CESIUM ACCUMULATION BY MICROORGANISMS - UPTAKE MECHANISMS, CATION COMPETITION, COMPARTMENTALIZATION AND TOXICITY
CESIUM ACCUMULATION BY MICROORGANISMS - UPTAKE MECHANISMS, CATION COMPETITION, COMPARTMENTALIZATION AND TOXICITY
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DOI：
10.1007/bf01569888
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发表时间：
1995-02-01
期刊：
影响因子：
--
通讯作者：
AVERY, SV
中科院分区：
文献类型：
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作者：
AVERY, SV
铯放射性同位素持续释放到环境中，重新引起了人们对微生物-铯相互作用的兴趣。铯在自然环境中几乎完全以一价阳离子Cs+的形式存在。尽管Cs+是一种弱刘易斯酸，与配体形成配合物的倾向较低，但其与生物必需碱阳离子Kt的化学相似性促进了高水平的代谢依赖性细胞内积累。微生物Cs+ (K+)的摄取通常由位于质膜上的单价阳离子运输系统介导。这些对碱阳离子的特异性差异很大，因此微生物在积累Cs+的能力上表现出很大的差异；在某些微生物中，Cs+似乎与K+具有相等或更大的转运亲和力。微生物Cs+的积累明显受到外部阳离子（如K+、Na+、NH4+和H+）存在的影响，并且通常伴随着细胞内K+的近似化学计量交换。然而，Cs+对缺乏ki的微生物培养物生长的刺激是有限的，有人提出，不是细胞中Cs+的存在抑制了生长，而是导致K+的损失。微生物对Cs+的耐受性增加可能是由于Cs+在液泡中的隔离或介导Cs+摄取的运输系统的活性和/或特异性的变化。虽然某些内部结构，如核糖体，在Cs+的存在下变得不稳定，并且已知Cs+在许多K+需要的酶的激活中很难替代K+，但Cs+诱导毒性的精确细胞内靶点尚未明确定义。
The continued release of caesium radioisotopes into the environment has led to a resurgence of interest in microbe-Cs interactions. Caesium exists almost exclusively as the monovalent cation Cs+ in the natural environment Although Cs+ is a weak Lewis acid thai exhibits a low tendency to form complexes with Ligands, its chemical similarity to the biologically essential alkali cation Kt facilitates high levels of metabolism-dependent intracellular accumulation. Microbial Cs+ (K+) uptake is generally mediated by monovalent cation transport systems located on the plasma membrane. These differ widely in specificity for alkali cations and consequently microorganisms display large differences in their ability to accumulate Cs+; Cs+ appears to have an equal or greater affinity than K+ for transport in certain microorganisms. Microbial Cs+ accumulation is markedly influenced by the presence of external cations, e.g. K+, Na+, NH4+ and H+, and is generally accompanied by an approximate stoichiometric exchange for intracellular K+. However, stimulation of growth of Ki-starved microbial cultures by Cs+ is limited and it has been proposed that it is not the presence of Cs+ in cells that is growth inhibitory but rather the resulting loss of K+. Increased microbial tolerance to Cs+ may result from sequestration of Cs+ in vacuoles or changes in the activity and/or specificity of transport systems mediating Cs+ uptake. The precise intracellular target(s) for Cs+ induced toxicity has yet to be clearly defined, although certain internal structures, e.g. ribosomes, become unstable in the presence of Cs+ and Cs+ is known to substitute poorly for K+ in the activation of many K+-requiring enzymes.