Silver nanoparticles-induced H₂O₂ triggers apoptosis-like death and is associated with dinF in Escherichia coli

Abstract

Silver nanoparticles (AgNPs) are the most widely used nanomaterials as antimicrobial agents. AgNPs have been shown to inhibit the growth of and induce apoptosis-like death in Escherichia coli. However, the precise mechanism of AgNPs-induced apoptosis-like death and association with DNA damage-inducible protein F (dinF), a gene of SOS response, is unknown. Here, AgNPs-contributing depletion of intracellular glutathione levels and deactivation of glutathione peroxidase were shown. This step, indicating disruption of the antioxidant system, resulted in overall oxidative stress. Furthermore, DNA oxidation was accompanied, leading to DNA fragmentation. In addition, AgNPs appeared to induce apoptosis-like death via the SOS response. We used sodium pyruvate – an H₂O₂ quencher – to study the contribution of H₂O₂, which showed attenuation of AgNPs-induced DNA damage, SOS response, and apoptosis-like death. In dinF mutant, the strain showed a higher degree of DNA damage and apoptotic features. In conclusion, AgNPs mediate apoptosis-like cell death by H₂O₂-induced oxidative DNA damage. Furthermore, our result demonstrates that dinF participates in this process, which further supports that AgNPs induces SOS response. Our findings may contribute to expanding the new applications of AgNP-based nanomaterials in biomedical fields.

Keywords:

• Apoptosis-like death
• DinF
• hydrogen peroxide
• oxidative stress
• silver nanoparticles

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or nonprofit sectors.