Gold nanoparticles induce a reactive oxygen species-independent apoptotic pathway in Escherichia coli.

Abstract

Gold nanoparticles (AuNPs) are a promising material for use in biological and biotechnological applications. While applications such as drug delivery, sensory probe, and organic photovoltaics have been widely evaluated, studies of the antimicrobial activity of AuNPs in therapeutic agents are lacking. In this study, the antibacterial activity and mode of action of AuNPs on Escherichia coli was focused. The membrane-impermeable dye SYTOX green was not taken up and membrane potential was depolarized by AuNPs. This demonstrated that AuNPs inhibit cell growth without directly causing membrane damage. Depolarization of membrane potential results in calcium uptake and processes such as bacterial apoptotic-like cell death. We confirmed that AuNPs induced DNA fragmentation resulting in apoptosis-like cell death in a TUNEL assay. FITC-VAD-FMK showed that caspase-like protein(s) such as RecA were activated, induced, and overexpressed. Additionally, elevated levels of intracellular reactive oxygen species (ROS) and decreased reduced glutathione were observed. In AuNP-treated cells, ROS elevation was not confirmed; however, glutathione was decreased. Based on these observations, AuNPs induce apoptotic-like death by severely damaging DNA and this was independent of ROS in E. coli.