Antiproliferative activity of some cis-/trans-platinum(II) complexes on HeLa cells.

Purpose of this work was to synthesize several cis-/trans- isomer pairs of the platinum(II) complexes, and study the extent and the mode of their antiproliferative activity on HeLa cells. Six platinum(II) isomer pairs have a general formula cis-/trans-[PtA2X2], where A is ligand: ammonia (NH3), pyridine (Py); and X is ligand: chloride ion (Cl-), bromide ion (Br-), iodide ion (I-), thiocyanato ion (SCN-); four compounds have different structural formulas, and these are cis-/trans-[Pt(NH2OH)2(NH3)2]Cl2, and cis-/trans-Pt(Gly)2, where Gly is bidentate glycinato ligand. Results of the MTT assay, showed that six cis- and one trans-platinum(II) complexes exhibited cytotoxicity (IC50) ranging between 5 and 33 microM. Most of the cis-platinum(II) isomers caused significant alteration of cell cycle phases progression, and induced apoptosis in degree that varied among different compounds, as evaluated using flowcytometry and morphological study. Spectrophotometric analysis (AAS) indicated that there is no correlation between intracellular platinum(II) accumulation and cytotoxicity of tested complexes.

Activity of glutathione peroxidase and superoxide dismutase in workers occupationally exposed to mercury.

According to previous research the lipid peroxidation process has a significant role in mercury toxicity. Since glutathione peroxidase (GPX) and superoxide dismutase (SOD) play a significant role in erythrocyte antioxidative defence, it is very important to determine their activity in occupationally exposed workers. The aim of this study was to assess the activity of antioxidative enzymes in the erythrocytes of workers occupationally exposed to mercury. We compared a group of 42 workers exposed to elemental mercury in a chloralkali plant (Hg group). The control group (C group) consisted of 75 subjects employed in lime production who had never been exposed to mercury or any toxic substance. The GPX activities in erythrocytes were significantly lower in the Hg group than in the control group (Hg group, 9.05 +/- 7.52 IU/gHb; C group 15.54 +/- 4.85 IU/gHb; p < 0.001). Also, SOD activity in the erythrocytes of workers occupationally exposed to mercury was significantly lower than in the control group (Hg group, 1280.7 +/- 132.3 IU/gHb; C group, 1377.9 +/- 207.5 IU/gHb; p < 0.006). The concentrations of mercury in blood were significantly higher in the Hg group compared to the control group (Hg group, 0.179 +/- 0.040 micromol/l; C group, 0.023 +/- 0.011 micromol/l; p < 0.001). Urine mercury concentrations were also significantly higher in the Hg group than in the control group (Hg group, 23.2 +/- 11.3 nmol/mmol creatinine; C group, 2.7 +/- 0.6 nmol/mmol creatinine; p < 0.001). The concentrations of selenium in erythrocytes were almost equal in both groups examined (Hg group, 62.9 +/- 8.72 microg/l; C group, 65.8 +/- 10.57 microg/l). Also, in the Hg group there were increased levels of erythrocyte malondialdehyde (Hg group, 138.58 +/- 33.85 micromol/l; C group 105.21 +/- 49.62 micromol/l; p < 0.001). On the basis of previous results, it can be concluded that occupational exposure to elemental mercury leads to increased lipid peroxidation in erythrocytes. Also, it can be postulated that this exposure leads to decreased activity of GPX and SOD in erythrocytes.