A wide variety of extracted and synthesised drug molecules have electr
on transfer capabilities which allow them to generate reactive oxygen
species (ROS). In particular, many antibiotics that kill or inhibit ba
cteria, yeasts and cancer cells readily transfer electrons to oxygen m
aking superoxide and hydrogen peroxide in the process. When suitable r
edox active forms of iron are available, Fenton chemistry occurs gener
ating the highly damaging hydroxyl radical. This type of chemistry is
very similar to that which evolved within phagocytic cells as part of
their microbial killing armoury. Many antibiotics, when used in model
systems, have well defined pharmacological actions against key cellula
r functions, but their clinical usefulness is also often demonstrable
at concentrations in vivo well below their in vitro minimum inhibitory
concentrations. These observations have led us to propose that a comm
on mechanism exists whereby phagocytic cells and antibiotics exploit t
he use of ROS for microbial killing.