Fernández Menéndez M J, Fell G S, Brock J H, Cannata J B
Bone and Mineral Research Unit, Hospital General de Asturias, Universidad de Oviedo, Spain.
Nephrol Dial Transplant. 1991;6(9):672-4. doi: 10.1093/ndt/6.9.672.
The investigation of different aluminium-binding agents and metabolic conditions that might act as critical factors in modulating aluminium absorption could yield valuable information in the understanding of aluminium gastrointestinal absorption. We evaluated the effect of iron depletion in aluminium uptake and the role of transferrin and citrate in aluminium incorporation by the intestinal epithelial cell line RIE1. Both complex, aluminium-citrate and aluminium-transferrin were prepared in a molar ratio of 2:1; both facilitated the aluminium uptake although a greater aluminium incorporation was found when aluminium was administered as aluminium-transferrin. This difference became even greater in the iron-depleted cells (normal cells vs iron-depleted cells): 7.7 +/- 1.4 versus 30 +/- 5.6 ng Al/micrograms DNA (P less than 0.05). From these and previous data it is possible to speculate that iron status could modulate the intestinal uptake of aluminium and that both transferrin and citrate would act as effective carriers in the incorporation of aluminium into mucosal cells.
研究不同的铝结合剂以及可能作为调节铝吸收关键因素的代谢条件，对于理解铝的胃肠道吸收可能会产生有价值的信息。我们评估了缺铁对铝摄取的影响，以及转铁蛋白和柠檬酸在肠上皮细胞系RIE1摄取铝过程中的作用。铝 - 柠檬酸复合物和铝 - 转铁蛋白复合物均以2:1的摩尔比制备；二者均促进了铝的摄取，不过当以铝 - 转铁蛋白形式给予铝时，发现有更多的铝被摄取。这种差异在缺铁细胞中（正常细胞与缺铁细胞相比）变得更加明显：分别为7.7±1.4与30±5.6 ng铝/微克DNA（P<0.05）。根据这些以及先前的数据可以推测，铁状态可能会调节肠道对铝的摄取，并且转铁蛋白和柠檬酸在铝进入黏膜细胞的过程中均作为有效的载体发挥作用。
