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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Mechanisms of protective functions of Escherichia coli polyamines against toxic effect of paraquat, which causes superoxide stress.

The toxic effect of paraquat, mainly caused by production of superoxide radicals, results in the induction of polyamine synthesizing enzymes and their products in cells of exponentially growing E. coli cultures. The activity of ornithine decarboxylase increases approximately twofold and the activity of lysine decarboxylase increases 1.4-fold. Unlike cadaverine, putrescine and spermidine stimulate expression of the soxRS regulon genes, and this depends on the polyamine concentration and is specific for different genes of the regulon. Of six genes studied, the maximum (to 130%), minimum (about 40%), and average (60-80%) stimulation was observed for the stress induction of nfo (endonuclease IV), sodA (superoxide dismutase), and the soxS gene of the transcriptional regulator, respectively. Addition of paraquat to exponentially growing E. coli culture results in oscillations of the topological state of DNA. Putrescine prevents the drop in the extent of DNA supercoiling caused by the damaging effect of free radicals during the first minutes of stress and increases it during the restoration (the peak of the transcriptional activity of the soxRS regulon genes). These effects are due to properties of putrescine as a DNA protector and modulator of its topological state. The ability of putrescine to decrease the mutation rate under conditions of superoxide stress induced by addition of paraquat is shown by the example of rifampicin resistance.[1]

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