[Experimental model for the study of molybdenosis in the primary copper deficiency in rats].

L Igarza, M A Quiroga, C Agostini M, N Auza
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Abstract

An experimental model in rats was evaluated to differentiate the effects between Copper deficiency and Molybdenosis. Sixty weaning rats (30 male and 30 female) received a diet with 70% complete powder milk (1 ppm Cu) and 30% maize meal (0.8-1.5 ppm Cu). Three experimental groups received the following mineral supplementation: copper deficiency (40 ppm Fe), molybdenosis (40 ppm Fe + 40 ppm Cu + 500 ppm Mo) and control (40 ppm Fe + 40 ppm Cu). The animals were weighed each 14 days. At 70 days of treatment were sacrificed. Blood and liver were sampled for analyzing hematocrit, ceruloplasmin activity and Cu and Mo liver concentration. Copper deficiency group had less serum ceruloplasmin activity. Cu and Mo liver concentration were higher in the animals with molybdenosis. We concluded that when Cu levels are higher than minimum requirement, feeding with high Mo, do not affect ceruloplasmin activity. In addition, high Mo liver concentration allows us to elucidate effects "per se" of molybdenosis.

[原发性缺铜大鼠钼中毒研究的实验模型]。
建立大鼠实验模型,探讨缺铜与钼中毒的关系。60只断奶大鼠(公母各30只)饲喂70%全奶粉(1 ppm Cu)和30%玉米粉(0.8 ~ 1.5 ppm Cu)的日粮。3个试验组分别给予缺铜(40 ppm Fe)、钼(40 ppm Fe + 40 ppm Cu + 500 ppm Mo)和对照组(40 ppm Fe + 40 ppm Cu)矿物质补充。每14天称重一次。治疗第70天处死。采集血液和肝脏,分析红细胞比容、铜蓝蛋白活性和肝脏铜、钼浓度。缺铜组血清铜蓝蛋白活性降低。钼中毒动物肝脏中Cu和Mo浓度较高。综上所述,当铜含量高于最低需要量时,高钼饲料不影响铜蓝蛋白活性。此外,高钼肝浓度使我们能够阐明钼中毒“本身”的影响。
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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