Guida L, Saidi Z, Hughes M N, Poole R K
Biosphere Sciences Division, King's College London, UK.
Arch Microbiol. 1991;156(6):507-12. doi: 10.1007/BF00245400.
The toxicity and binding of aluminium to Escherichia coli has been studied. Inhibition of growth by aluminium nitrate was markedly dependent on pH; growth in medium buffered to pH 5.4 was more sensitive to 0.9 mM or 2.25 mM aluminium than was growth at pH 6.6-6.8. In medium buffered with 2-(N-morpholino)ethanesulphonic acid (MES), aluminium toxicity was enhanced by omission of iron from the medium or by use of exponential phase starter cultures. Analysis of bound aluminium by atomic absorption spectroscopy showed that aluminium was bound intracellularly at one type of site with a Km of 0.4 mM and a capacity of 0.13 mol (g dry wt)-1. In contrast, binding of aluminium at the cell surface occurred at two or more sites with evidence of cooperativity. Addition of aluminium nitrate to a weakly buffered cell suspension caused acidification of the medium attributable to displacement of protons from cell surfaces by metal cations. It is concluded that aluminium toxicity is related to pH-dependent speciation [with Al(H2O)6(3+) probably being the active species] and chelation of aluminium in the medium. Aluminium transport to intracellular binding sites may involve Fe(III) transport pathways.
已对铝对大肠杆菌的毒性和结合情况进行了研究。硝酸铝对生长的抑制作用明显取决于pH值;在缓冲至pH 5.4的培养基中生长比在pH 6.6 - 6.8时对0.9 mM或2.25 mM铝更为敏感。在用2 -(N - 吗啉代)乙磺酸(MES)缓冲的培养基中,培养基中缺铁或使用指数生长期起始培养物会增强铝的毒性。通过原子吸收光谱法分析结合铝表明,铝在一种类型的位点上细胞内结合,其Km为0.4 mM,容量为0.13 mol(干重g)-1。相比之下,铝在细胞表面的结合发生在两个或更多位点,有协同作用的证据。向弱缓冲的细胞悬液中添加硝酸铝会导致培养基酸化,这是由于金属阳离子将质子从细胞表面置换所致。得出的结论是,铝的毒性与pH依赖性物种形成[可能以Al(H2O)6(3+)为活性物种]以及培养基中铝的螯合有关。铝向细胞内结合位点的转运可能涉及Fe(III)转运途径。