A Role of Iron Ions in the SOS DNA Repair Response Induced by Nitric Oxide in Escherichia coli

M. V. Stupakova¹, I. I. Lobysheva^2*, V. D. Mikoyan², A. F. Vanin², and S. V. Vasilieva¹

¹Institute of Biochemical Physics, Russian Academy of Sciences, ul. Kosygina 4, Moscow, 117334 Russia; fax: (7-095) 137-4101

²Institute of Chemical Physics, Russian Academy of Sciences, ul. Kosygina 4, Moscow, 117977 Russia; fax: (7-095) 938-2156; E-mail: irlobysh@polymer.chph.ras.ru

^* To whom correspondence should be addressed.

Received September 1, 1999; Revision received November 18, 1999

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An induction of the SOS DNA repair response by physiological nitric oxide donors (dinitrosyl iron complexes (DNIC) with thiols and S-nitrosothiols (RSNO)) was studied in E. coli cells. DNIC with thiols were the most effective SOS-inducers. Being more toxic, RSNO mediated a similar response at 10-100 µM, but they were inactive at concentrations above 0.5 mM. Pretreatment of the cells with chelating agents, o-phenanthroline and picolinic acid, prevented induction of the SOS response by all NO-donors used and led to a decrease in the DNIC-type EPR signal that appeared after incubation of the cells with DNIC or S-nitrosoglutathione (GSNO). Analysis of these effects revealed a dual role of iron ions in reactivity and toxicity of the NO-donating agents. On one hand, they could stabilize GSNO in the form of less toxic DNIC, and, on the other hand, they took part in the formation of the SOS-inducing signal by NO-donating agents.

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KEY WORDS: SOS-response, E. coli, nitric oxide, iron, gene expression

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