Ljunggren O, Fredholm B B, Lerner U H
Department of Oral Pathology, Umeå University, Sweden.
Acta Physiol Scand. 1991 Jun;142(2):267-73. doi: 10.1111/j.1748-1716.1991.tb09156.x.
In order to elucidate the possible role of polyamines in the mobilization of mineral from long-term bone cultures stimulated with parathyroid hormone we have measured the activity of ornithine decarboxylase in osteoblasts, the levels of polyamines in calvarial bone and determined the effect of added polyamines and inhibitors of polyamine biosynthesis on calcium mobilization. Parathyroid hormone (10 nmol l-1) stimulated omithine decarboxylase activity by approximately 50% in both cultured bone cells of osteoblastic phenotype, UMR 106 and in mouse calvarial osteoblast-like cells. In mouse calvaria the levels of putrescine and spermidine were increased by parathyroid hormone after 24 hours. The levels of spermine were very low and were unchanged by parathyroid hormone. The two polyamine synthesis inhibitors alpha-difluoromethylornithine (DFMO; 2 mmol l-1) and methylglyoxal-bis-guanylhydrazone (MGBG; 50 mu mol l-1) did not significantly affect the mobilization of 45Ca from parathyroid hormone-stimulated bones. All three polyamines, putrescine, spermidine and spermine, inhibited the mobilization of 45Ca induced by parathyroid hormone in a dose-dependent manner. The inhibition induced by putrescine was reversible. In summary, we have shown that parathyroid hormone increases the accumulation of polyamines in bone, but the effect is small. Furthermore, inhibition of polyamine biosynthesis does not reduce parathyroid hormone-induced mineral mobilization and the addition of polyamines leads to a reduced rather than a stimulated mineral mobilization. Thus, polyamines do not seem to be critically involved in the changes in bone resorption induced by parathyroid hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
为了阐明多胺在甲状旁腺激素刺激的长期骨培养物中矿物质动员过程中可能发挥的作用，我们测定了成骨细胞中鸟氨酸脱羧酶的活性、颅盖骨中多胺的水平，并确定了添加的多胺和多胺生物合成抑制剂对钙动员的影响。甲状旁腺激素（10 nmol l-1）在成骨细胞表型的培养骨细胞UMR 106和小鼠颅盖成骨样细胞中，使鸟氨酸脱羧酶活性提高了约50%。在小鼠颅盖骨中，24小时后腐胺和亚精胺水平因甲状旁腺激素而升高。精胺水平非常低，且不受甲状旁腺激素影响。两种多胺合成抑制剂α-二氟甲基鸟氨酸（DFMO；2 mmol l-1）和甲基乙二醛双脒腙（MGBG；50 μmol l-1）对甲状旁腺激素刺激的骨骼中45Ca的动员没有显著影响。腐胺、亚精胺和精胺这三种多胺均以剂量依赖方式抑制甲状旁腺激素诱导的45Ca动员。腐胺诱导的抑制作用是可逆的。总之，我们已经表明甲状旁腺激素会增加骨中多胺的积累，但作用较小。此外，抑制多胺生物合成并不会降低甲状旁腺激素诱导的矿物质动员，而添加多胺会导致矿物质动员减少而非增强。因此，多胺似乎并非关键参与甲状旁腺激素诱导的骨吸收变化。（摘要截短至250字）
