Alekseeva I A, Spiricheva V B, Blazhevich N V, Sokolova S V, Pereverzeva O G
Vopr Med Khim. 1982 Sep-Oct;28(5):71-8.
Deficiency of vitamin D in rats led to impairment of Ca2+ absorption in intestine, hypocalcemia, decrease in specific weight of femur diaphyses, decrease in content of Ca2+ and in the ratio Ca2+/hydroxyproline in diaphyses and epiphyses. These patterns were normalized after daily administration of cholecalciferol (vitamin D3) at a dose of 500 ng (20 IU) into rats within 5 days. I alpha, 25-dihydroxycalciferol at a daily dose of 30 ng stimulated absorption of Ca2+ in intestine, increased the specific weight of diaphyses and content of Ca2+ in diaphysis, but content of Ca2+ in blood and epiphyses was not normalized. Increase in 1,25 (OH)2D3 dose up to 300 ng caused a decrease in the rate of mineralization of diaphyses and epiphyses with simultaneous elevation of the Ca2+ content in blood. 24, 25-dihydroxycalciferol at a dose of 250 ng stimulated effectively both diaphyses and epiphyses mineralization, at the same time the effect was also maintained after 10-fold increase of the dose.
大鼠维生素D缺乏导致肠道钙吸收受损、低钙血症、股骨骨干比重降低、骨干和骨骺中钙含量及钙/羟脯氨酸比值降低。在5天内每天给大鼠腹腔注射500 ng(20 IU)胆钙化醇(维生素D3)后,这些指标恢复正常。每天剂量为30 ng的1α,25-二羟维生素D3刺激肠道钙吸收,增加骨干比重和骨干钙含量,但血液和骨骺中的钙含量未恢复正常。将1,25(OH)2D3剂量增加至300 ng会导致骨干和骨骺矿化速率降低,同时血液中钙含量升高。剂量为250 ng的24,25-二羟维生素D3有效刺激骨干和骨骺矿化,同时剂量增加10倍后效果依然维持。