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Volume 272, Number 41, Issue of October 10, 1997 pp. 25573-25575
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

A Mechanism for Complementation of the sodA sodB Defect in Escherichia coli by Overproduction of the rbo Gene Product (Desulfoferrodoxin) from Desulfoarculus baarsii

(Received for publication, June 3, 1997, and in revised form, July 14, 1997)

Stefan I. Liochev and Irwin Fridovich

From the Department of Biochemistry, Duke University Medical Center, Durham, North Carolina 27710

Overexpression of rbo in Escherichia coli prevents the inactivation of the [4Fe-4S]-containing fumarases that otherwise occurs in the sodA sodB strain. It similarly protects against the increased sensitivity toward H2O2, which is imposed by the lack of SOD A and SOD B. These results would be explained on the basis of scavenging of Obardot 2 within the cells by RBO. This interpretation was supported by measurements of intracellular scavenging of Obardot 2 by the lucigenin luminescence method. Since SOD activity could not be detected in dilute extracts, of the RBO-overexpressing sodA sodB strain, we propose that RBO catalyzes the reduction of Obardot 2 at the expense of cellular reductants such as NAD(P)H. A similar mechanism may apply to other instances of complementation of SOD defects by non-SOD genes.


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