The challenge of optimizing both performance and safety in nanomaterials hinges on our ability to resolve which structural features lead to desired properties. It has been difficult to draw meaningful conclusions about biological impacts from many studies of nanomaterials due to the lack of nanomaterial characterization, unknown purity, and/or alteration of the nanomaterials by the biological environment. To investigate the relative influence of core size, surface chemistry, and charge on nanomaterial toxicity, we tested the biological response of whole animals exposed to a matrix of nine structurally diverse, precision-engineered gold nanoparticles (AuNPs) of high purity and known composition. Members of the matrix include three core sizes and four unique surface coatings that include positively and negatively charged headgroups. Mortality, malformations, uptake, and elimination of AuNPs were all dependent on these parameters, showing the need for tightly controlled experimental design and nanomaterial characterization. Results presented herein illustrate the value of an integrated approach to identify design rules that minimize potential hazard.

The present study was designed to characterize the interaction of choline with the M₁ subtype of the muscarinic acetylcholine receptor. Using Chinese hamster ovary cells transfected with neuronal nitric oxide synthase and the cloned human M₁ receptor (CHO hM₁/nNOS cells), we investigated choline’s effects on production of nitric oxide and elevation of intracellular [Ca²⁺]. Choline showed the properties of a full agonist in inducing the sustained plateau of increased intracellular [Ca²⁺], although it was only a partial agonist in inducing the larger, transient [Ca²⁺] peak. Choline was also found to act as a full agonist in stimulating the production of nitric oxide. These results have implications for efforts in the clinical treatment of dementia.