Lerner U, Fredholm B B
Biochim Biophys Acta. 1983 May 25;757(2):226-34. doi: 10.1016/0304-4165(83)90113-7.
The effect of 2-chloroadenosine on bone resorption was studied in calvarial bones from 6-7-day-old mice in organ culture. 2-Chloroadenosine stimulated the mobilization of minerals (40Ca, 45Ca) and increased the degradation of matrix ([3H]proline) from the bones. The nucleoside also caused an increased release of beta-glucuronidase, a lysosomal enzyme. In doses above 30 microM 2-chloroadenosine was cytotoxic, as evidenced by an increased release of lactate dehydrogenase. 2-Chloroadenosine-stimulated resorption could be inhibited by calcitonin, increased concentration of phosphate in culture medium, cortisone, dexamethasone, indomethacin, naproxen, meclofenamic acid and 5,8,11,14-eicosatetraynoic acid. 2-Chloroadenosine was much more sensitive to inhibition by dexamethasone than was parathyroid hormone. The response to the maximal dose of 2-chloroadenosine could not be enhanced by parathyroid hormone, 1 alpha-hydroxyvitamin D-3 and prostaglandin E2. An exposure to 2-chloroadenosine for 12 h was not sufficient to produce prolonged resorption. The results suggest that 2-chloroadenosine stimulated bone resorption by a process which is dependent on osteoclastic activity. The possibility that the effect of 2-chloroadenosine, either directly or indirectly, is related to formation of prostaglandins is discussed in the light of the above data.
在器官培养中，研究了2-氯腺苷对6-7日龄小鼠颅骨骨吸收的影响。2-氯腺苷刺激了矿物质（40Ca、45Ca）的动员，并增加了骨基质（[3H]脯氨酸）的降解。该核苷还导致溶酶体酶β-葡萄糖醛酸酶的释放增加。剂量高于30μM时，2-氯腺苷具有细胞毒性，乳酸脱氢酶释放增加证明了这一点。降钙素、培养基中磷酸盐浓度增加、可的松、地塞米松、吲哚美辛、萘普生、甲氯芬那酸和5,8,11,14-二十碳四烯酸可抑制2-氯腺苷刺激的骨吸收。2-氯腺苷比甲状旁腺激素对地塞米松的抑制作用更敏感。甲状旁腺激素、1α-羟基维生素D-3和前列腺素E2不能增强对最大剂量2-氯腺苷的反应。暴露于2-氯腺苷12小时不足以产生长期的骨吸收。结果表明，2-氯腺苷通过依赖破骨细胞活性的过程刺激骨吸收。根据上述数据，讨论了2-氯腺苷的作用直接或间接与前列腺素形成相关的可能性。
