Burnatowska-Hledin M A, Doyle T M, Eadie M J, Mayor G H
J Lab Clin Med. 1986 Aug;108(2):96-102.
We examined the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in both hypercalcemic and hypocalcemic rat models and the effect of exogenous 25-hydroxyvitamin D3 (25(OH)D3) on serum and tissue aluminum (Al) burdens. Rats fed a 0.2% Al diet received daily subcutaneous injections of either 1,25(OH)2D3 (80.9 ng/kg, n = 5 and 809 ng/kg, n = 8), 25 (OH)D3 (809 ng/kg, n = 4, and 8090 ng/kg, n = 8) or propylene glycol vehicle for 18 days. Rats given 809 ng/kg of 1,25(OH)2D3 were hypercalcemic and when compared with pair-fed controls had higher serum (33.1 vs. 14.3 micrograms/L, P less than 0.01), bone (21.2 vs. 13.2 micrograms/gm, P less than 0.01), and kidney (6.5 vs. 2.0 micrograms/gm, P less than 0.01) but not brain (1.2 vs. 1.5 micrograms/gm) or liver (0.9 vs. 0.8 micrograms/gm dry tissue) Al concentration. The lower dose of 1,25(OH)2D3 had no effect on serum or tissue Al. Treatment with 25(OH)D3 did not increase serum Ca and Al or tissue Al concentration. To dissociate a specific effect of exogenous 1,25(OH)2D3 from the concurrent hypercalcemia, endogenous production of 1,25(OH)2D3 was stimulated. Animals were fed a low Ca diet until hypocalcemia developed and were then divided into four groups: one given low Ca (n = 7) for 21 days, one given low Ca plus 0.2% Al (n = 7) for 21 days, one returned to a normal Ca diet (n = 4) for 30 days, and one returned to a normal Ca diet for 9 days and continued with a normal diet plus 0.2% Al (n = 5) for 21 days. Hypocalcemic rats fed the Al diet, when compared with hypocalcemic controls, had higher serum (143.6 vs. 31.8 micrograms/L, P less than 0.01), bone (16.0 vs. 2.9 micrograms/gm, P less than 0.01), and kidney (8.2 vs. 2.8 micrograms/gm, P less than 0.005) but not brain (3.4 vs. 2.3 micrograms/gm) or liver (3.8 vs. 2.3 micrograms/gm) Al concentrations. Serum, bone, and kidney Al concentration was also significantly higher than that in normocalcemic rats fed the Al diet. These results indicate that pharmacologic doses of 1,25(OH)2D3 and dietary hypocalcemia enhance gastrointestinal Al absorption and serum, kidney, and bone Al concentration.
我们研究了1,25 - 二羟维生素D3（1,25(OH)2D3）在高钙血症和低钙血症大鼠模型中的作用，以及外源性25 - 羟维生素D3（25(OH)D3）对血清和组织铝（Al）负荷的影响。喂食0.2%铝饮食的大鼠每天皮下注射1,25(OH)2D3（80.9 ng/kg，n = 5和809 ng/kg，n = 8）、25(OH)D3（809 ng/kg，n = 4和8090 ng/kg，n = 8）或丙二醇载体，持续18天。给予809 ng/kg 1,25(OH)2D3的大鼠出现高钙血症，与配对喂食的对照组相比，血清（33.1对14.3微克/升，P小于0.01）、骨骼（21.2对13.2微克/克，P小于0.01）和肾脏（6.5对2.0微克/克，P小于0.01）中的铝浓度更高，但脑（1.2对1.5微克/克）或肝脏（0.9对0.8微克/克干组织）中的铝浓度无差异。较低剂量的1,25(OH)2D3对血清或组织铝无影响。用25(OH)D3治疗未增加血清钙、铝或组织铝浓度。为了将外源性1,25(OH)2D3的特定作用与同时发生的高钙血症区分开来，刺激了1,25(OH)2D3的内源性产生。动物喂食低钙饮食直至出现低钙血症，然后分为四组：一组给予低钙饮食（n = 7）21天，一组给予低钙饮食加0.2%铝（n = 7）21天，一组恢复正常钙饮食（n = 4）30天，一组恢复正常钙饮食9天，然后继续正常饮食加0.2%铝（n = 5）21天。与低钙血症对照组相比，喂食铝饮食的低钙血症大鼠血清（143.6对31.8微克/升，P小于0.01）、骨骼（16.0对2.9微克/克，P小于0.01）和肾脏（8.2对2.8微克/克，P小于0.005）中的铝浓度更高，但脑（3.4对2.3微克/克）或肝脏（3.8对2.3微克/克）中的铝浓度无差异。血清、骨骼和肾脏中的铝浓度也显著高于喂食铝饮食的正常钙血症大鼠。这些结果表明，药理剂量的1,25(OH)2D3和饮食性低钙血症会增强胃肠道铝吸收以及血清、肾脏和骨骼中的铝浓度。
