Iwami K, Moriyama T
Department of Public Health, Nara Medical University, Japan.
Arch Toxicol. 1993;67(5):352-7. doi: 10.1007/BF01973707.
Cadmium(Cd) has been thought to disturb the bone metabolism directly. The mechanism for the bone lesion is unknown, however. To examine the effects of cadmium on bone metabolism, we compared its effects on osteoblasts and osteoclasts in vitro. We used an established cell line, MC3T3-E1, as osteoblasts and tartrate resistant acid phosphatase (TRACP)-positive multi-nucleated cells (MNC) formed by a bone marrow culture system as osteoclasts. Alkaline phosphatase (ALP) activity was decreased by 10(-7) M Cd and DNA content and hydroxyproline content of osteoblastic cells were decreased by 10(-5) M Cd. Cadmium at 10(-7) M inhibited the osteoclastic cell formation from mouse bone marrow in the presence of 10(-8) M 1 alpha, 25(OH)2 vitamin D3. A 100-fold higher concentration of zinc(Zn) simultaneously added to the cadmium-containing medium prevented the toxicity of cadmium to osteoclastic cells as observed in the culture of osteoblastic cells. These results indicate that both bone formation and bone resorption are inhibited by cadmium. The responses of osteoclasts and osteoblasts to cadmium in this culture system were the same and the responses of cadmium-damaged osteoblasts and osteoclasts to zinc were also similar. These results suggest that another mechanism by which cadmium could cause bone damage should be considered in addition to the specific induction of osteoclastic cells by Cd.
镉(Cd)被认为会直接干扰骨代谢。然而,骨损伤的机制尚不清楚。为了研究镉对骨代谢的影响,我们在体外比较了其对成骨细胞和破骨细胞的作用。我们使用已建立的细胞系MC3T3-E1作为成骨细胞,并用骨髓培养系统形成的抗酒石酸酸性磷酸酶(TRACP)阳性多核细胞(MNC)作为破骨细胞。10^(-7) M的镉可降低碱性磷酸酶(ALP)活性,10^(-5) M的镉可降低成骨细胞的DNA含量和羟脯氨酸含量。在存在10^(-8) M 1α,25(OH)2维生素D3的情况下,10^(-7) M的镉抑制了小鼠骨髓中破骨细胞的形成。在含镉培养基中同时添加高100倍浓度的锌(Zn),可防止镉对破骨细胞的毒性,这与在成骨细胞培养中观察到的情况相同。这些结果表明,镉同时抑制骨形成和骨吸收。在该培养系统中,破骨细胞和成骨细胞对镉的反应相同,镉损伤的成骨细胞和破骨细胞对锌的反应也相似。这些结果表明,除了镉对破骨细胞的特异性诱导外,还应考虑镉导致骨损伤的另一种机制。