Evaluation of tellurium toxicity in transformed and non-transformed human colon cells

Diphenyl ditelluride (DPDT) and tellurium tetrachloride (TeCl4) 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 TeCl4 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 TeCl4 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 TeCl4 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 TeCl4 treatment in necrosis. GSH/GSSG ratio shifts indicate oxidative mechanisms are involved.

► HT-29, Caco-2 and CCD-18Co cells treatment with Te compounds resulted cytotoxicity. ► DPDT caused apoptosis in HT-29 and CCD-18Co cells and TeCl4 treatment caused necrosis. ► Intrinsic pathway was involved in HT-29 and CCD-18Co cells treated with DPDT. ► No release of caspase 3/7 or 9 was observed in TeCl4 treated cells. ► Altered GSH/GSSG ratios in HT-29 and CCD-18Co cells suggest oxidative process.