Raja Kishor B, Jafri Shahnaz E, Peters Timothy J, Simpson Robert J
Department of Clinical Biochemistry, King's College London, London, UK.
Biometals. 2006 Oct;19(5):547-53. doi: 10.1007/s10534-005-5919-4.
Absorption from food is an important route for entry of the toxic metal, cadmium, into the body. Both cadmium and iron are believed to be taken up by duodenal enterocytes via the iron regulated, proton-coupled transporter, DMT1. This means that cadmium uptake could be enhanced in conditions where iron absorption is increased. We measured pH dependent uptake of (109)Cd and (59)Fe by duodenum from mice with an in vitro method. Mice with experimental (hypoxia, iron deficiency) or hereditary (hypotransferrinaemia) increased iron absorption were studied. All three groups of mice showed increased (59)Fe uptake (p<0.05) compared to their respective controls. Hypotransferrinaemic and iron deficient mice exhibited an increase in (109)Cd uptake (p<0.05). Cadmium uptake was not, however, increased by lowering the medium pH from 7.4 to 6. In contrast, (59)Fe uptake (from (59)FeNTA(2)) and ferric reductase activity was increased by lowering medium pH in control and iron deficient mice (p<0.05). The data show that duodenal cadmium uptake can be increased by hereditary iron overload conditions. The uptake is not, however, altered by lowering medium pH suggesting that DMT1-independent uptake pathways may operate.
食物中的吸收是有毒金属镉进入人体的重要途径。镉和铁都被认为是通过铁调节的质子偶联转运体DMT1被十二指肠肠上皮细胞摄取。这意味着在铁吸收增加的情况下,镉的摄取可能会增强。我们用体外方法测量了来自小鼠十二指肠的(109)镉和(59)铁的pH依赖性摄取。研究了实验性(缺氧、缺铁)或遗传性(低转铁蛋白血症)铁吸收增加的小鼠。与各自的对照组相比,所有三组小鼠的(59)铁摄取均增加(p<0.05)。低转铁蛋白血症和缺铁小鼠的(109)镉摄取增加(p<0.05)。然而,通过将培养基pH从7.4降至6,镉摄取并未增加。相反,在对照和缺铁小鼠中,通过降低培养基pH,(59)铁摄取(来自(59)FeNTA(2))和铁还原酶活性增加(p<0.05)。数据表明,遗传性铁过载条件可增加十二指肠镉摄取。然而,降低培养基pH并不会改变摄取,这表明可能存在不依赖DMT1的摄取途径。