Reduced Iron-Containing Clay Minerals as Antibacterial Agents

Previous work documented' the general-antibacterial mechanism of iron containing clays that involved hydroxyl radical (center dot OH) production from soluble Fe2+, and attack of cell membrane and intracellular proteins. Here we explore the role of clay structural Fe(II) in center dot OH production at near neutral pH and identify a lipid involved in the antibacterial process. Structural Fe(III) in nontronite NAu-2 was reduced (rNAu-2) and E. cali, a model bacterium, was exposed to rNAu-2 in-oxic suspension. The antibacterial activity of rNAu-2 was dependent on pH and Fe(II) concentration, where E. coli were completely killed at pH 6, but survived at pH 7 and 8. In the presence of a center dot OH scavenger or in anaerobic atmosphere, E. coli survived better, suggesting that cell death may be caused by center dot OH generated from oxidation of structural Fe(II) in-rNAu-2. In-situ imaging evealed damage of a membrane lipid, cardiolipin, in,the' polar region of E. coli cells, where reactive oxygen species and redox-active labile Fe were enriched, Our results advanCe the previous antibacterial-modelf by demonstrating that the structural Fe(II) is the primary source of center dot OH, which damage's cardiolipin, triggers the influx of soluble Fe2+ into the cell, and ultimately leads, to cell-death. (GRAPHICS)