The role of element homeostasis in neoplastic disease pathogenesis is be-yond question. The imbalance of trace elements precisely underlies the ini-tiation and promotion of tumor pathology. The aim of the study was to...The role of element homeostasis in neoplastic disease pathogenesis is be-yond question. The imbalance of trace elements precisely underlies the ini-tiation and promotion of tumor pathology. The aim of the study was to in-vestigate blood and tissue macroelements, microelements and hemoproteins level in brain tumors and their intermolecular interactions. Samples of blood and brain tumor tissues were investigated. Detection of myoglobin level was implemented by the reaction of passive hemagglutination and immunoturbidimetric test. Catalase activity was determined by the method of Beer and Sizer. Free radical activity was determined by the method of induced biochemiluminescence. Microelements level was investigated by usage of atomic emission spectrometry. To build the networks of studied hemoprotein interactions with signaling pathways of proteins, expressed in brain tumors, molecular interaction databases (STRING, BioGrid) were used. Modern databases of signaling pathways (KEGG) suggest that in normal cells hypoxia can lead to HIF-1A protein synthesis. ROS synthesis inhibits the PHD enzyme and triggers the release of calcium ions, and increases proliferation. Calcium ions are triggering factor of apoptosis and cell proliferation. Myoglobin can possibly be the cell adaptation factor towards hypoxia, oxidative stress and element homeostasis violation, and myoglobin level decreasing can additionally stimulate proliferation, by apoptosis inhibition.展开更多
文摘The role of element homeostasis in neoplastic disease pathogenesis is be-yond question. The imbalance of trace elements precisely underlies the ini-tiation and promotion of tumor pathology. The aim of the study was to in-vestigate blood and tissue macroelements, microelements and hemoproteins level in brain tumors and their intermolecular interactions. Samples of blood and brain tumor tissues were investigated. Detection of myoglobin level was implemented by the reaction of passive hemagglutination and immunoturbidimetric test. Catalase activity was determined by the method of Beer and Sizer. Free radical activity was determined by the method of induced biochemiluminescence. Microelements level was investigated by usage of atomic emission spectrometry. To build the networks of studied hemoprotein interactions with signaling pathways of proteins, expressed in brain tumors, molecular interaction databases (STRING, BioGrid) were used. Modern databases of signaling pathways (KEGG) suggest that in normal cells hypoxia can lead to HIF-1A protein synthesis. ROS synthesis inhibits the PHD enzyme and triggers the release of calcium ions, and increases proliferation. Calcium ions are triggering factor of apoptosis and cell proliferation. Myoglobin can possibly be the cell adaptation factor towards hypoxia, oxidative stress and element homeostasis violation, and myoglobin level decreasing can additionally stimulate proliferation, by apoptosis inhibition.
