[慢性氢氧化铝中毒大鼠钙的生长和代谢]。

S Mahieu, M L Calvo, N Millen, M Gonzalez, M C Contini
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引用次数: 0

摘要

在氢氧化铝慢性中毒大鼠(80毫克/公斤体重-体重-摄入量-每周3次,持续6个月)和对照大鼠(3至26周龄)中研究了铝对生长的影响。生长数据根据Parks的喂养生长理论进行评估。在中毒期结束时,通过钙平衡和在45ca++的帮助下测定骨Ca++的增加和吸收速率来研究钙代谢。采用间接法研究甲状旁腺功能。与对照组相比,治疗大鼠的渐近体重和食物转化为生物量的初始效率显著下降。两组之间的食物摄取量没有差异。铝既不影响峰值生长速率,也不影响达到成熟所需的时间。治疗组大鼠钙平衡明显低于对照组。与此同时,脸部排出的钙也显著增加,这可能是由于肠道吸收减少所致。在所有处理过的大鼠中,观察到骨小梁表面大量的铝和骨骼钙++质量的减少。然而,当以100克体重表示时,后者没有差异。与对照组相比,治疗组骨钙的吸积率明显降低,而骨钙的吸收率没有变化。在铝处理组中,Vo+/Vo-降低所显示的骨转换减少伴随着钙恢复速度的减慢,这与甲状旁腺对钙缺乏的反应有间接关系。在我们研究的模型中,骨转换减少可能是由骨中的铝沉积引起的;然而,可能存在相关因素,如甲状旁腺激素分泌功能障碍,或其受体在骨水平上的亲和力降低。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Growth and metabolism of calcium in rats chronically poisoned with aluminium hydroxide].

The effects of aluminum on growth have been studied in rats chronically poisoned with aluminum hydroxide (80 mg/kg b.w.-i.p.-three times a week, during 6 months) and in control rats, between 3 and 26 weeks of age. The growth data was evaluated according to Parks 'theory of feeding an growth. At the end of the poisoning period, the calcium metabolism was studied through a balance of calcium and the determination of bone Ca++ accretion and resorption rates with the aid of 45Ca++. The parathyroid glands function was studied using an indirect method. Treated rats showed a significant decrease in asymptotic weights and in the initial efficiency of food conversion into biomass regarding controls. No differences were observed in food intake between both group. Aluminum affected neither the peak growth rate nor the time necessary to attain maturity. The calcium balance in treated rats was significantly less than in the control group. This was accompanied by a significant increase in the calcium excreted by faces, caused perhaps by a less intestinal absorption. An important amount of aluminum on the surface of the trabecular bone and a reduction in the skeletal Ca++ mass, was observed in all treated rats. Nevertheless there are no differences in the latter when expressed for 100 g of body weight. The rate of skeletal Ca++ accretion was found to be significantly decreased in treated group with respect to controls, without any changes in the bone Ca resorption rate. The reduction in bone turnover revealed by the decrease of Vo+/Vo- was accompanied by less recovery velocity of calcemia in the aluminum treated group, being indirectly related to the parathyroid gland response to calcium depletion. In the model that we studied the decreased bone turnover could have been caused by deposits of aluminum in bone; however there could exist associated factors such as dysfunction in the secretion of PTH, or less affinity between its receptors at the bone level.

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