Cell viability modulation through changes of Ca2+-dependent signalling pathways

The aim of the study was to determine the correlations between intracellular calcium ion level and a cell's ability to survive. The intracellular concentration of Ca2+ ions, maintained through different mechanisms, plays an important role in signalling in cells. The deregulation of these mechanisms by various cell stressors (e.g. cytotoxic agents) can disturb Ca2+ homeostasis and influence Ca2+-dependent signalling pathways in the cell. Perturbations of intracellular electrochemical equilibrium may lead to changes in cell function or even to cell death. According to some experimental results, one of the cell stressors may be exposure to magnetic fields (MF). Because of the wide distribution of MF sources in our environment, magnetic fields have recently been intensively examined in relation to the occurrence of cancer. Nevertheless, two questions still remain unanswered: Is the influence of MF on cells positive or negative, and what mechanism(s) underlie the effects of MF action on cells? Most studies focus on the influence of MF on Ca2+ ion fluxes as calcium ions play the role of intracellular second messengers, triggering many signalling cascades. Physical models assuming the mechanisms generating the disturbance of ionic transport and/or the dysfunction of ion–protein complexes in cells due to MF action have been widely discussed in the literature, but a detailed explanation of experimental results is still awaited.The dynamics of the concentration of intracellular calcium ions can be detected by various methods, including optical and non-optical techniques. This review combines an insight into basic intracellular Ca2+ regulative mechanisms and common techniques used to detect changes in Ca2+ concentration inside the cell. The emphasis here is on the determination of Ca2+ regulative mechanisms developed in non-excitable cells (e.g. U937 cells, HeLa, etc.), which are probably mainly involved in cell responses to external stress (e.g. MF stimuli).