Processes regulating cellular metal accumulation and physiological effects: Phytoplankton as model systems

被引:314
作者
Sunda, WG [1 ]
Huntsman, SA [1 ]
机构
[1] NOAA, Natl Marine Fisheries Serv, Beaufort Lab, Beaufort, NC 28516 USA
关键词
membrane transport of metals; phytoplankton; cellular metal accumulation; metal toxicity;
D O I
10.1016/S0048-9697(98)00226-5
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Trace metals exist in a variety of redox states and coordination species which markedly influences their geochemical behavior and biological availability. Most exist in natural waters as metal cations that are complexed to varying degrees by inorganic and organic ligands. Metal ions are generally taken up into cells by membrane transport proteins designed for acquisition of nutrient metals (Mg, Fe, Mn, Zn, Co, Cu, Mo). Organic ligands compete with these transport proteins for binding metal ions, and consequently, organic complexation substantially decreases metal uptake rates. Typically, the chelated metal is not directly available for cellular uptake, and metal uptake is controlled by either the concentration of free aquo ions or that of kinetically labile inorganic species. The coordination sites of transport proteins, however, are not entirely specific for intended nutrient metals, and consequently will bind with and transport non-nutritive or toxic metals. Competition for membrane transport sites and for intracellular metabolic binding sites can substantially influence the uptake of both nutrient and toxic metals and resultant effects on growth rate. Such growth rate effects provide feedback on cellular metal concentrations since the amount of metal accumulated within cells represents a balance between the rate of metal uptake and the cellular growth rate, the effective biodilution rate. Phytoplankton have provided useful model systems for investigating the processes and associated chemical and biological factors regulating cellular metal accumulation and resultant physiological effects. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:165 / 181
页数:17
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