Mahieu S, Calvo M L, Millen N, Gonzalez M, Contini M C
Cátedra Fisiología Humana, Facultad de Bioquímica y Cs. Biológicas, Universidad Nacional del Litoral, Ciudad Universitaria, Santa Fé, Argentina.
Acta Physiol Pharmacol Ther Latinoam. 1998;48(1):32-40.
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.
研究了氢氧化铝慢性中毒大鼠（80毫克/千克体重，腹腔注射，每周三次，持续6个月）和对照大鼠在3至26周龄期间铝对生长的影响。根据帕克斯的喂养与生长理论评估生长数据。在中毒期结束时，通过钙平衡以及借助45Ca++测定骨Ca++的积聚和吸收速率来研究钙代谢。使用间接方法研究甲状旁腺功能。与对照组相比，处理后的大鼠在渐近体重以及食物转化为生物量的初始效率方面显著降低。两组之间在食物摄入量上未观察到差异。铝既不影响峰值生长速率，也不影响达到成熟所需的时间。处理后大鼠的钙平衡显著低于对照组。这伴随着粪便中钙排泄的显著增加，这可能是由于肠道吸收减少所致。在所有处理后的大鼠中均观察到小梁骨表面有大量铝以及骨骼Ca++质量减少。然而，以100克体重表示时，后者并无差异。发现处理组的骨骼Ca++积聚速率相对于对照组显著降低，而骨Ca吸收速率没有任何变化。铝处理组中Vo+/Vo-的降低所揭示的骨转换减少伴随着血钙恢复速度减慢，这与甲状旁腺对钙缺乏的反应间接相关。在我们研究的模型中，骨转换减少可能是由于铝在骨中的沉积所致；然而，可能存在相关因素，如甲状旁腺激素分泌功能障碍，或其在骨水平的受体之间亲和力降低。
