity and by coadministered drug and drink which affect gastric acidity.
 ...
PMID:The bioavailability of sulpiride taken as a film-coated tablet with sodium bicarbonate, cimetidine, natural orange juice or hydrochloric acid. 255 11

Fresh Cheddar cheese whey was inoculated with ca. 10(6) Staphylococcus aureus/ml and held at 4, 25, and 37 degrees C for 48 h. Numbers of staphylococci decreased in whey at 25 and 37 degrees C and decreased or remained constant in whey at 4 degrees C. When Cheddar cheese whey was neutralized with sodium hydroxide before inoculation with ca. 10(2) or 10(6) S. aureus/ml, numbers of the bacterium increased at all incubation temperatures. Viability of S. aureus strains in whey butter made from inoculated whey cream (from Cheddar cheese whey) was determined. Whey cream was either neutralized to a titratable acidity of .15% or untreated before inoculation with ca. 10(4) S. aureus/ml. Butter churned from the whey cream was held at 4, 25, and 30 degrees C for up to 4 wk. Viability of S. aureus was enhanced in lightly salted (1%) whey cream butter and in butter made from neutralized whey cream. Strains of S. aureus did not survive in unsalted or in salted (1.5%) butter made from untreated whey cream.
 ...
PMID:Fate of Staphylococcus aureus in whey, whey cream, and whey cream butter. 262 38

This study was conducted to determine the effect of a high protein diet on calcium metabolism in rat. Wistar strain male rats (50 days old) were divided into 5 groups (day 0): control diet (18% casein); high protein diet (18% casein +20% lactalbumin); high protein and 0.1% sodium bicarbonate diet; high protein and 0.2% sodium bicarbonate diet; and high protein and 0.4% sodium bicarbonate diet. On days 0, 1, 3, 5, 7, 9, urine samples were collected and, at the same time, feces were collected from half of the animals in each group. Urinary titratable acidity (TA-HCO3-), ammonium ion (NH4+), and net acid excretion (NAE) were measured as an index of acid-base balance in rat body. Urinary volume was rapidly increased and the increase of urinary volume continued throughout the study in rats fed the high protein diet. Urinary excretions of calcium and phosphorus were increased after day 3 and day 1, respectively, in rats fed the high protein diet. The high protein diet depressed calcium absorption and elevated phosphorus absorption from the digestive tract in rats fed the high protein diet. The high protein diet decreased TA-HCO3-, which was closely correlated with the decrease of NAE. Sodium bicarbonate supplementation to the high protein diet had little effect on urinary calcium excretion and NAE. This study suggested that there was no relationship between metabolic acidosis and hypercalciuria in rats fed the high protein diet.
 ...
PMID:Effects of high protein diet and sodium bicarbonate supplementation on calcium metabolism in rats. 263 82

Cells of Schizosaccharomyces pombe TMB 1138, which are capable of metabolizing-malate, was immobilized in calcium alginate gel to carry out maloalcoholic fermentation. Four milliliters of cell suspension containing about 2.0 X 10(7) cells were entrapped in 16 ml of sodium alginate solution in order to prepare 2% Na-alginate (w/v) gel bead. After activation by incubating at 28 degrees C for 24 h in grape juice, 300 beads of immobilized cells were inoculated into the fermentation medium. After fermentation was proceeded at 25 or 28 degrees C for 24 h by shaking, it could metabolize L-malate completely and the total acidity was also reduced. Under the same condition for batch fermentation, it was found that the utilization of L-malic acid was over 97% for the first 7 days in fermentation medium, 85% for the first 4 days in grape juice and 87% for the first 4 days in wine. Furthermore, for the continuous fermentation in wine, the conversion of L-malic acid reached 92% in 24 h and could be maintained at 75% in the following 9 days.
 ...
PMID:Maloalcoholic fermentation by immobilized Schizosaccharomyces pombe. 263 4

Sucralfate protects the stomach against a number of experimental damaging agents and is efficacious in the treatment of peptic ulcer disease. It binds with acidity to the base of an ulcer to form a protective barrier. Sucralfate also enhances prostaglandin synthesis and release in the mucosa. In this study, the rat stomach was examined to determine sucralfate's interaction with gastric mucus. Mucus in the rat stomach forms a distinct and continuous blanket. In snap-frozen samples, pretreatment with phosphate-buffered saline as a control shows a layer of mucus of homogeneous structure thinner than the homogeneous layer after pretreatment with antibodies developed against rat gastric mucus. Pretreatment with the surface protective agent sucralfate shows some increase in the thickness of mucus with a thin dense sublayer adjacent to the epithelium and a less dense-appearing outer zone of variable thickness. Analysis of x-rays generated by the electron beam on windows of mucus and epithelium showed the expected gradients of sodium, potassium, chloride, and sulfur. The percentage of aluminum and sulfur in the mucus was higher in sucralfate-treated samples than in controls. Interaction between sucralfate and gastric mucus needs further investigation.
 ...
PMID:Sucralfate interactions with gastric mucus. 273 36


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>