Brzóska Małgorzata M, Majewska Katarzyna, Moniuszko-Jakoniuk Janina
Department of Toxicology, Medical University of Białystok, Mickiewicza 2c, 15-222 Białystok, Poland.
Arch Toxicol. 2005 May;79(5):277-88. doi: 10.1007/s00204-005-0650-z. Epub 2005 Apr 1.
This study was aimed at assessing the effect of cadmium (Cd) intoxication on the risk of deformities and fractures of the growing bone on a female rat model of human exposure to this metal. For this purpose, bone mineral density (BMD) and mechanical properties of the proximal and distal ends and diaphysis of the femur were investigated in female Wistar rats exposed to 1, 5, and 50 mg Cd L(-1) in drinking water for 3, 6, 9, and 12 months since weaning. Daily Cd doses received from the drinking water during the treatment period were in the ranges 0.059-0.219, 0.236-1.005, and 2.247-9.649 mg kg(-1) body weight at 1, 5, and 50 mg Cd L(-1), respectively. Biomechanical properties of the femoral proximal and distal ends were evaluated in a compression test and those of the femoral diaphysis in a cutting test with loading perpendicular to the bone longitudinal axis in all tests. Cd dose- and exposure duration-dependently affected the mineralization and mechanical properties of the bone tissue at various locations of the femur. Exposure to 1 mg Cd L(-1) (corresponding to low human exposure) during skeletal development weakened the fracture strength of the femoral neck and of the trabecular bone at the level of the distal end of the femur and affected the elastic properties of the cortical bone at the femoral diaphysis. At the higher levels of Cd treatment, the adverse action generally occurred after shorter exposure than at 1 mg Cd L(-1) and was more seriously advanced. The Cd-induced weakening in the bone biomechanical properties at particular sites of the femur correlated with the decreased bone mineralization. The results indicate that even low exposure to Cd may affect the mineralization and biomechanical properties of growing bone, thus increasing the risk of fractures.
本研究旨在通过人类暴露于镉（Cd）的雌性大鼠模型，评估镉中毒对生长中骨骼畸形和骨折风险的影响。为此，对断奶后饮用含1、5和50 mg Cd L(-1)的饮用水3、6、9和12个月的雌性Wistar大鼠的股骨近端、远端和骨干的骨矿物质密度（BMD）及力学性能进行了研究。在治疗期间，从饮用水中摄入的每日镉剂量分别为1、5和50 mg Cd L(-1)时，体重每千克分别为0.059 - 0.219、0.236 - 1.005和2.247 - 9.649 mg。在所有测试中，通过压缩试验评估股骨近端和远端的生物力学性能，通过垂直于骨纵轴加载的切割试验评估股骨干的生物力学性能。镉剂量和暴露持续时间对股骨不同部位的骨组织矿化和力学性能有依赖性影响。在骨骼发育期间暴露于1 mg Cd L(-1)（相当于人类低暴露水平）会削弱股骨颈和股骨远端小梁骨的骨折强度，并影响股骨干皮质骨的弹性性能。在较高镉处理水平下，一般比1 mg Cd L(-1)暴露更短时间后就会出现不良作用，且更为严重。镉诱导的股骨特定部位骨生物力学性能减弱与骨矿化减少相关。结果表明，即使低水平暴露于镉也可能影响生长中骨骼的矿化和生物力学性能，从而增加骨折风险。
