Hu Zhiqiang, Chandran Kartik, Grasso Domenico, Smets Barth F
Environmental Engineering Program, University of Connecticut, Storrs, Connecticut 06269-2037, USA.
Environ Sci Technol. 2003 Feb 15;37(4):728-34. doi: 10.1021/es025977d.
The goal of this study was to explore the relationship between metal extracellular sorption, intracellular accumulation, and nitrification inhibition. Metal sorption on nitrifying biomass was rapid and could be described by linear partitioning with partition coefficients (Kp) of 20.3 +/- 0.1, 0.4 +/- 0.0, 0.1 +/- 0.0, and 0.2 +/- 0.0 L/g biomass chemical oxygen demand for Cu, Zn, Ni, and Cd, respectively. On the other hand, intracellular Zn, Ni, and Cd concentrations continued to increase with time beyond 12 h after metal addition, whereas intracellular Cu attained equilibrium after 4 h. Metal internalization kinetics could be described by an intraparticle diffusion model, with characteristic diffusion time constants (td) of 9.4, 64.6, 80.5, and 66.1 h for Cu, Zn, Ni, and Cd, respectively. Ultimate internalized percentages of the total cell-associated metal were 1.4 +/- 0.0, 4.3 +/- 0.5,7.6 +/- 1.0, and 2.7 +/- 0.2% for Cu, Zn, Ni, and Cd, respectively. Nitrification inhibition was not a function of the sorbed metal fraction but correlated well with intracellular Zn, Ni, or Cd fractions. An intraparticle diffusion model coupled with a saturation-type biological toxicity model fit the inhibition data for varying initial Cd concentrations and exposure periods. In contrast, no relationship between intracellular or sorbed Cu concentrations and nitrification inhibition was observed. In the presence of 1 mM Cu, less than 13.3 +/- 10.5% cells remained viable as compared to 72.8 +/- 7.5,104.8 +/- 1.7, and 84.7 +/- 7.0% (assumed 100% viable cells in metal-free control) in the presence of 1 mM Zn, Ni, and Cd, respectively. Hence, the observations that inhibition by metals such as Zn, Ni, and Cd is related to their intracellular fraction and the slow kinetics of metal internalization indicate that metal inhibition can easily be underpredicted from short-term batch assays. Furthermore, the inhibitory mechanism of Cu was very different from Zn, Ni, and Cd and may involve rapid loss of membrane integrity.
本研究的目的是探讨金属细胞外吸附、细胞内积累与硝化抑制之间的关系。金属在硝化生物量上的吸附很快，可用线性分配来描述，铜、锌、镍和镉的分配系数（Kp）分别为20.3±0.1、0.4±0.0、0.1±0.0和0.2±0.0 L/g生物量化学需氧量。另一方面，添加金属12小时后，细胞内锌、镍和镉的浓度随时间持续增加，而细胞内铜在4小时后达到平衡。金属内化动力学可用颗粒内扩散模型描述，铜、锌、镍和镉的特征扩散时间常数（td）分别为9.4、64.6、80.5和66.1小时。细胞相关金属的最终内化百分比，铜、锌、镍和镉分别为1.4±0.0、4.3±0.5、7.6±1.0和2.7±0.2%。硝化抑制不是吸附金属分数的函数，但与细胞内锌、镍或镉分数密切相关。颗粒内扩散模型与饱和型生物毒性模型相结合，适合不同初始镉浓度和暴露时间的抑制数据。相比之下，未观察到细胞内或吸附的铜浓度与硝化抑制之间的关系。在存在1 mM铜的情况下，与分别存在1 mM锌、镍和镉时72.8±7.5%、104.8±1.7%和84.7±7.0%（假设无金属对照中100%活细胞）相比，存活细胞少于13.3±10.5%。因此，锌、镍和镉等金属的抑制作用与其细胞内分数以及金属内化的缓慢动力学有关的观察结果表明，从短期批量试验中很容易低估金属抑制作用。此外，铜的抑制机制与锌、镍和镉非常不同，可能涉及膜完整性的快速丧失。
