Brzóska Malgorzata M, Moniuszko-Jakoniuk Janina
Department of Toxicology, Medical University of Białystok, Mickiewicza 2C street, 15-222 Białystok, Poland.
Toxicol Sci. 2004 Dec;82(2):468-77. doi: 10.1093/toxsci/kfh275. Epub 2004 Sep 16.
In this study, based on a rat model of human environmental exposure to cadmium (Cd), it has been examined whether low-level lifetime Cd exposure increases the risk of vertebral osteoporosis and vertebrae fractures in the elderly. For this purpose, the lumbar vertebral bodies (L4 or L3) of control and Cd-exposed (1 mg Cd/l in drinking water for 24 months) female Wistar rats were assigned to densitometric, radiographic, biomechanical (compression test), and biochemical studies, as well as to assess their dimensions and chemical composition. The exposure to Cd affected the mineral status of the L4. The decreased mineral content, density (BMD) and bone mineral area of the vertebral body together with the unchanged ratio of non-organic and organic components indicate osteoporotic nature of the Cd-induced changes. The activity of alkaline phosphatase in the L3 decreased. Cd also influenced the mechanical properties of the L4. The yield load and ultimate load decreased indicating a weakness in the vertebral body compression strength. Stiffness of the L4 decreased and the displacement at ultimate increased suggesting its enhanced susceptibility to deformities. Indeed, in the Cd group vertebral deformities (in 30% of females) or even fractures (in 40% of females), including those with disruption of bone continuity were evident. Z-score values for the L4 BMD revealed vertebral osteopenia in 30% and osteoporosis in 70% of the Cd-exposed females. The results allow for the conclusion that low lifetime exposure to Cd may become an important factor increasing the risk of lumbar spine osteoporosis with vertebral deformities and fractures in the elderly.
在本研究中,基于人类环境镉(Cd)暴露的大鼠模型,研究了低水平终生镉暴露是否会增加老年人椎体骨质疏松和椎体骨折的风险。为此,将对照组和镉暴露组(饮用水中含1 mg Cd/l,持续24个月)雌性Wistar大鼠的腰椎椎体(L4或L3)用于骨密度测定、放射学、生物力学(压缩试验)和生化研究,以及评估其尺寸和化学成分。镉暴露影响了L4的矿物质状态。椎体矿物质含量、密度(BMD)和骨矿物质面积降低,同时无机和有机成分比例不变,表明镉诱导的变化具有骨质疏松的性质。L3中碱性磷酸酶的活性降低。镉还影响了L4的力学性能。屈服载荷和极限载荷降低,表明椎体抗压强度减弱。L4的刚度降低,极限位移增加,表明其对畸形的易感性增强。事实上,在镉组中,椎体畸形(30%的雌性)甚至骨折(40%的雌性)明显,包括那些骨连续性中断的情况。L4 BMD的Z评分显示,30%的镉暴露雌性存在椎体骨质减少,70%存在骨质疏松。结果表明,终生低剂量镉暴露可能成为增加老年人腰椎骨质疏松伴椎体畸形和骨折风险的一个重要因素。