Evidence for several steps in luteolin uptake by is presented. The first step is highly reversible and strongly pH dependent absorption, greatly enhanced at acidic pH. Studies with liposomes suggest that this step consists of a passive dissolution of the flavonoid in its non-ionized state in the lipidic matrix of the membrane. This first step is enhanced in bacteria killed by high temperature. The second step, a slower and more stable accumulation, is not pH dependent. The nature of the sites involved in this more stable binding remains to be determined. Low temperature and treatment with the metabolic inhibitor potassium cyanide resulted in an increase of luteolin uptake and a decrease of extrusion of flavonoids, suggesting an active extrusion process. Studies with spheroplasts or isolated membranes showed that under physiological conditions most of the luteolin was entrapped in the outer membrane while only a small amount was kept in the cytoplasmic membrane. Arguments are presented supporting the view that has developed a mechanism to keep luteolin in its membranes which helps avoid the toxic effect of the flavonoid on the respiratory chain by trapping most of it in the outer membrane and to maintain the operon in a transcriptionally active form in conditions where this strong inducer is no longer exuded by the host plant.


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