Anti-Bacterial Mechanisms for Ag+ , Cu2+, and Zn2+ Ion Solutions against Staphylococcus Aureus and Escherichia Coli

Abstract

Abstract: Antibacterial mechanism of Ag+ ion solution against S. aureus had been found that Ag+-induced S. aureus may inactivate PGN synthesis transglycosylase TG and transpeptidase TP. Bacteriolysis of S. aureus PGN cell wall, in which wall teichoic acids control PGN synthesis crosslinking TP, is due to the inhibition of PGN elongation by enhancing the activities of PGN autolysins; amidase AmiA and AmiE, and PGN hydrolase Lysostaphin-like endopeptidase (Glycine-Glycine bond cleavage). Against E. coli, the antibacterial mechanism of Ag+ ion solution had been found that bacteriolysis and destruction of E.coli cell wall by silver ions are caused by the destruction of outer membrane structure owing to the activation of endopeptidase of lipoprotein at C-, and N-terminals, and inhibition of PGN elongation due to the damage of PGN synthetic enzyme of silver-protein Amidase in periplasmic space, and PGN autolysins of Amidase, Peptidase, and Carboxypeptidase. Bacteriolysis and destruction of E.coli cell wall are due to the damage of LPS synthesis, destructing of outer membrane structure by degrading of lipoprotein at C-, N-terminals, owing to inhibition of PGN formations by inactivation of carboxypeptidase and TP-endopeptidase, and activities of PGN autolysins of amidase, peptidase and carboxypeptidase. Bacteriolysis of S.aureus PGN cell wall by Cu2+ ions is thought to be due to inhibition of PGN elongation owing to the damages of PGN synthetic TG/TP and the activations of PGN autolysin, AmiA. Bacteriolysis of E.coli cell wall by Cu2+ ions occurs by destruction of outer membrane structure due to degradation of lipoprotein at N-, C-terminals, damage of TP enzyme and activations of PGN autolysins. Furthermore, deletion of PGN autolysin also becomes bacteriolytic factor. It is thought that the activations of these PGN autolysins by Zn2+ ions could be enhanced the inhibitions of PGN elongation simultaneously, with bacteriolysis of S. aureus PGN cell wall. Bacteriolysis of E. coli cell wall by Zn2+ ions are due to destruction of outer membrane structure by degrading of lipoprotein at C-, Nterminals, owing to PGN formation inhibition by activities of PGN autolysins of amidase and carboxypeptidase-transpeptidase Ag+,Cu2+,Zn2+ ions-induced ROS generation of O2 - and H2O2 and ROS-mediated oxidative stress in bacterial cell lead to killing by stress damage for silver ions, cell membrane damages due to high reactive •OH and OH－are formed by Haber-Weiss and Fenton reactions for Cu2+ ions, and DNA molecular damage for Zn2+ ions.