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Background/Purpose: Nanobacteria, known to date as self-replicating, nano-scale size organisms, smaller than bacteria. However, whether these are living organisms or agglomeration of biomolecules was one of the most controversial issues for many years. One of the reasons for debate is their lack of any genetic material. Although many studies investigate whether nanobacteria are the cause of diseases that affect human health, the discussions did not reach a conclusion. While most studies try to unravel the structures of nanobacteria, some studies investigated their effects on diseases. It has been proposed that pathological calcifications in kidney and dental pulp stones, as well as calcifications in heart valves and arteries, might be caused by nanobacteria. In this study, we investigated the effects and molecular structures of nanobacteria on the formation of atheroma plaques that cause atherosclerosis. Methods: Nanobacteria grown from atheroma plaques in cell culture medium were analysed by scanning electron microscope (SEM) and energy dispersive X-ray spectroscopy (EDS). Macromolecules of nanobacteria were separated by SDS-polyacrylamide gel electrophoresis and their sensitivity to protease and nucleases was tested. After determining their resistance to nucleases and susceptibility to proteinase K, protein profiles were determined by quadrupole time-of-flight mass spectrometry (QTOF-MS). Results: In SEM, spherical structures with sizes ranging from 80 to 900 nm were visualized. EDS analyses showed that very low concentration of phosphorus (P: 0.3 %) indicated absence of nucleic acids. The resistance was observed to proteases. Also, protein profiles indicated human proteins, with a high percentage of albumin. Conclusion: It was determined that nanobacteria derived from atheroma plaque were structures composed of human proteins. The findings confirmed the theory that nanobacteria are non-living structures formed by a mechanism called biocrystallization. Although the accumulation of nanobacteria may be a contributing element to the creation of atheroma plaque, it is possible that the etiological components that initiate the formation of the plaque are not nanobacteria. |
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