Modulation of intracellular calcium homeostasis by trimethyltin chloride in human tumour cells

Neuroblastoma SY5Y and cervix adenocarcinoma HeLa S3

Ana Maria Florea, Frank Splettstoesser, Elke Dopp, Albert W. Rettenmeier, Dietrich Busselberg

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Physiological modifications of intracellular Ca2+ ([Ca 2+]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 (Me 3SnCl; 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 μM ∼125.6%; 5 μM ∼130.1%; 500 μM ∼145% in HeLa S3 cells and 0.5 μM ∼133.3%; 5 μM ∼136.1%; 500 μM ∼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: ∼109% (no calcium added) versus ∼117% (2 mM calcium; 5 μM TMT) in HeLa cells. This difference was similar in neuroblastoma SY5Y cells, were ∼127% versus ∼136% increase (5 μM 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.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalToxicology
Volume216
Issue number1
DOIs
Publication statusPublished - 1 Dec 2005
Externally publishedYes

Fingerprint

Neuroblastoma
Cervix Uteri
Tumors
Adenocarcinoma
Homeostasis
Cells
Modulation
Calcium
HeLa Cells
Neoplasms
Trimethyltin Compounds
trimethyltin chloride
Neuronal Plasticity
Poisons
Cell proliferation
Cytotoxicity
Muscle Contraction
Confocal Microscopy
Plasticity
Neurotransmitter Agents

Keywords

  • Calcium homeostasis
  • HeLa S3
  • Human cervix adenocarcinoma
  • Human neuroblastoma SY5Y
  • Human tumour cells
  • TMT
  • Trimethyltin chloride

ASJC Scopus subject areas

  • Toxicology

Cite this

Modulation of intracellular calcium homeostasis by trimethyltin chloride in human tumour cells : Neuroblastoma SY5Y and cervix adenocarcinoma HeLa S3. / Florea, Ana Maria; Splettstoesser, Frank; Dopp, Elke; Rettenmeier, Albert W.; Busselberg, Dietrich.

In: Toxicology, Vol. 216, No. 1, 01.12.2005, p. 1-8.

Research output: Contribution to journalArticle

Florea, Ana Maria ; Splettstoesser, Frank ; Dopp, Elke ; Rettenmeier, Albert W. ; Busselberg, Dietrich. / Modulation of intracellular calcium homeostasis by trimethyltin chloride in human tumour cells : Neuroblastoma SY5Y and cervix adenocarcinoma HeLa S3. In: Toxicology. 2005 ; Vol. 216, No. 1. pp. 1-8.
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abstract = "Physiological modifications of intracellular Ca2+ ([Ca 2+]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 (Me 3SnCl; TMT) modulates calcium homeostasis in cervix adenocarcinoma (HeLa S3) cells [Florea, A.-M., Dopp, E., B{\"u}sselberg, 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 μM ∼125.6{\%}; 5 μM ∼130.1{\%}; 500 μM ∼145{\%} in HeLa S3 cells and 0.5 μM ∼133.3{\%}; 5 μM ∼136.1{\%}; 500 μM ∼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: ∼109{\%} (no calcium added) versus ∼117{\%} (2 mM calcium; 5 μM TMT) in HeLa cells. This difference was similar in neuroblastoma SY5Y cells, were ∼127{\%} versus ∼136{\%} increase (5 μM 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.",
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