Cannata J B, Gómez Alonso C, Fernández Menéndez M J, Fernández Soto I, McGregor S, Menéndez-Fraga P, Brock J H
Bone and Mineral Research Unit, Hospital General de Asturias, Universidad de Oviedo, Spain.
Nephrol Dial Transplant. 1991;6(9):637-42. doi: 10.1093/ndt/6.9.637.
In this study we have evaluated the haematological consequences of chronic aluminium (Al) overload. We have also investigated 'in vivo' whether aluminium overload may modulate gastrointestinal iron (Fe) absorption and 'in vitro' whether the presence of aluminium may influence the cellular uptake of iron. The in vivo studies were performed in rats with normal renal function and the in vitro experiments were done using the rat intestinal epithelial cell line RIE-1. The results demonstrate that aluminium deposit in tissues even with normal renal function. The intraperitoneal aluminium loading resulted in serum and tissue aluminium increases comparable with concentrations found in aluminium-intoxicated renal patients. The aluminium intoxication was accompanied by a microcytic anaemia with a haematological pattern similar to that observed in iron-deficiency anaemia. Nevertheless, iron absorption was significantly reduced despite an increased total iron binding capacity (TIBC). In addition, aluminium was also able to reduce in vitro cellular uptake of iron in the RIE-1 intestinal cell line. These experimental results demonstrate that aluminium interferes with iron absorption and iron transfer, and suggest that these mechanisms may be responsible for maintaining and even increasing the anaemia observed in aluminium overload.
在本研究中,我们评估了慢性铝(Al)过载的血液学后果。我们还“在体内”研究了铝过载是否可能调节胃肠道铁(Fe)的吸收,以及“在体外”研究了铝的存在是否可能影响铁的细胞摄取。体内研究在肾功能正常的大鼠中进行,体外实验则使用大鼠肠上皮细胞系RIE - 1完成。结果表明,即使肾功能正常,铝也会在组织中沉积。腹腔内铝负荷导致血清和组织铝含量增加,与铝中毒肾病患者体内发现的浓度相当。铝中毒伴有小细胞性贫血,其血液学模式与缺铁性贫血中观察到的相似。然而,尽管总铁结合能力(TIBC)增加,但铁吸收显著降低。此外,铝还能够在体外降低RIE - 1肠细胞系中铁的细胞摄取。这些实验结果表明,铝会干扰铁的吸收和转运,并表明这些机制可能是导致铝过载时贫血维持甚至加重的原因。