Abstract

Antibiotics are ubiquitous in the iron-rich environments but their roles in microbial reduction of Fe(III) oxides are still unclear. Using ampicillin and Geobacter soli, this study investigated the underlying mechanism by which antibiotic regulated microbial reduction of Fe(III) oxides. Results showed that sub-minimal inhibitory concentrations (sub-MIC) of ampicillin significantly affected ferrihydrite reduction by G. soli, with a stimulatory effect at 1/64 and 1/32 MIC and an inhibitory effect at 1/8 MIC. Increasing ampicillin concentration resulted in increasing cell length and decreasing bacterial zeta potential that were beneficial for ferrihydrite reduction, and decreasing outer membrane permeability that was unfavorable for ferrihydrite reduction. The respiratory metabolism ability was enhanced by 1/64 and 1/32 MIC ampicillin and reduced by 1/8 MIC ampicillin, which was also responsible for regulation of ferrihydrite reduction by ampicillin. The ferrihydrite reduction showed a positive correlation with the redox activity of extracellular polymeric substances (EPS) which was tied to the cytochrome/polysaccharide ratio and the content of α-helices and β-sheet in EPS. These results suggested that ampicillin regulated microbial Fe(III) oxide reduction through modulating the bacterial morphology, metabolism activity and extracellular electron transfer ability. Our findings provide new insights into the environmental factors regulating biogeochemical cycling of iron.

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