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Characterization of isolated and cultured chick osteoclasts: The effects of acetazolamide, calcitonin, and parathyroid hormone on acid production
Author(s) -
Hunter Susan J.,
Schraer Harald,
Gay Carol V.
Publication year - 1988
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650030308
Subject(s) - acetazolamide , calcitonin , parathyroid hormone , endocrinology , medicine , chemistry , carbonic anhydrase , intracellular ph , acid phosphatase , carbonic anhydrase inhibitor , calcium , intracellular , biochemistry , enzyme
The effects of acetazolamide, calcitonin (CT), and parathyroid hormone (PTH) on acid production in isolated osteoclasts has been investigated. Osteoclasts were isolated from the endosteum of 3‐week chick tibias and were maintained under culture conditions for 5 days. The cells were treated with acetazolamide (10 ×4 M and 10 −7 M ), CT (1 mU/ml and 0.31 mU/ml) and PTH (6.5 U/ml and 0.40 U/ml) for 1, 3, 6, and 18 hr. The cells were stained with acridine orange and the intensity of fluorescence measured by a light microscope photometer. Acetazolamide treatment resulted in a steady decline in intracellular acidity, suggesting that carbonic anhydrase plays a major role in acid production in isolated osteoclasts. Treatment with PTH produced a decline in acidity at 1 hr, followed by a peak at 3 hr and then a decline at 6 and 18 hr. The transient increase in acidity may be due to activation of carbonic anhydrase by PTH. Calcitonin treatment also resulted in a decline in cell acidity which was similar, but less pronounced than that resulting from acetazolamide treatment. These results indicate that calcitonin may mediate osteoclast activity by alterations in intracellular acid production.