کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2582771 | 1561701 | 2016 | 9 صفحه PDF | دانلود رایگان |
• 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.
Journal: Environmental Toxicology and Pharmacology - Volume 43, April 2016, Pages 216–224