 | REACTIVE OXYGEN SPECIES: FROM RADIATION TO MOLECULAR BIOLOGY: A Festschrift in Honor of Daniel L. Gilbert
Copyright © 2000 by the New York Academy of Sciences
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Annals of the New York Academy of Sciences 899:69-87 (2000)
© 2000 New York Academy of Sciences
Genetic Responses to Free Radicals: Homeostasis and Gene Control
BEATRIZ GONZÁLEZ-FLECHAa AND
BRUCE DEMPLEb,c
aPhysiology Program, Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA
bDivision of Toxicology, Department of Cancer Cell Biology, Harvard School of Public Health, Boston, Massachusetts 02115, USA
cAddress for correspondence: Voice: 617-432-3462; Fax: 617-432-2590/432-0377.
e-mail: bdemple{at}hsph.harvard.edu
Gene regulation mechanisms have evolved allowing cells to fine-tune the level of "endogenous" oxidative stress and to cope with increased free radicals from external sources. Levels of H 2O 2 are tightly controlled in E. coli by OxyR, which is activated by H 2O 2 to increase scavenging activities and limit H 2O 2 generation by the respiratory chain. Sub-micromolar levels of H 2O 2 are maintained in mammalian tissues, though the regulatory systems that govern this control are unknown. Excess superoxide triggers the soxRS system in E. coli, which is controlled by the oxidant-sensitive iron-sulfur centers of the SoxR protein. Nitric oxide activates SoxR by a different modification of the iron-sulfur centers. The soxRS regulon mobilizes diverse functions to scavenge free radicals and repair oxidative damage in macromolecules, and other mechanisms that exclude many environmental agents from the cell. Mammalian cells also sense and respond to sub-toxic levels of nitric oxide, activating expression of heme oxygenase 1 through stabilization of its mRNA. These inductions give rise to adaptive resistance to nitric oxide in neuronal and other cell types.
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