Physiological modifications of intracellular Ca2+ ([Ca2+]i) levels trigger and/or regulate a diversity of cellular activities (e.g.
neurotransmitter release, synaptic plasticity, muscular contraction, cell proliferation), while
calcium overloads could result in cytotoxicity. Previously, we have shown that
trimethyltin chloride (Me3SnCl; TMT) modulates
calcium homeostasis in cervix
adenocarcinoma (HeLa S3) cells [Florea, A.-M., Dopp, E., Büsselberg, D., 2005. TMT induces elevated
calcium transients in HeLa cells: types and levels of response. Cell
Calcium 37, 252-258]. Here we compare [Ca2+]i-changes induced by
trimethyltin chloride in
neuroblastoma SY5Y and HeLa S3 cells using
calcium-sensitive
dyes (
fluo-4/AM (
fluo-4) and rhod-2/AM (rhod-2)) and
laser scanning microscopy (LSM). TMT-induced
calcium elevations in
neuroblastoma SY5Y as well as in HeLa S3 cells. [Ca2+]i rose to a sustained plateau or to transient spikes. Overall, the detected averaged increase of the maximum
calcium elevation were: 0.5 microM approximately 125.6%; 5 microM approximately 130.1%; 500 microM approximately 145% in HeLa S3 cells and 0.5 microM approximately 133.3%; 5 microM approximately 136.1%; 500 microM approximately 147.1% in
neuroblastoma SY5Y cells. The
calcium rise derived from internal stores did not significantly depend on the presence of
calcium in the external
solution: approximately 109% (no
calcium added) versus approximately 117% (2 mM
calcium; 5 microM TMT) in HeLa cells. This difference was similar in
neuroblastoma SY5Y cells, were approximately 127% versus approximately 136% increase (5 microM TMT) were measured. Staining of
calcium stores with
rhod-2 showed a TMT-induced [Ca2+]i-decrease in the stores followed by an increase of the
calcium concentration in the nuclei of the two cell lines tested. Our results suggest that toxic effects in human tumour cells after exposure to
trimethyltin compounds might be due to an elevation of [Ca2+]i.