Anderson C, Danylchuk K D
J Environ Pathol Toxicol. 1979 Mar-Apr;2(4):1151-9.
A previous report had suggested that chronic cadmium intoxication interfered with calcium accumulation in bone and suggested that the mechanism may be a parathyroid-induced bone resorption. We measured C-terminal parathyroid hormone levels in the blood of four male standardized research beagles chronically exposed during 6 months to 25 ppm cadmium chloride in their drinking water while at the same time we performed measurements of the parameters of haversian bone remodelling activity. We failed to demonstrate any statistically significant difference in levels of this hormone in the experimental dogs before or during the exposure, or between samples obtained from the experimental dogs at the end of their period of exposure and normal untreated control dogs from the same colony. We conclude that in the early stages of chronic cadmium intoxication before there is evidence suggestive of intestinal or renal malfunction that may secondarily involve the parathyroid glands, the alteration observed in haversian bone remodelling rates is not mediated through abnormalities of function of the parathyroid glands.
先前的一份报告表明，慢性镉中毒会干扰骨骼中的钙积累，并指出其机制可能是甲状旁腺引起的骨吸收。我们测量了四只雄性标准化研究比格犬血液中的甲状旁腺激素C端水平，这些比格犬在6个月内长期饮用含有25 ppm氯化镉的水，同时我们还对哈弗斯骨重塑活动的参数进行了测量。我们未能证明在暴露前或暴露期间，实验犬体内这种激素的水平有任何统计学上的显著差异，也未能证明在暴露期结束时从实验犬采集的样本与来自同一群体的未处理正常对照犬的样本之间存在差异。我们得出结论，在慢性镉中毒的早期阶段，在有证据表明肠道或肾脏功能障碍可能继发累及甲状旁腺之前，哈弗斯骨重塑率的改变并非由甲状旁腺功能异常介导。
