Borelli Primavera, Blatt Solange, Pereira Juliana, de Maurino Beatriz Beutler, Tsujita Maristela, de Souza Ana Cristina, Xavier José Guilherme, Fock Ricardo Ambrósio
Laboratório Hematologia Experimental, Departmento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Brazil.
Br J Nutr. 2007 Feb;97(2):307-14. doi: 10.1017/S0007114507172731.
Protein-energy malnutrition is a syndrome in which anaemia together with multivitamin and mineral deficiency may be present. The pathophysiological mechanisms involved have not, however, yet been completely elucidated. The aim of the present study was to evaluate the pathophysiological processes that occur in this anaemia in animals that were submitted to protein-energy malnutrition, in particular with respect to Fe concentration and the proliferative activity of haemopoietic cells. For this, histological, histochemical, cell culture and immunophenotyping techniques were used. Two-month-old male Swiss mice were submitted to protein-energy malnutrition with a low-protein diet (20 g/kg) compared with control diet (400 g/kg). When the experimental group had attained a 20 % loss of their original body weight, the animals from both groups received, intravenously, 20 IU erythropoietin every other day for 14 d. Malnourished animals showed a decrease in red blood cells, Hb concentration and reticulocytopenia, as well as severe bone marrow and splenic atrophy. The results for serum Fe, total Fe-binding capacity, transferrin and erythropoietin in malnourished animals were no different from those of the control animals. Fe reserves in the spleen, liver and bone marrow were found to be greater in the malnourished animals. The mixed colony-forming unit assays revealed a smaller production of granulocyte-macrophage colony-forming units, erythroid burst-forming units, erythroid colony-forming units and CD45, CD117, CD119 and CD71 expression in the bone marrow and spleen cells of malnourished animals. These findings suggest that, in this protein-energy malnutrition model, anaemia is not caused by Fe deficiency or erythropoietin deficiency, but is a result of ineffective erythropoiesis.
蛋白质 - 能量营养不良是一种可能伴有贫血以及多种维生素和矿物质缺乏的综合征。然而，其中涉及的病理生理机制尚未完全阐明。本研究的目的是评估在遭受蛋白质 - 能量营养不良的动物中，这种贫血所发生的病理生理过程，特别是关于铁浓度和造血细胞的增殖活性。为此，使用了组织学、组织化学、细胞培养和免疫表型分析技术。将两个月大的雄性瑞士小鼠用低蛋白饮食（20 g/kg）进行蛋白质 - 能量营养不良处理，与对照饮食（400 g/kg）相比。当实验组体重减轻达到其原始体重的20%时，两组动物每隔一天静脉注射20 IU促红细胞生成素，共14天。营养不良的动物表现出红细胞、血红蛋白浓度降低和网织红细胞减少，以及严重的骨髓和脾脏萎缩。营养不良动物的血清铁、总铁结合力、转铁蛋白和促红细胞生成素的结果与对照动物无差异。发现营养不良动物脾脏、肝脏和骨髓中的铁储备更多。混合集落形成单位分析显示，营养不良动物骨髓和脾脏细胞中粒细胞 - 巨噬细胞集落形成单位、红系爆式集落形成单位、红系集落形成单位以及CD45、CD117、CD119和CD71的表达产生较少。这些发现表明，在这个蛋白质 - 能量营养不良模型中，贫血不是由缺铁或促红细胞生成素缺乏引起的，而是无效造血的结果。
