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)

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.
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PMID:Humoral and ionic regulation of osteoclast acidity. 243 48

Changes in the acidity of osteoclasts were evaluated by direct measurement of the fluorescent intensity of osteoclasts exposed to acridine orange, a fluorescent weak base which becomes concentrated in acid-containing subcellular compartments. Parathyroid hormone (PTH) produced dose-dependent increases in fluorescent intensity; maximal increases in intensity occurred at doses between 3 and 10 micrograms PTH/ml of culture medium. Acetazolamide, a potent inhibitor of carbonic anhydrase, inhibited the increase in fluorescence induced by PTH, but this drug was less effective in reducing fluorescence in maximally than in submaximally stimulated osteoclasts, indicating that either more enzyme or more resistant enzyme was present in the PTH-stimulated cells. Because increased fluorescence of acridine orange is a sign of greater acidity, these results suggest that (1) PTH stimulates the acidity of osteoclasts, (2) carbonic anhydrase activity is necessary for maximum acidity, and (3) carbonic anhydrase is activated by PTH.
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PMID:Stimulation of carbonic anhydrase in osteoclasts by parathyroid hormone. 393 90