奈米科技被譽為是二十一世紀最重要的科技之一，其蓬勃發展的結果雖可對各產業帶來劃時代的革命，但同時也免不期然的將會讓這些對生態造成何種影響仍不明確的新興物質排入環境中，使其發展的背後仍有隱憂。因此，了解奈米材料的傳輸、宿命及毒性，甚至更進一步地研究這類物質會對生態及人類健康帶來的衝擊為何，對於奈米科技的永續發展將極有助益，而探究人造奈米顆粒與微生物之間的相互作用則可視為推估這類材料潛在生態風險的第一步。然而，近期文獻雖已指出含鎘量子點在風化過程中，會因為鎘離子的溶出而對微生物產生制菌性或殺菌性的毒性效應，但文獻對於胞外化學物種組成在過程中如何影響量子點最後毒性作用的探討仍相當缺乏。有鑒於此，為釐清一般不具鎘抗性基因的原核細胞的鎘攝取機制，本研究利用革蘭氏陰性菌 Escherichia coli K-12 (ATCC 25404)為模式生物，以其存活率多寡做為鎘攝入的指標，在操縱試驗培養液化性的狀態下，探討胞外化學物種組成對於含鎘量子點所造成的微生物毒性之影響，並藉此推論及評估量子點潛在的生態衝擊程度。實驗結果證實原先設定的假說，即「溶解鎘主要以自由型態的鎘離子Cd2+進入菌株細胞中，且細胞對鎘的攝取過程主要依賴主動運輸此等機制」。這些結果意味著當水相系統維持在以自由態的鎘離子為優勢物種時，量子點將有可能對生態帶來最大的毒性衝擊。

Recent advances in nanotechnology have created numerous and promising applications in all sectors of society; as a result, large scale developments of engineered nanomaterials (ENMs) have increased the likelihood of the release of these novel materials to the environment. Yet, the behavior of these nanomaterials in the environment is still poorly understood, thus raising the concerns of their potential ecological health risks. Given that microbes are the foundation of many ecosystems, a better understanding of the factors that control the microbial toxicity of ENMs is crucial for their sustainable use. To date, available data have indicated that toxicity of quantum dots (QDs) to bacteria is predominantly attributed to the release of toxic inorganic ions, in particular metal species, from weathered QD-cores. Hence, extracellular metal speciation is considered to play an important role in determining the ultimate toxicity of QDs towards microbial cells. In this study, we conducted exposure experiments to investigate the importance of cadmium (Cd) speciation in toxicity to pure cultures of Escherichia coli K-12 (ATCC 25404), a known Gram-negative strain lacking metal resistance czc genes in its genome and thus can be used as a model organism to represent generic non-resistant bacterial cells. Variable chloride chemistry experiments were carried out to modify Cd(II) speciation in assay media, and cell death or growth inhibition was used as an indicator of toxicity. Results show that the toxicity of Cd decreased along the chloride gradient where the severest growth inhibition occurred at the lowest salinity. Under the experimental conditions, inhibition was not a function of the total Cd(II) concentration but strongly correlated with free Cd2+ concentration. In addition, when strong chelating agents such as citrate and EDTA were supplemented to the assay medium, the Cd2+ concentrations were also modulated, resulting in reduced deleterious effects. As such, Cd toxicity to non-czc-mediated Cd resistant bacteria seemed to be explained by the free ion activity model (FIAM). We further examined if energy dependence of Cd uptake was required by strain K-12. Interestingly, differential viability was not observed when starved cells were exposed to media containing Cd(II) and variable chloride concentrations, suggesting that active transport may be the underlying uptake mechanism of Cd in this strain. Together, these results suggest that Cd toxicity to non-resistant bacterial cells is directly proportional to the uncomplexed, free Cd activity in solution, and uptake of Cd may be mediated via an energy-dependent transport system. Accordingly, on the basis of the predictions from the FIAM, these results also suggest that except for acidic and oligotrophic environments, under circumneutral and alkaline conditions cadmium-based QDs may not pose a significant threat to the ecosystem.

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