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Evaluation of tellurium toxicity in transformed and non-transformed human colon cells
1Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St John's University, Queens, NY 11439, USA.
Abstract:
Diphenyl ditelluride (DPDT) and tellurium tetrachloride (TeCl(4)) were evaluated for toxicity in transformed (HT-29, Caco-2) and non-transformed colon cells (CCD-18Co). Significant decreases in viability were observed with DPDT exposure in HT-29 (62.5-1000 μM), Caco-2 (31.25-1000 μM) and CCD-18Co cells (500-1000 μM) and with TeCl(4) in HT-29 (31.25-1000 μM), Caco-2 (31.25-1000 μM) and CCD-18Co cells (500-1000 μM). Light microscopy confirmed viability analysis. Significant increases in caspase 3/7 and 9 activity were observed with DPDT in HT-29 (500-1000 μM) and CCD-18Co cells (1000 μM) indicating apoptosis. No significant increases in caspases were seen with TeCl(4) indicating necrosis. Apoptosis or necrosis was confirmed with fluorescent staining (FITC-Annexin, Hoechst 33342 and Ethidium Homodimer). Significant decreases in GSH/GSSG ratio were observed with DPDT in HT-29 (62.5-1000 μM), and CCD-18Co cells (1000 μM) and with TeCl(4) in HT-29 (62.5-1000 μM) and CCD-18Co cells (250-1000 μM). We concluded that cells treated with DPDT resulted in apoptosis and TeCl(4) treatment in necrosis. GSH/GSSG ratio shifts indicate oxidative mechanisms are involved.
Insights
Diphenyl ditelluride (DPDT) induces apoptosis in colon cells, while tellurium tetrachloride (TeCl4) causes necrosis. Both compounds decrease cell viability and alter the glutathione redox state, suggesting oxidative stress mechanisms in toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Biochemistry
Background:
- Organotellurium compounds exhibit diverse biological activities.
- Understanding the cytotoxic mechanisms of diphenyl ditelluride (DPDT) and tellurium tetrachloride (TeCl4) is crucial for assessing their potential applications and risks.
Purpose of the Study:
- To evaluate the toxicity of DPDT and TeCl4 in human colon cell lines.
- To determine the mode of cell death (apoptosis vs. necrosis) induced by these compounds.
- To investigate the role of oxidative stress in their cytotoxic effects.
Main Methods:
- Cell viability assays (MTT or similar) were performed on transformed (HT-29, Caco-2) and non-transformed (CCD-18Co) colon cells.
- Light microscopy was used to confirm observations from viability assays.
- Caspase 3/7 and 9 activity assays were conducted to detect apoptosis.
- Fluorescent staining (FITC-Annexin V, Hoechst 33342, Ethidium Homodimer) was employed to confirm apoptosis or necrosis.
- Glutathione (GSH/GSSG) ratio was measured to assess oxidative stress levels.
Main Results:
- Both DPDT and TeCl4 significantly reduced cell viability across all tested colon cell lines in a dose-dependent manner.
- DPDT exposure led to significant increases in caspase 3/7 and 9 activity, indicating apoptosis.
- TeCl4 treatment did not significantly increase caspase activity, suggesting necrosis as the primary mode of cell death.
- Both compounds caused significant decreases in the GSH/GSSG ratio, indicating the involvement of oxidative stress.
Conclusions:
- DPDT induces apoptosis in colon cells, whereas TeCl4 induces necrosis.
- Both compounds exhibit cytotoxic effects on colon cells through mechanisms involving oxidative stress.
- The differential induction of apoptosis and necrosis by DPDT and TeCl4 highlights distinct cellular responses to these organotellurium compounds.
