Adequate dietary calcium mitigates osteopenia induced by chronic lead exposure in adult rats.

H E Gruber, Y Ding, A A Stasky, M Meyer, M R Pandian, D Pandian, N D Vaziri, J Grigsby, H C Gonick
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引用次数: 5

Abstract

The purpose of the present study was to investigate bone changes in the adult rat exposed to low lead levels during intake of normal dietary calcium and to contrast these findings with data from our earlier studies performed with animals receiving low dietary calcium concurrent with lead exposure. The present study exposed adult rats to 100 ppm lead via drinking water for 12 weeks and assessed bone histology, 1,25-dihydroxyvitamin D, 25(OH)vitamin D and parathyroid hormone levels. No osteopenia was evident by quantitative bone histology, and circulating levels of 1,25-dihydroxyvitamin D, 25(OH) vitamin D and parathyroid hormone were normal. Bone ash findings documented incorporation of significant amounts of lead into bone mineral. These findings document absence of interference with vitamin D metabolism, absence of secondary hyperparathyroidism and absence of osteopenia following 12 weeks of low lead exposure in the adult rat maintained on normal calcium intake. Results stress the importance of adequate calcium intake in our elderly population who may be exposed to cumulative, low-level lead exposure.

适当的膳食钙减轻成年大鼠慢性铅暴露引起的骨质减少。
本研究的目的是研究在摄入正常膳食钙的情况下暴露于低铅水平的成年大鼠的骨骼变化,并将这些发现与我们早期对摄入低钙同时暴露于铅的动物进行的研究数据进行对比。本研究将成年大鼠通过饮用水暴露在百万分之百的铅环境中12周,并评估其骨组织、1,25-二羟基维生素D、25(OH)维生素D和甲状旁腺激素水平。定量骨组织学检查未见骨质减少,血液中1,25-二羟基维生素D、25(OH)维生素D及甲状旁腺激素水平正常。骨灰的发现记录了大量铅与骨矿物质的结合。这些发现证明,在正常钙摄入的成年大鼠低铅暴露12周后,维生素D代谢没有受到干扰,继发性甲状旁腺功能亢进没有发生,骨质减少也没有发生。结果强调,对于可能暴露于累积的低水平铅暴露的老年人群,摄入足够的钙是非常重要的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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