Tumour cell uptake G2-M accumulation and cytotoxicity of NAMI-A on TS/A adenocarcinoma cells

Anticancer Res. 2001 May-Jun;21(3B):1893-8.

Abstract

The ruthenium(III) complex imidazolium trans-imidazoledimethylsulfoxide-tetrachlororuthenate (NAMI-A) was tested on TS/A adenocarcinoma cells to evaluate the relationship between cell uptake, cell cycle arrest and cytotoxicity. The in vitro challenge of TS/A cells with 10(-4) M NAMI-A for 15 minutes to 4 hours showed a partial reduction of cell growth only after 4 hour exposure. In the same experimental conditions NAMI-A caused the increase of cells in G2-M cell cycle phase directly proportional on the length of treatment, and the ruthenium uptake by tumour cells, measured by flameless atomic absorption spectroscopy, that increases up to 2 hours of treatment and then reaches a plateau. The arrest of cell cycle in the pre-mitotic G2-M phase was transient and completely reversed by 48 hours after treatment. This study showed that the effect of NAMI-A on the cell cycle of TS/A cells is not strictly related to NAMI-A uptake as is the effect on tumour cell proliferation.

MeSH terms

  • Adenocarcinoma / drug therapy*
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / toxicity*
  • Cell Cycle / drug effects
  • Cell Division
  • Dimethyl Sulfoxide / analogs & derivatives
  • Dimethyl Sulfoxide / pharmacokinetics*
  • Dimethyl Sulfoxide / toxicity*
  • Flow Cytometry
  • G2 Phase*
  • Mitosis*
  • Organometallic Compounds / pharmacokinetics*
  • Organometallic Compounds / toxicity*
  • Ruthenium / pharmacology
  • Ruthenium Compounds
  • Spectrophotometry, Atomic
  • Time Factors
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • Organometallic Compounds
  • Ruthenium Compounds
  • imidazolium-bis(imidazole)dimethylsulfoxideimidazotetrachlororuthenate(III)
  • Ruthenium
  • Dimethyl Sulfoxide