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Journal of Bacteriology, March 2002, p. 1556-1564, Vol. 184, No. 6
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.6.1556-1564.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Involvement of Superoxide Dismutases in the Response of Escherichia coli to Selenium Oxides

Magali Bébien,1 Gilles Lagniel,2 Jérôme Garin,3 Danièle Touati,4 André Verméglio,1* and Jean Labarre2

CEN/Cadarache-DSV-DEVM Laboratoire de Bioénergétique Cellulaire, Univ-Méditérranée CEA 1000, 13108 Saint Paul-Lez-Durance Cedex,1 CEA/Saclay-DSV-DBCM Service de Biochimie et Génétique Moléculaire, Laboratoire de PhysioGénomique, 91191 Gif-sur-Yvette Cedex,2 CEA/Grenoble-DSV-DBMS-CP, 38054 Grenoble,3 Institut Jacques Monod, CNRS-Universités Paris 6 et Paris 7, 75251 Paris Cedex 05, France4

Received 19 July 2001/ Accepted 23 November 2001

Selenium can provoke contrasting effects on living organisms. It is an essential trace element, and low concentrations have beneficial effects, such as the reduction of the incidence of cancer. However, higher concentrations of selenium salts can be toxic and mutagenic. The bases for both toxicity and protection are not clearly understood. To provide insights into these mechanisms, we analyzed the proteomic response of Escherichia coli cells to selenate and selenite treatment under aerobic conditions. We identified 23 proteins induced by both oxides and ca. 20 proteins specifically induced by each oxide. A striking result was the selenite induction of 8 enzymes with antioxidant properties, particularly the manganese and iron superoxide dismutases (SodA and SodB). The selenium inductions of sodA and sodB were controlled by the transcriptional regulators SoxRS and Fur, respectively. Strains with decreased superoxide dismutase activities were severely impaired in selenium oxide tolerance. Pretreatment with a sublethal selenite concentration triggered an adaptive response dependent upon SoxRS, conferring increased selenite tolerance. Altogether, our data indicate that superoxide dismutase activity is essential for the cellular defense against selenium salts, suggesting that superoxide production is a major mechanism of selenium toxicity under aerobic conditions.

* Corresponding author. Mailing address: CEN/Cadarache DSV-DEVM, Laboratoire de Bioénergétique Cellulaire, F-13108 St. Paul-Lez-Durance Cedex, France. Phone: (33) 442254630. Fax: (33) 442254701. E-mail: avermeglio{at}cea.fr.

Journal of Bacteriology, March 2002, p. 1556-1564, Vol. 184, No. 6
0021-9193/02/$04.00+0     DOI: 10.1128/JB.184.6.1556-1564.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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