| Summary: | Understanding the electrochemical stability or corrosion behaviour of metallic nanoparticles in aqueous environments is of central importance in the fields of catalysis, sensing and nano-electronics. The electrochemical stability of silver nanoparticles (AgNPs) was investigated as a function of applied potential, pH and particle size. The direct voltammetric measurements of the Ag oxidation potential indicate that the electrochemical stability of nanoparticles (NPs) is different from their bulk metal, suggesting that theoretically derived energy diagrams for a bulk material might not always be accurate for NPs. In order to understand interactions of nanomaterials (NMs) with biological systems, the cellular environment can be considered as an electrochemical cell, since metal ion release is a major pathway underlying their potential toxicity. NPs inhaled from the air into the deep lung first contact with the lung lining fluid where they have the potential to translocate into other organs like the brain, liver, spleen and heart via blood circulation. Here, this thesis specifically focuses on the impact of AgNMs on two major organs, the lung and brain. AgNMs as potential occupational and environmental hazards may raise health and safety concerns. For this reason, there is a need to assess the interaction of NMs with biological systems for early prediction of their cytotoxicity. The stability of AgNPs in dipalmitoylphosphatidylcholine (DPPC), the major component of lung surfactant, was investigated as a function of pH. TEM images revealed that the AgNPs were coated with a DPPC layer serving as a semi-permeable layer, improving their dispersion and delaying ions release in the lung. Furthermore, these studies suggested that size, stability and chemical composition of NP have to be taken into account in the evaluation of NP cytotoxicity. These observations have important implications for predicting the potential reactivity of AgNPs in the lung and the environment. In response to potential neurotoxicity, studies have shown that AgNPs can cross the blood brain barrier (BBB) via the systemic blood supply and then localise inside the brain, causing neurodegeneration, but much less is known about the distribution of AgNMs and their interaction with protein complexes inside the brain cells. Interaction of microglia with AgNMs, as well as their uptake, cytotoxicity and processing inside cells were investigated. The findings demonstrate that Ag2S formation acts as an ion trap for free Ag+, significantly limiting short term toxicity effects with important consequences for the neuro safety of AgNMs. In order to manipulate particular NPs features with favourable bio-availability and bio-distribution, not only NP uptake into cells, but also a fundamental understanding of the NPs-protein complex is necessary.
|
|---|
