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Comparison of the effects of stimulators and inhibitors of resorption on the release of lysosomal enzymes and radioactive calcium from fetal bone in organ culture. [/sup 45/Ca, rats]

Journal Article · · Endocrinology; (United States)
OSTI ID:6503364

The release of lysosomal enzymes, collagenase, and previously incorporated /sup 45/Ca from fetal rat long bones cultured in a chemically defined medium is compared. Parathyroid hormone (PTH) and prostaglandin E/sub 2/ increased the release of ..beta..-glucuronidase, acetylglucosaminidase, and cathepsin D, but showed little effect on collagenase activity in the medium at 48 h. The dose-response relations for ..beta..-glucuronidase and /sup 45/Ca release were similar. However, the increase in lysosomal enzyme release was proportionally greater and occurred earlier than the increase in /sup 45/Ca release. PTH also caused a significant increase in total ..beta..-glucuronidase activity in bone plus medium. Several agents which stimulate /sup 45/Ca release at an optimal concentration, but not at a higher concentration, including dibutyryl cAMP, isobutylmethylxanthine, and the calcium ionophore, A23187, all increased lysosomal enzyme release at the concentration which increased /sup 45/Ca release. Three inhibitors of bone resorption (calcitonin, cortisol, and colchicine) blocked lysosomal enzyme release at the same time that /sup 45/Ca release decreased. When the bones escaped from calcitonin inhibition, both /sup 45/Ca and lysosomalenzyme release increased. While colchicine blocked both lysosomal enzymes and /sup 45/CA release, it actually increased the release of bone collagenase, and together with PTH or prostaglandin E/sub 2/ caused a large increase in free collagenase activity in the medium. These data indicate that lysosomal enzyme release is closely linked to bone resorption and suggest that lysosomal enzymes may have a primary role in initiating resorption, perhaps by acting on noncollagenous matrix or tissue components before mineral removal and collagen degradation.

Research Organization:
Univ. of Connecticut Health Center, Farmington
OSTI ID:
6503364
Journal Information:
Endocrinology; (United States), Journal Name: Endocrinology; (United States) Vol. 103:6; ISSN ENDOA
Country of Publication:
United States
Language:
English

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