Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2582771 | Environmental Toxicology and Pharmacology | 2016 | 9 Pages |
•Exposure of HT-29 and CCD-18Co cells to DPDT and TeCl4 causes Te accumulation.•Te treatment of HT-29 & CCD-18Co cells induces HO-1 confirming oxidative stress.•Te treatment of HT-29 & CCD-18Co cells shows varied gene alterations.
The current study evaluated the potential of TeCl4 and DPDT to accumulate within cells and cause oxidative stress. HO-1, antioxidant gene expression and protein alterations were studied.•Significant Te accumulation was observed in HT-29 cells (500–1000 μM DPDT; 125–1000 μM TeCl4) and CCD-18Co cells (500 μM DPDT and TeCl4).•Significant increases in HO-1 were observed with 250–1000 μM DPDT and 62.5–1000 μM TeCl4 in HT-29 cells and in 500–1000 μM DPDT and 62.5–1000 μM TeCl4 in CCD-18Co cells.•In CCD-18Co cells, a significant increase in COX-2 was observed at 500–1000 μM DPDT and 125–1000 μM TeCl4.•Significant increase in NQO1 was observed with exposure to 500–1000 μM DPDT and TeCl4.•In HT-29 cells, increased CYGB was noted at concentrations of 500–1000 μM DPDT and TeCl4, while significant increases were noted in NCF-1at 1000 μM DPDT and TeCl4.•No change in MT-3 and GSR were observed in either cell line.