J. Hoerter et al., ROLE OF ENTEROBACTIN AND INTRACELLULAR IRON IN CELL LETHALITY DURING NEAR-UV IRRADIATION IN ESCHERICHIA-COLI, Photochemistry and photobiology, 64(3), 1996, pp. 537-541
In Escherichia coli, fur mutants that constitutively express their nat
ive iron chelating agent, enterobactin, are significantly more sensiti
ve to near-UV radiation (NUV) than wild type, An entA mutant, which is
incapable of synthesizing enterobactin, is equal to wild type in resi
stance to NUV irradiation, However, the addition of Fe+3 enterobactin
but not Al+3 enterobactin to entA cell suspensions just prior to irrad
iation results in an increased sensitivity to NUV irradiation, A fes m
utant, which is unable to reduce and release iron from enterobactin, i
s significantly more sensitive to NUV irradiation than wild type. The
addition of nontoxic levels of H2O2 (5 mu M) just prior to irradiation
significantly increases sensitivity of both fur and fes mutants, Thes
e results suggest that one mechanism by which NUV irradiation leads to
cell lethality is by creating a transient iron overload, producing ve
ry favorable conditions for the production of highly deleterious free
radicals through a variety of mechanisms that lead to oxidative stress
and DNA damage including lethal and mutagenic lesions, These results
are consistent with the hypothesis that enterobactin is an endogenous
chromophore for NUV and contributes to cell lethality via the destruct
ion of its ligand, releasing Fe+2 into the cytoplasm to catalyze the p
roduction of highly reactive hydroxyl radicals and other toxic oxygen
species via the Haber-Weiss reaction.