FomA protein

The coordination of Cu(ii) ions by the Ac-KGHGNGEEGTPTVHNE-NH2 (1L) peptide – a FomA protein fragment of Fusobacterium nucleatum – and its cyclic analogue: cyclo(KGHGNGEEGTPTVHNE) (2L) was studied by potentiometric titration, spectroscopic methods (UV-Vis, CD, EPR) and mass spectrometry (MS). Both the ligands contain two histydyl residues located in the third and fourteenth position of the peptide chain. For the 1L and 2L ligands mono- and dinuclear complexes were identified and studied in an aqueous solution. At the pH range characteristic of the intestinal environment (5.5–7.5), copper(ii) complexes were identified and their formation constants were determined. The same forms of the complexes with respectively the linear peptide and the cyclic peptide show similar stability, but greater than that reported in the literature for complexes with the same coordination mode. Moreover, the 1L peptide and its complex exhibit an α-helix structure, whereas the 2L peptide adopts this seconda...

Explanation of carcinogenesis processes may certainly contribute to the prevention and development of novel methods for cancer treatment. In this paper we considered the probable relationship between the presence of Fusobacterium nucleatum in colon and its possible influence on the development of colorectal cancer. For this purpose, intracellular and/or extracellular generation of reactive oxygen species (ROS) by mouse colon carcinoma cells (CT26) were stimulated by two fragments of FomA adhesin from F. nucleatum and their complexes with copper(II): Cu(II)-Ac-KGHGNG-NH 2 (1Cu) and Cu(II)-Ac-PTVHNE-NH 2 (2Cu). Incubation of the cells with copper complexes was followed with ICP-MS technique. The overall generation of ROS was shown by means of fluorescence spectroscopy with two proper probes, whereas identification of ROS was achieved by the spin trapping technique and EPR measurements. As a result, an abundant production of the hydroxyl radicals, both inside and outside the cells, was observed upon the stimulation of the CT26 cells with the copper complexes. Clearly both compounds induced strong oxidation stress which triggered a radicals' cascade that finally resulted in the pronounced lipid peroxidation. The later was