• 文献标题:   Graphene Induces Formation of Pores That Kill Spherical and Rod-Shaped Bacteria
  • 文献类型:   Article
  • 作  者:   PHAM VTH, TRUONG VK, QUINN MDJ, NOTLEY SM, GUO YC, BAULIN VA, AL KOBAISI M, CRAWFORD RJ, IVANOVA EP
  • 作者关键词:   graphene nanosheet film, bactericidal effect, edge densitie, pore formation, single mean field simulation
  • 出版物名称:   ACS NANO
  • ISSN:   1936-0851 EI 1936-086X
  • 通讯作者地址:   Swinburne Univ Technol
  • 被引频次:   120
  • DOI:   10.1021/acsnano.5b03368
  • 出版年:   2015

▎ 摘  要

Pristine graphene, its derivatives, and composites have been widely reported to possess antibacterial properties. Most of the studies simulating the interaction between bacterial cell membranes and the surface of graphene have proposed that the graphene-induced bacterial cell death is caused either by (1) the insertion of blade-like graphene-based nanosheets or (2) the destructive extraction of lipid molecules by the presence of the lipophilic graphene. These simulation studies have, however, only take into account graphene-cell membrane interactions where the graphene is in a dispersed form. In this paper, we report the antimicrobial behavior of graphene sheet surfaces in an attempt to further advance the current knowledge pertaining to graphene cytotoxicity using both experimental and computer simulation approaches. Graphene nanofilms were fabricated to exhibit different edge lengths and different angles of orientation in the graphene sheets. These substrates were placed in contact with Pseudomonas aeruginosa and Staphylococcus aureus bacteria, where it was seen that these substrates exhibited variable bactericidal efficiency toward these two pathogenic bacteria. It was demonstrated that the density of the edges of the graphene was one of the principal parameters that contributed to the antibacterial behavior of the graphene nanosheet films. The study provides both experimental and theoretical evidence that the antibacterial behavior of graphene nanosheets arises from the formation of pores in the bacterial cell wall, causing a subsequent osmotic imbalance and cell death.