Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, 210009 Nanjing, China.
Nutrients. 2019 Apr 15;11(4):849. doi: 10.3390/nu11040849.
Estimation of the skeleton-protective effects of Ca in Cd-induced bone damage is helpful in the assessment of Cd health risk. The aim of this study was to identify whether Ca supplementation during exposure to different population-relevant doses of Cd can prevent Cd-induced bone damage under the tolerable upper intake level of Ca supplementation. Young female Sprague-Dawley rats were given different population-relevant doses of Cd (1, 5, and 50 mg Cd/kg diet) and Ca supplementation (0.4% Ca supplementation) intervention. Ca supplementation significantly decreased Cd-induced bone microstructure damage, increased bone biomechanics ( < 0.05), serum bone formation marker level ( < 0.05) and expression of osteogenic gene markers exposure to the 5 and 50 mg Cd/kg diets. However, it had no impact on these indicators under the 1 mg Cd/kg diets, with the exception of expression of osteogenic marker genes. Ca supplementation significantly decreased serum Klotho level ( < 0.05), and fibroblast growth factor 23/Klotho-associated gene expression in the kidney and bone showed significant changes. In conclusion, Ca supplementation has a positive effect on bone formation and bone quality against the damaging impact of Cd, especially with exposure to the 5 mg and 50 mg Cd/kg diet, which may be related to its impact on the fibroblast growth factor 23/Klotho axis.
评估钙在镉诱导的骨骼损伤中的保护作用有助于评估镉的健康风险。本研究旨在确定在可耐受的钙补充摄入量水平下,暴露于不同人群相关剂量的镉时补充钙是否可以预防镉诱导的骨骼损伤。将年轻雌性 Sprague-Dawley 大鼠给予不同人群相关剂量的镉(1、5 和 50mg/kg 饮食)和钙补充(0.4% 钙补充)干预。钙补充显著降低了镉诱导的骨微结构损伤,增加了骨生物力学(<0.05)、血清骨形成标志物水平(<0.05)和骨生成基因标志物的表达,而暴露于 5 和 50mg/kg 饮食中的这些标志物没有影响,除了骨生成标志物基因的表达。钙补充显著降低了血清 Klotho 水平(<0.05),肾脏和骨骼中成纤维细胞生长因子 23/Klotho 相关基因的表达也发生了显著变化。总之,钙补充对骨骼形成和骨质量具有积极作用,可抵抗镉的破坏作用,尤其是在摄入 5mg 和 50mg/kg 镉饮食时,这可能与其对成纤维细胞生长因子 23/Klotho 轴的影响有关。