Brzóska M M, Majewska K, Moniuszko-Jakoniuk J
Department of Toxicology, Medical University of Białystok, Mickiewicza 2C, 15-222 Białystok, Poland.
Food Chem Toxicol. 2005 Oct;43(10):1507-19. doi: 10.1016/j.fct.2005.04.008.
The influence of exposure to cadmium (Cd) during skeletal development on the risk of bone fractures at the stage of skeletal maturity was investigated on a female rat model of human exposure. The tibias of rats treated with 1, 5 or 50 mg Cd/l in drinking water for 3, 6, 9 and 12 months (since weaning) were used. The exposure to Cd dose- and time-dependently influenced the tibia bone mineral density (BMD) and chemical composition. In skeletally matured animals, at each level of the exposure to Cd, the BMD at the whole tibia and its diaphysis as well as the percentage of minerals content in the bone, including the content of zinc, copper and iron, were decreased compared to control. Moreover, in the 50 mg Cd/l group, the percentage of organic components content increased. The Cd-induced changes, at all levels of exposure, resulted in weakening in the yield strength and fracture strength of the tibia (a three-point bending test of the diaphysis and compression test with vertical loading) of the skeletally matured females. A very important and clinically useful finding of this study is that a decrease (even by several percent) in the tibia BMD results in weakness in the bone biomechanical properties and that the BMD may predict the risk of its fracture at the exposure to Cd. Moreover, the results together with our previous findings seem to suggest that tibia, due to higher vulnerability of its diaphysis, compared to the femoral diaphysis, to damage by Cd may be more useful than femur to investigate the effect of Cd on the cortical bone. The present study revealed that a low exposure to Cd (1 mg Cd/l), corresponding to low human environmental exposure, during the skeletal development affects the tibia mineral status leading to weakening in its mechanical properties at the skeletal maturity. The findings allow for the conclusion that environmental exposure to Cd during childhood and adolescence may enhance the risk of low BMD and fractures at adulthood.
在人类暴露的雌性大鼠模型上，研究了骨骼发育期间接触镉（Cd）对骨骼成熟阶段骨折风险的影响。使用在饮用水中添加1、5或50 mg Cd/l处理3、6、9和12个月（自断奶起）的大鼠胫骨。镉暴露对胫骨骨矿物质密度（BMD）和化学成分有剂量和时间依赖性影响。在骨骼成熟的动物中，与对照组相比，在每个镉暴露水平下，整个胫骨及其骨干的BMD以及骨中矿物质含量的百分比，包括锌、铜和铁的含量均降低。此外，在50 mg Cd/l组中，有机成分含量的百分比增加。在所有暴露水平下，镉诱导的变化导致骨骼成熟雌性大鼠胫骨的屈服强度和断裂强度减弱（骨干的三点弯曲试验和垂直加载的压缩试验）。本研究一个非常重要且具有临床意义的发现是，胫骨BMD降低（即使降低几个百分点）会导致骨骼生物力学性能减弱，并且BMD可能预测镉暴露时的骨折风险。此外，这些结果与我们之前的发现似乎表明，由于胫骨骨干比股骨干更容易受到镉的损伤，因此在研究镉对皮质骨的影响方面，胫骨可能比股骨更有用。本研究表明，在骨骼发育期间低剂量接触镉（1 mg Cd/l），相当于低水平的人类环境暴露，会影响胫骨矿物质状态，导致其在骨骼成熟时机械性能减弱。这些发现可以得出结论，儿童期和青春期环境接触镉可能会增加成年期低BMD和骨折的风险。
