Cu(II)-reduction by <Emphasis Type="Italic">Escherichia coli</Emphasis> cells is dependent on respiratory chain components |
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Authors: | Sabrina?I?Volentini Ricardo?N?Farías Luisa?Rodríguez-Montelongo Email author" target="_blank">Viviana?A?RapisardaEmail author |
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Institution: | 1.Departamento Bioquímica de la Nutrición,Instituto Superior de Investigaciones Biológicas (Consejo Nacional de Investigaciones Científicas y Técnicas-Universidad Nacional de Tucumán),San Miguel de Tucumán,Argentina;2.Instituto de Química Biológica “Dr Bernabé Bloj” (Universidad Nacional de Tucumán),San Miguel de Tucumán,Argentina |
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Abstract: | Copper is both an essential nutrient and a toxic element able to catalyze free radicals formation which damage lipids and
proteins. Although the available copper redox species in aerobic environment is Cu(II), proteins that participate in metal
homeostasis use Cu(I). With isolated Escherichia coli membranes, we have previously shown that electron flow through the respiratory chain promotes cupric ions reduction by NADH
dehydrogenase-2 and quinones. Here, we determined Cu(II)-reductase activity by whole cells using strains deficient in these
respiratory chain components. Measurements were done by the appearance of Cu(I) in the supernatants of cells exposed to sub-lethal
Cu(II) concentrations. In the absence of quinones, the Cu(II)-reduction rate decreased ~70% in respect to the wild-type strain,
while this diminution was about 85% in a strain lacking both NDH-2 and quinones. The decrease was ~10% in the absence of only
NDH-2. In addition, we observed that quinone deficient strains failed to grow in media containing either excess or deficiency
of copper, as we have described for NDH-2 deficient mutants. Thus, the Cu(II)-reduction by E. coli intact cells is mainly due to quinones and to a lesser extent to NDH-2, in a quinone-independent way. To our knowledge, this
is the first in vivo demonstration of the involvement of E. coli respiratory components in the Cu(II)-reductase activity which contributes to the metal homeostasis. |
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