Abstract
Just when it seemed that scientists had a handle on how antibiotics kill bacteria and how their power could be amplified, new evidence has emerged that casts doubt on that approach. In 2007, James J. Collins and coworkers at Boston University presented evidence that all bacteria-killing antibiotics do their jobs by inducing the formation of reactive oxygen species (ROS) ( CE Cell, DOI: 10.1016/j.cell.2007.06.049). The reactive molecules damage bacterial cells. The three antibiotics the Collins group used—norfloxacin (a quinolone), ampicillin (a β-lactam), and kanamycin (an aminoglycoside)—target different bacterial functions. The scientists hoped to show that a common mechanism could provide a way to make bacteria more sensitive to antibiotics. But now it seems the research results may have been too good to be true. Two studies from other research groups report that the same antibiotics used in Collins’ study don’t kill bacteria with ROS after ...
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