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蛋白质能量营养不良会使造血祖细胞停滞在 G0/G1 细胞周期阶段,从而改变细胞的生成率。

Protein-energy malnutrition halts hemopoietic progenitor cells in the G0/G1 cell cycle stage, thereby altering cell production rates.

机构信息

Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Laboratório de Hematologia Experimental, Universidade de São Paulo, São Paulo, Brasil.

出版信息

Braz J Med Biol Res. 2009 Jun;42(6):523-30. doi: 10.1590/s0100-879x2009000600008.

Abstract

Protein energy malnutrition (PEM) is a syndrome that often results in immunodeficiency coupled with pancytopenia. Hemopoietic tissue requires a high nutrient supply and the proliferation, differentiation and maturation of cells occur in a constant and balanced manner, sensitive to the demands of specific cell lineages and dependent on the stem cell population. In the present study, we evaluated the effect of PEM on some aspects of hemopoiesis, analyzing the cell cycle of bone marrow cells and the percentage of progenitor cells in the bone marrow. Two-month-old male Swiss mice (N = 7-9 per group) were submitted to PEM with a low-protein diet (4%) or were fed a control diet (20% protein) ad libitum. When the experimental group had lost about 20% of their original body weight after 14 days, we collected blood and bone marrow cells to determine the percentage of progenitor cells and the number of cells in each phase of the cell cycle. Animals of both groups were stimulated with 5-fluorouracil. Blood analysis, bone marrow cell composition and cell cycle evaluation was performed after 10 days. Malnourished animals presented anemia, reticulocytopenia and leukopenia. Their bone marrow was hypocellular and depleted of progenitor cells. Malnourished animals also presented more cells than normal in phases G0 and G1 of the cell cycle. Thus, we conclude that PEM leads to the depletion of progenitor hemopoietic populations and changes in cellular development. We suggest that these changes are some of the primary causes of pancytopenia in cases of PEM.

摘要

蛋白质能量营养不良(PEM)是一种常导致免疫缺陷伴全血细胞减少的综合征。造血组织需要高营养供应,细胞的增殖、分化和成熟以恒定和平衡的方式发生,对特定细胞谱系的需求敏感,并依赖于干细胞群体。在本研究中,我们评估了 PEM 对造血某些方面的影响,分析了骨髓细胞的细胞周期和骨髓中祖细胞的百分比。2 月龄雄性瑞士小鼠(每组 7-9 只)接受低蛋白饮食(4%)或自由摄入对照饮食(20%蛋白质)进行 PEM。当实验组在 14 天后失去约 20%的初始体重时,我们收集血液和骨髓细胞以确定祖细胞的百分比和细胞周期各阶段的细胞数量。两组动物均用 5-氟尿嘧啶刺激。在第 10 天进行血液分析、骨髓细胞组成和细胞周期评估。营养不良的动物表现出贫血、网织红细胞减少和白细胞减少。他们的骨髓细胞数量减少,祖细胞耗竭。营养不良的动物的细胞周期 G0 和 G1 阶段的细胞也比正常动物多。因此,我们得出结论,PEM 导致造血祖细胞群体耗竭和细胞发育改变。我们认为这些变化是 PEM 中全血细胞减少的一些主要原因。

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