The fluorescent detection of biothiols and antimicrobial study based on copper(I) iodide coordination polymer

In a previous communication, we reported a new method of synthesis of stable metallic copper nanoparticles (Cu-NPs), which had high potency for bacterial cell filamentation and cell killing. The present study deals with the mechanism of filament formation and antibacterial roles of Cu-NPs in E. coli cells. Our results demonstrate that NP-mediated dissipation of cell membrane potential was the probable reason for the formation of cell filaments. On the other hand, Cu-NPs were found to cause multiple toxic effects such as generation of reactive oxygen species, lipid peroxidation, protein oxidation and DNA degradation in E. coli cells. In vitro interaction between plasmid pUC19 DNA and Cu-NPs showed that the degradation of DNA was highly inhibited in the presence of the divalent metal ion chelator EDTA, which indicated a positive role of Cu(2+) ions in the degradation process. Moreover, the fast destabilization, i.e. the reduction in size, of NPs in the presence of EDTA led us to propose that the nascent Cu ions liberated from the NP surface were responsible for higher reactivity of the Cu-NPs than the equivalent amount of its precursor CuCl2; the nascent ions were generated from the oxidation of metallic NPs when they were in the vicinity of agents, namely cells, biomolecules or medium components, to be reduced simultaneously.

This work investigates the role of oxidation state in the antibacterial activity of copper oxide nanoparticles (NPs). This work investigates the role of oxidation state in the antibacterial activity of copper oxide nanoparticles (NPs). The findings add strong support to a contact killing mechanism of copper oxides (CuO and Cu 2 O) through which bacteria initially suffer severe damage to the cell envelope. Then further damage ensues by an independent pathway of each copper oxide nanoparticle. Formation of copper( i )–peptide complex from cuprous oxide (Cu 2 O) and free radical generation from cupric oxide (CuO) were identified as key sources of toxicity towards E.coli . Cu 2 O rapidly inactivated Fumarase A, an iron sulphur cluster enzyme suggesting the cuprous state of copper binding to the proteins. This inactivation was not noticed in CuO. The percentage of biocidal/bacteriostatic activity is closely related to the oxidation state of the copper oxides. In the case of E.coli , Cu 2 O nanoparticles showed more efficient antibacterial activity and higher affinity to the bacterial cells. CuO nanoparticles produced significant ROS in terms of super oxides while Cu 2 O did not. The diminishing defective emission peaks of Cu 2 O after incubation with microbes strongly suggest the formation of protein complexes. This work is carried out to enable better understanding of the mechanistic pathways of copper oxide nanoparticles.